1 / 22

Carbon Monoxide Poisoning

Carbon Monoxide Poisoning.ppt

baktijp
Download Presentation

Carbon Monoxide Poisoning

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Environmental MedicineCarbon Monoxide PoisoningBarotraumaCaisson Disease Don Hudson, D.O., FACEP/ACOEP

  2. Introduction • Medicine related to physical phenomena • Barotrauma and temperature • But first, carbon monoxide poisoning • Consider Mass Injuries

  3. Carbon monoxide • Colorless, odorless tasteless non-irritant gas from incomplete combustion of organic materials • 1-2% COHb in non-smokers, 5-6% in smokers. • Approx. 1,000 people die /year from CO poisoning. Less now natural gas has replaced coal gas.

  4. Toxicity • 1985 - 1365 deaths - 475 admissions & 10 deaths in hospitals in the UK. • 3800 die per annum in US • > 10,000 days at work lost • Main cause of death in children • Recent deaths in Anchorage

  5. Toxicity • Common sources • car exhausts (lethal in closed garage in <10 min) (NB catalysts) • Unserviced heating systems • Fires - all sorts • Methylene chloride (paint stripper) • Some types of insulations

  6. Physiology • Binds to Hb with an affinity 200-250 times that of oxygen. • Forms carboxyhemoglobin, reducing the total oxygen-carrying capacity of blood and shifting O2 dissociation curve to the left. • Alters shape of Hb molecule making it less ready to release O2. • Binds to cellular proteins e.g. cytochrome oxidase similarly to cyanide. • t½ 250 min in air

  7. Clinical manifestations • Varied • Depends on • CO concentration • length of exposure • general health of exposed person • Infants, elderly, CVS disease, anemia, lung disease and patients with increased metabolic rate are at risk

  8. Chronic exposure to low concentrations • Headache, fatigue, dizziness, difficulty in concentration, paraesthesia, chest pain, palpitations, visual disturbances, nausea, diarrhea, abdominal pain. • Can easily be mistaken for other illnesses. • Should be considered in vague presentations.

  9. Acute poisoning • Clinical findings do NOT correlate well with CO concentrations • <10% - asymptomatic • 10-30% - headache, mild exertional dyspnea, “gastro-enteritis”. • Coma, seizures, cardiorespiratory arrest if >60% • Live patients are pale, NOT pink.

  10. Neuropsychiatric problems • Insidious • Intellectual deterioration, memory impairment, Parkinsonism, akinetic mutism; damage to any area but especially globus pallidus, cerebral cortex, hippocampus and substantia nigra. • Personality changes - not for better

  11. Treatment • Remove from source • 100% O2 by close-fitting facemask - intubate and ventilate EARLY if unconscious as high incidence of regurgitation is present. • Dissociation from Hb occurs readily - elimination t½ <50 min with 100% O2 • Hyperbaric treatment at 2.5bar reduces this to 22 minutes and dissolves enough O2 to meet needs of body without Hb.

  12. Results of hyperbaric therapy • First used successfully in Glasgow in 1960s. • Reduces morbidity from 43% to <5%. • Can even be used in late-presenting cases with high CO levels. • Early treatment associated with better outcomes • General support also necessary.

  13. Hyperbaric Therapy • Currently there is no medical facility, in Anchorage, equipped to do this. • There is only one outside vendor available to perform this service. • The staffing of the chamber is a major problem.

  14. Blast injury • 6 separate mechanisms of injury: • Blast wave. Transient high pressure wave • Cellular disruption at air-tissue interface • perforated eardrum at +1bar • “blast lung” at +1.75 bar • shearing at tissue planes - submucosal/serosal bleed • sudden expansion of compressed trapped gas in bowel or blood vessels leading to perforation or air embolism • Blast lung often delayed up to 48 hours • Rare in survivors (0.6%)

  15. Blast injury mechanisms • Blast wind • In the immediate vicinity will fragment bodies • Further away will produce blast limb avulsions • Blast transportation leading to secondary impact injuries • Injuries from flying debris/secondary missiles

  16. Blast injury mechanisms • Missiles • Bomb fragments (casing, elements deliberately included - nuts, nails, ball-bearings) • Secondary missiles picked up by blast wind; glass, pieces of vehicles etc

  17. Blast injury mechanisms • Flash burns • Crush injuries - from falling masonry, pieces of vehicle etc • Psychological effects - particularly with terrorist weapons.

  18. Blast injury treatment • ABC - but try to avoid ventilating patients with lung injury • Care with extremities crushed for prolonged periods • Preserve all and any debris and its location for forensic analysis

  19. Caisson disease- Bends • Gas dissolves in blood in proportion to ambient pressure. • Rapid reductions in pressure cause bubbles to form in the tissues • Risk factors: multiple dives, rapid ascent, poor discipline & flying home • Presents 1-36 hours later - can be anywhere in the world

  20. Presentations of Caisson disease • Throbbing muscle and joint pain • Migrating skin mottling/rashes • Coughs and chest pain • CNS signs • headache • seizures • deafness/ nystagmus • mood changes

  21. Treatment of Caisson diseaseor BENDS • Act rapidly • Avoid aspirin and opiates • Recompress urgently. • Recompression <30min after onset of symptoms >80% respond • After 6hour delay 50% respond • Fly (Cab Alt)as low as practicable

  22. Summary • CO season • Blast and pressure disease • Comments? • Questions?

More Related