Colourless, odourless, non-flammable gas which is heavier than air. In its solid form (dry ice) it is whitish in colour and acts as a corrosive.
· Fire extinguisher.
· Carbonation of soft drinks.
· Shielding gas during welding processes.
· Synthesis of urea, for dry ice, and organic synthesis.
Four stages have been described, depending on the arterial oxygen saturation:
–– %O2 Saturation: 90%
–– Night vision: decreased.
–– %O2 Saturation: 82 to 90%
–– Respiratory rate: compensatory increase
–– Pulse: compensatory increase
–– Night vision: decreased further
–– Performance ability: somewhat reduced
–– Alertness: somewhat reduced
–– Symptoms may begin in those with significant pre-existing cardiac, pulmonary, or haematologic diseases.
–– %O2 Saturation: 64 to 82%
–– Compensatory mechanisms become inadequate –– Air hunger
–– Tunnel vision
–– Visual acuity: reduced
–– Numbness and tingling of extremities
–– Poor judgement
–– Memory loss
–– Decreased ability for escape from toxic environment.
–– %O2 Saturation: 60 to 70% or less
–– Deterioration in judgement and co-ordination may occur in 3 to 5 minutes or less
–– Total incapacitation and unconsciousness follow rapidly.
Unconsciousness leading to death will occur when the atmospheric oxygen concentration is reduced to 6 to 8% or less. Concentrations up to 35% CO2 have an exciting effect upon both circulation and respiration. Concentrations above 35% have a depressing effect upon both circulation and respiration. Bradycardia progressing to asystole may occur in the absence of signs of cyanosis following inhalation exposure to 99.97% carbon dioxide. Investigators suggest hypercapnia and acidosis may contribute to the cause of cardiac arrest.
Dermal exposure to solid carbon dioxide (“dry ice”) may cause frostbite injury. Severe tissue burns have been reported.
Arterial blood gases are useful to assess the degree of hypox-aemia.
· Move patient from the toxic environment to fresh air.
· Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis. perform endotracheal intubation, and provide assisted ventilation as required.
· If hypoxia has been severe or prolonged, carefully evaluate for neurologic sequelae and provide supportive treatment as indicated.
Treatment of frostbite:
o Freeze injury associated with dermal exposure to “dry ice” is unlike frostbite in that the damage occurs within seconds and rewarming is not beneficial.
o Some investigators suggest that freeze injuries of this nature should be managed much like a thermal burn.
o Burn surgeons should be consulted in the more severe cases.
o Do not institute rewarming unless complete rewarming can be assured; refreezing thawed tissue increases tissue damage. Place affected area in a water bath with a temperature of 40 to 420C for 15 to 30 minutes until thawing is complete. Some authors suggest that an antibacterial (hexachlorophene or povidone-iodine) be added to the bath water.
· Correct systemic hypothermia.
· Rewarming may be associated with increasing pain, requiring narcotic analgesics.
o Digits should be separated by sterile absorbent cotton; no constrictive dressings should be used. Protective dressings should be changed twice per day. Perform daily hydrotherapy for 30 to 45 minutes in warm water 400C. This helps debride devitalised tissue and maintain range of motion.
o The injured extremities should be elevated and should not be allowed to bear weight.
o Prophylactic antibiotics are recommended by some investigators.
o Topical aloe vera may decrease tissue destruction and should be applied every 6 hours.
o Ibuprofen is a thromboxane inhibitor and may help reduce tissue loss. Adult dose of 200 mg every 12 hours is recommended.
· Most cases are accidental resulting from inadvertent build- up of CO2 in a confined space.
· Dry ice can generate toxic concentrations of CO . Release of carbon dioxide from rising colder, deep water producing a deadly cloud of gas has been postulated to explain the deaths associated with the Lake Nyos disaster of August 21, 1986, Lake Monoun disaster of August 1984, and Dieng Plateau, Indonesia disaster of February 20, 1979. Survivors of the Lake Nyos disaster in August, 1986 were noted to have superficial blisters which healed rapidly. Characteristics of the blisters suggested that they were the result of depriving the skin of oxygen. Hospitalised and outpatient survivors had symptoms compatible with exposure to a suffocating gas. Many survivors had lost consciousness for hours (6 to 36 hours) after the incident. Cough, headache, fever, weakness or malaise, and limb swelling were frequently noted (10% or more incidence) among the victims. Evidence after the incident suggested a slow build-up of carbon dioxide deep in the lake, followed by its release as a cold, suffocating aerosol. Dogs, cats, cattle, goats, chickens, snakes, and frogs were also found dead in their tracks. Insect life was noted to be absent for approximately 24 hours following the incident.
· Excess levels of carbon dioxide, ammonia, and other asphyxiant gases have been theorised to accumulate at the face of a sleeping infant. If the infant is unable to change its position or breathing pattern, sudden infant death syndrome (SIDS) may result from asphyxiation. Asphyxia may be due to an excess of CO2 and abnormal reflex actions connected with breathing and swallowing.
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