04 toxic gases

8/12/2019 04 Toxic Gases

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By

Dr.Nirmala Perera


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Irritant Gases- causes irritation of therespiratory tract

Simple Asphyxiants- interferes withgaseous exchange only. They are notabsorbed


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Clinical Asphyxiants- Are absorbed into thelungs and causes various actions

Eg combines with Hb

Causes haemolysis

Interfere with cellular oxidation

Depress the brain and causes respiratory depressionand paralysis


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Simple asphyxiant gas

Sources- In anaesthesia,

Industrial- eg. Mines, disused wells, pits, shipholds, burning of lime, wood & coal, BreweriesMineral water plants


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Normal levels- O.3% > 3% - Headache, drowsiness, dizziness,

giddiness, muscle weakness ( prevents runningaway from the area)

10% - loss of consciousness

25-30% - minimal fatal concentration

60- 80% Instance collapse and death (tissueanoxia)


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It is odourless, rapidly absorbed when inhaled andcombines with haemoglobin to form carboxy-haemoglobin which is stable than oxy-

haemoglobin.

The affinity of CO for Hb is more than Oxygen


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Coal gas

Exhaust fumes of motor vehicles and other engines

Incomplete combustion in closed surroundings

Industrial gases

Circumstances : Suicidal and accidental


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The symptoms depends on the bloodconcentration of CO

Up to 20% - no symptoms

3%- street cleaners, traffic policemen

5%- heavy smokers


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20% - Headache, dizziness and malaise

30% - giddiness & mild shortness of breath

40% - Confusion, in-coordination, staggering,fatigue of muscles


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50%- drunken gait, slurred speech,incoordination, exhaustion, vomiting, flushing,

sweating & pink colour of skin (mimicsdrunkenness and drug intoxication)

60% - respiratory distress, dilated pupils, loss of

consciousness 70% - coma & death


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History of exposure

Pink colour

Clinical features

Blood analysis( 5-10ml of blood with anti-coagulant)


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Pink colour of the skin, hypostasis, blood andinternal organs

Symmetrical softening of the basal ganglia

Hypostatic pneumonia (delayed death)


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SOURCES

Cyanide Gas

Fumigation of ships

Spraying in fruit orchards


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Cyanide saltsUsed in electroplanting, goldplating, photography & engraving

Laboratory useCyanide capsules

Cyanogenic Glycosides in plantmaterial


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SUICIDE- Biting of cyanide capsule by terrorists Ingestion of liquid potash by those in thejewellery/electroplating trade

Ingestion by laboratory workers

ACCIDENTAL Faulty fumigating techniques Laboratory accidents Plant material

HOMICIDAL Introduced into food or drink War gas used in world war 1 Gas chambers in Germans in world war II Execution by cyanide gassing/ingestion (USA)


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TWO FOLD ACTION

Inhibits the enzyme Cytochrome Oxidase

Acts as a corrosive because of its alkaline radical


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The rapidly absorbed cyanide is carried to thetissues in the blood stream

A cellular poison Strong affinity between cyanide and cytochrome

oxidase

Interfere with cellular utilization of oxygen

The cell cannot use oxygen although there isabundance of it in the blood stream

Cause cellular anoxia- Histotoxic or cytotoxic

anoxia


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SMALL DOSES Vertigo, headache, difficulty in breathing, loss of

muscle power & giddiness

LARGE DOSES Rapid loss of consciousness, collapse, twitching,

convulsions & death

The same is true for higher concentration of cyanidevapour


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History

Clinical features

Pink colour of extremities Smell of bitter almonds in the breath

The ability to smell is an inherited character.


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Red colour of skin, hypostasis, blood andvascular organs

Odour of bitter almonds or may be ammonia

Diffusely red mucosa of the GIT with orwithout areas of corrosion

Remnants of the capsule with cut injuries inthe mouth


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Embalming with formalin will rapidly

destroy cyanide

Postmortem decomposition produce tracesof cyanide


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Carbon dioxide- Accidental poisoning Co Suicidal and accidental poisoning

possible

CN- Suicidal and accidental poisoningpossible


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04 toxic gases

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