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.

Carbon monoxide1 | P a g e

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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

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,

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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 People suffering from anemia Smokers People engaged in intense physical activity in a poorly ventilated

area contaminated with carbon monoxide People living at altitude

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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:

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.

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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 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

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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

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

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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 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

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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.

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---

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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 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.

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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: Mild to moderate cases( 25% - 30%COHB )

o Malaise, flu-like symptoms, fatigueo Dyspnea o Chest pain, palpitationso Lethargyo Confusiono Depressiono Hallucination, confabulation

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o Agitationo Nausea, vomitingo Abdominal paino Headache, drowsinesso Dizziness, weaknesso 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 disturbanceo Syncopeo seizureso Memory and gait

disturbanceso Bizarre neurologic

symptomso comao Mild fever

COHb Levels and Symptomatology

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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 signso Tachycardiao Hypertension or hypotensiono Hyperthermiao 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")

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10%Asymptomatic or may have headaches

20%Dizzyness, nausea, and syncope

30% Visual disturbances

40% Confusion and syncope

50% Seizures and coma

60%Cardiopulmonary dysfunction and death

More than 70-80%%

death

Toxic Gases

Pallor is present early more often . Ophthalmologic

o Flame-shaped retinal hemorrhageso 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

1 .History and clinical picture:

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

make the diagnosis.

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 intoxicationI) 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 showsbilaterally 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.

* Blood oxygen tension is a determinant of the rate of carboxyhemoglobin elimination.

*This therapy should be used until:

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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 CO from hemoglobin. While breathing

room air, this process is too slow it takes about 300 minutes. While on a 100% oxygen non-rebreather mask,

this time is reduced to about 90 minutes; with hyperbaric oxygen

therapy, the time is shortened to 32 minutes.

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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Oxygen % Half-Life (min.)

21 (room air) 240 - 300

80 80 - 100

100 50 - 70

100 (at 3 atm.)

20 - 25

Toxic Gases

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): 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

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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.

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

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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.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.

Prognosis28 | P a g e

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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. 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.

Chlorine Gas

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#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 Household accidents

involving the inappropriate mixing of hypochlorite cleaning solutions with acidic agents

Transportation releases Swimming pool chlorination tablet accidents

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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

permissible air levels may be difficult until irritative symptoms are present.

#Mechanism of activity

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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 :

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.

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#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 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

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# To summarized::

#Clinical picture:History:

Cough (52-80%) Shortness of breath (20-51%) Chest pain (33%)

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Burning sensation in the throat and substernal area (14%) Nausea or vomiting (8%) Ocular and nasal irritation (4-6%) Choking 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

InternationalInternationally, 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.

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DiagnosisLaboratory 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.

TreatmentPrehospital 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 function,

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whereas treatment in the supine position was associated with further compromise of pulmonary gas exchange.

Sodium bicarbonate oThe 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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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

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

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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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