1 / 76

Inhalational Poisoning

Inhalational Poisoning. Dr. CC Lau. Classification. Simple asphyxiants Chemical asphyxiants Pulmonary irritants Systemic toxicants. Factors. Concentration Duration of exposure Environment (enclosed space) Vapour density Toxic particle size and solubility Patient factors

moe
Download Presentation

Inhalational 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. Inhalational Poisoning Dr. CC Lau

  2. Classification • Simple asphyxiants • Chemical asphyxiants • Pulmonary irritants • Systemic toxicants

  3. Factors • Concentration • Duration of exposure • Environment (enclosed space) • Vapour density • Toxic particle size and solubility • Patient factors • (presence of fire / explosion, thermal unjuries)

  4. Oxygen • Essential for cellular respiration • “Oxygenation” affected by • Respiration suppression (opioids) • “Dilution” of oxygen in air • Simple asphyxiants (no direct toxic effect) • Interfere with gas exchange • Pulmonary irritants • Systemic toxic effects • affect oxygen binding to Hb (CO, Met-Hb) • Interfere with cellular respiration (Chemical asphyxiants, CN, CO, H2S)

  5. Simple Asphyxiants • Pathophysiology • Displace oxygen >> lowering FiO2 • Not irritating and no direct systemic toxic effect • Clinical effects due to HYPOXIA

  6. Clinical Findings Goldfrank’s Toxicologic Emergencies, 6th Edition

  7. Simple Asphyxiants • Carbon dioxide • Fire accident, dry ice, fire extinguishers, refrigerant • Nitrogen • Chromatography, fertilizer, cryogenic agent, scuba diving • Noble Gases • Welding operations, lasers, illumination

  8. Simple Asphyxiants • Hydrocarbon Gases • Methane • Natural gas, marsh gas, fire damp • Ethane • Natural gas, refrigerant • Propane • Fuel, solvent • Butane • Fuel, solvent

  9. Cameroon Lake Nyos

  10. Nearly 2,000 people perished down slope of LAKE NYOS in August, 1986, when a large volume of poisonous gas was suddenly released from the lake late one evening. People simply "went to sleep" that night, and few ever awoke. • Lake Nyos was a young volcanic maar, and that carbon dioxide of volcanic origin had been released from solution in the lake's waters. • CO2 is continuing to be supplied to the lake, and that other gas-release events are inevitable in the future. Permanent habitations in vulnerable areas down slope is now prohibited.

  11. Treatment for Simple Asphyxiants • 100% oxygen • Remove from exposure • ABCs and supportive care • Rapid resolution of symptoms unless end-organ damage has occurred

  12. Pulmonary Irritants • Direct toxic effect on the respiratory tract • Most severe - Acute Lung Injury (ALI) • Characterized by pulmonary inflammation and alveolar filling

  13. Pulmonary Irritants • Pathophysiology • As simple asphyxiants (at high concentration) • Direct local effects on mucosal surface

  14. Pulmonary Irritants • Site and onset of injury depends upon particle size and solubility (those with smaller particle size and low solubility can pass to more distal airways) • High solubility • Upper airway • Eyes • Nose • Low solubility • Lower respiratory tract

  15. Pulmonary Irritants

  16. Ammonia (NH3) Plastics, explosives, fertilizer, cleaning agent Hydrogen Chloride Pyrolysis of PVCs Commercial chemicals Sulphur Dioxide By-product found in smelting and oil refining Smog Dose-related bronchospasm Pulmonary Irritants - Examples

  17. Pulmonary Irritants - Clinical Effects • High water solubility gases • Rapidly irritating • Upper airways and eyes affected • Glottic inflammation may compromise airway • Prolonged exposure can result in bronchial/pulmonary effects

  18. Pulmonary Irritants - Clinical Effects • Intermediate water solubility gases • Delay to irritation concentration dependent • Low concentration or less irritating agents affect lower airways • May be delayed to ALI

  19. Pulmonary Irritants - Examples • Chlorine (Cl2) • Oxidizing agent; many industrial uses • Chemical warfare gas WWI • Swimming pool tablets; water treatment, compressed gas for direct chlorination of pool • Intermediate water solubility • HCl + HOCl >> ocular and upper airway irritation >> coughing, hoarseness, pulmonary oedema

  20. Pulmonary Irritants - Examples • Phosgene (COCl2) • Weapon of mass destruction WWI • Pleasant odor >> promote deep and prolonged breathing • Relatively water insoluble • Dissolution >> liberation of hydrochloric acid and reactive oxygen species • DELAYED onset of ALI, may be nearly a day

  21. Pulmonary Irritants – Clinical Effects • Low water solubility gases • Generally non-irritating • Exposure often prolonged resulting in pulmonary effects • May have pleasant smell • Bronchospasm • Delayed ALI • Bronchiolitis obliterans (BOOP)

  22. Nitrogen Dioxide • Silo filler’s disease • Inhalation due to accumulation of nitrogen dioxide from bacterial conversion of nitrates from fresh grains • Limited water solubility >> lower airway problem, slow conversion of nitrogen oxide to nitric acid in alveoli >> delayed alveolar injury • High conc. may lead to acute symptoms • “triphasic illness” • Delayed – bronciolitis obliterans

  23. Pulmonary Irritants - Treatment • General management • Remove from exposure • ABCs and supportive care; oxygen • -agonists • No role for steroids (except for bronchiolitis obliterans)

  24. Pulmonary Irritants - Treatment • Specific management • Aerosolized bicarbonate (2% solution) • Nebulized sodium bicarbonate for chlorine exposure • 1 part NaHCO3:3 parts water/saline • May also work for hydrogen chloride • Reduces symptoms; no data on outcome Chisolm CD. Ann Emerg Med, 1989;18:466

  25. Pulmonary Irritants - Treatment • Observation • No delayed toxicity from highly water soluble agents • Observe for durations of symptoms • Decreased solubility increases risk of ALI; onset may be delayed. • Admit for 24 hours / patient instructions • arrange follow-up (bronchiolitis obliterans)

  26. Simple vs Chemical Asphyxiants • All gases can act as simple asphyxiants • Chemical asphyxiants interfere with oxygen utilization by the body • Carbon monoxide • Hydrogen sulphide (H2S) • Cyanide

  27. Carbon Monoxide

  28. Carbon monoxide • Epidemiology - Leading cause of poisoning morbidity & mortality in US - Between 50 and 5000 deaths reported annually - about 1/2 suicides - about 1/3 are fire victims

  29. Sources of CO • Incomplete combustion of any carbonaceous material - Fires, particularly coal and wood

  30. Other Sources of CO • Methylene chloride - Found in paint and varnish removers - Metabolized to CO in the liver - Toxicity may be delayed 4-8 hours after exposure

  31. Risk factors for CO toxicity • Extremes of age • Pregnant women (fetus) • Pre-existing coronary artery disease

  32. Kinetics • Rapidly absorbed across alveolar membranes • Binds hemoglobin (Hb) with approximately 250 times greater affinity than oxygen • T1/2

  33. Pathophysiology • Carboxyhemoglobin (COHb) does not carry oxygen   O2 content in blood • Binding to myoglobin  impaired O2 extraction  myocardial & skeletal muscle hypoxia • Induces lipid peroxidation in CNS neurological sequelae *

  34. Glycolysis (cytosol) Glucose ADP+ NAD+ ATP NADH NADH NAD+ Lactate Pyruvate Pyruvate dehydrogenase complex Cori Cycle I III IV Acetyl-CoA Q Cyto C CoA-SH NADH O2 H2O NADH NAD+ NAD++ Electron Transport Chain (inner mitochondrial membrane) Inhibited by CO, CN, H2S Kreb’s Cycle (mitochondrial matrix) FADH2 NAD++ FADH NADH Impaired by hypoxemia ATP NADH NAD++

  35. Lipid peroxidation in the CNS

  36. Clinical Presentation • Acute symptoms are due to tissue hypoxia: heart and brain most affected - CNS: headache, dizziness, blurry vision, altered mental status, ataxia, seizures, coma - CVS: exertional dyspnea,  HR,  RR, hypotension, palpitations, angina, weakness, dysrhythmias, myocardial ischemia

  37. Clinical Presentation • Renal: acute renal failure • Musculoskeletal: rhabdomyolysis • Ocular: venous engorgement, rarely blindness • Dermal: bullae; cherry-red color (seen with severe exposure, generally after patient expires)

  38. Normal: 1-2%; higher in smokersPoor correlation with symptoms (expecially chronic exposure)Do not predict development of delayed sequelae COHb levels

  39. Outcome • 12% persistent CNS signs or symptoms • 12% delayed neurologic sequelae (overall) • 25% in severe patients • 2% death

  40. Delayed Neurologic Sequelae • Deterioration after lucid period of 2 days to 4 weeks (mean 15 days) • Elderly appear to be most susceptible • Most cases associated with LOC during acute phase • Characterized by: dementia, amnesia, apathy, hypokinesia, ataxia, tremor, memory impairment, parkinsonism

  41. Prognosis of Delay Neurologic Symptoms • Mild symptoms: • almost 100% resolution within 2 months • Severe symptoms: • 75% resolution within 1 yr • Mean 3-6 months

  42. Management • Remove from exposure; ABC’s • 100% O2 by non-breather mask • Check COHb level • Assess for evidence of end organ damage • Pregnancy test • Hyperbaric oxygen if indicated

  43. Reasons for HBO • COHb half-life • Displaces CO from myoglobin and cytochrome oxidase •  O2 content of blood and improves O2 delivery •  lipid peroxidation • Improved neurological outcome

  44. HBO Therapy • Goulon et al, Paris, 1962-69 • For CO and anoxia from coal gas • Experience with 302 patients Rx with HBO • HBO within 6 hrs: 13.5% mortality • HBO greater than 6 hrs: 30.1% mortality Goulon M, J Hyperbaric Med 1986;1:23

  45. HBO Randomized Clinical Trials Mild toxicity n= 65 Thom 1995 Weaver 2002 Raphael 1989 Mathieu 1996 Scheinkestel 1999 All, n= 150 All, n =629 Non-comatose, n - 299 All, n = 191 0.1 0.25 0.5 1 2 4 Benefit harm

  46. Randomized-controlled, double-blinded trials

  47. Hyperbaric Oxygen (HBO) • Indications 1) End organ damage - syncope, coma, seizures - myocardial ischemia or life-threatening dysrhythmia - persistent symptoms after treatment with normobaric O2

  48. Recommendations for HBO 2) COHb levels (regardless of symptoms) - > 25% - > 15% in pregnant woman Fetus • Fetal Hgb  affinity for CO • Lower PO2 3) Other considerations - abnormal neuropsychiatric exam - metabolic acidosis - inability to oxygenate

More Related