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Hazardous Material Medical Care Gas and Toxic Inhalation

October 28, 2003. Gases and Toxic Inhalation. 2. Outline. Inhalation exposureAsphyxiantsSimple asphyxiantsSystemic asphyxiantIrritant gases Smoke inhalationSemiconductors gases. October 28, 2003. Gases and Toxic Inhalation. 3. Inhalation exposure. The most common hazardous material exposureI

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Hazardous Material Medical Care Gas and Toxic Inhalation

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    1. October 28, 2003 Gases and Toxic Inhalation 1 Hazardous Material Medical Care Gas and Toxic Inhalation ?.?. ????? ?????? ?????????????????? ?????????????? ??? ???????????????????? ??????????????????????????????? ?????????????????????????? ??????????? ????? toxbuster@hotmail.com

    2. October 28, 2003 Gases and Toxic Inhalation 2 Outline Inhalation exposure Asphyxiants Simple asphyxiants Systemic asphyxiant Irritant gases Smoke inhalation Semiconductors gases

    3. October 28, 2003 Gases and Toxic Inhalation 3 Inhalation exposure The most common hazardous material exposure Involves large number of cases Low potential for secondary contamination Asphyxiant: Simple asphyxiant Systemic asphyxiants

    4. October 28, 2003 Gases and Toxic Inhalation 4 Simple asphyxiants Displace oxygen from ambient air Decrease FiO2 Inadequate oxygen for hemoglobin saturation No pharmacological effects Needs high ambient concentration to cause asphyxia Situations: Confined space High ambient concentration -- compressed liquefied gas

    5. October 28, 2003 Gases and Toxic Inhalation 5 Simple asphyxiants: Clinical manifestations Symptoms of hypoxia CVS and CNS effects predominate No hypercapnia No dyspnea until severe hypoxia Many cases pass out and die before developing obvious symptoms

    6. October 28, 2003 Gases and Toxic Inhalation 6

    7. October 28, 2003 Gases and Toxic Inhalation 7 Simple asphyxiants: specific agents Noble gases: Helium, argon, xenon Short chain-aliphatic hydrocarbon gases: methane, ethane, propane, butane Carbon dioxide Nitrogen gases

    8. October 28, 2003 Gases and Toxic Inhalation 8 Simple asphyxiants: treatment Decontamination: not needed Removal from exposure Respiratory support Supplemental oxygen Ventilation if needed No role of hyperbaric oxygen

    9. October 28, 2003 Gases and Toxic Inhalation 9 Systemic asphyxiants Carbon monoxide Cyanide Hydrogen sulfide

    10. October 28, 2003 Gases and Toxic Inhalation 10 Carbon monoxide (CO) A leading cause of death from poisoning in western countries Carbon monoxide: product of combustion of organic materials Colorless, odorless and non-irritating gas Major sources in Thailand: Smoke inhalation Exposure to methylene chloride (paint remover): inhalation, skin, ingestion conversion into carbon monoxide

    11. October 28, 2003 Gases and Toxic Inhalation 11 Carbon monoxide poisoning CO is inhaled and absorbed at the rate proportional to respiration Confined to blood and 15% to tissue predominately myoglobin Elimination by gas exchange with half-life 4-6 hours at room air CO 200-250 times affinity to hemoglobin when compared to oxygen Shift oxyhemoglobin dissociation curve leftward CO 60 times affinity to myoglobin when compared to oxygen

    12. October 28, 2003 Gases and Toxic Inhalation 12

    13. October 28, 2003 Gases and Toxic Inhalation 13 Acute carbon monoxide poisoning ‘Flu-like symptoms’ Headache and dizziness Nausea, weakness, difficulty with concentration Mild tachycardia and tachypnea Syncope, seizures, altered mental status Acute metabolic acidosis Cherry red skin

    14. October 28, 2003 Gases and Toxic Inhalation 14 Anginal chest pain in patients with predisposing coronary artery disease Ischemic heart disease, cardiac arrhythmias and complications of IHD Acute carbon monoxide poisoning

    15. October 28, 2003 Gases and Toxic Inhalation 15 Acute carbon monoxide poisoning: Diagnosis History: exposure history Acute unconsciousness/ acute metabolic acidosis Pulse oximetry may overestimate oxygen saturation; thus ABG should be used. Confirmation: Carboxyhemoglobin

    16. October 28, 2003 Gases and Toxic Inhalation 16 Normal (non-smoker): 5% or less/Normal smoker: up to 12% Serious toxicity with level 25% or more A comatose person may have a level close to zero. Elevation of carboxyhemoglobin just confirms the poisoning. In a patient with altered mental status, CT scan may show hypodensity change in globus pallidus and subcortical white matter as early as 6 hours after severe poisoning Acute carbon monoxide poisoning: Carboxyhemoglobin

    17. October 28, 2003 Gases and Toxic Inhalation 17

    18. October 28, 2003 Gases and Toxic Inhalation 18 Removal from exposure 100% oxygen therapy Promotes tissue oxygenation Enhance CO elimination Half-life of 1-2 hours Treat until patients become asymptomatic, CarboxyHb< 10% Acute carbon monoxide poisoning: Management

    19. October 28, 2003 Gases and Toxic Inhalation 19 40% of cases treated, completely recovered and appear fine. Return of symptoms on day 20-40 Headache, memory and learning problems Parkinsonism Symptomatic treatment 50% recover and 50% permanent symptoms Acute carbon monoxide poisoning: long-term complications

    20. October 28, 2003 Gases and Toxic Inhalation 20 Cyanide poisoning A powerful cellular poisoning Inhalation exposure Hydrogen cyanide gas Combustion products Other exposures: Ingestion Cyanide salts Cyanogenic plants Iatrogenic: infusion of degraded nitroprusside

    21. October 28, 2003 Gases and Toxic Inhalation 21 Rapidly absorbed from respiratory tract Distribute to RBC and tissues Elimination by forming thiocyanate and excrete in urine Half-life of 2.5 days in persons with normal renal function Binds to Ferric ion in cytochrome a-a3: enzyme in mitochondria catalyzing electron transfer to oxygen Cyanide poisoning

    22. October 28, 2003 Gases and Toxic Inhalation 22

    23. October 28, 2003 Gases and Toxic Inhalation 23 Cyanide poisoning: Clinical manifestation Inhalation: Immediate onset Low concentration (50 ppm or less): anxiety, restlessness, dyspnea, palpitation, headache Higher concentration (100 ppm): death in 30 minute, tachycardia, tachypnea, syncope, seizures High dose (250 ppm): Immediate onset: seizures, bradycardia or asystole, CVS collapse, respiratory depression, coma

    24. October 28, 2003 Gases and Toxic Inhalation 24 Cyanide poisoning: Diagnosis History Exposure: laboratories, jewelry, metal works Clinical manifestation Rapid onset and progression of manifestations Arterialization of veins in fundoscopy Severe type B lactic acidosis Confirmation: erythrocyte cyanide level (< 50 mcg/L), retrospective

    25. October 28, 2003 Gases and Toxic Inhalation 25 Removal from exposure 100% oxygen Cyanide antidote may not be needed for inhalation victims who are asymptomatic or recovered before presentation Cyanide antidote kit: Amyl nitrite Sodium nitrite Sodium thiosulfate Cyanide poisoning: treatment

    26. October 28, 2003 Gases and Toxic Inhalation 26 Sodium nitrite Induces ‘methemoglobinemia’: Hb with Fe3+ Cyanide binds with Fe3+ Sodium nitrite 300 mg ( 10 ml of 3% NaNO2) IV over 5-10 minutes Hypotension due to vasodilation Amyl nitrite in cases of Non-medical personal No available IV line

    27. October 28, 2003 Gases and Toxic Inhalation 27 Sodium thiosulfate Enhances cyanide elimination from the body Sodium thiosulfate donates sulfur atom to rhodanase-catalyzed reactions to form thiosulfate Thiosulfate excreted in urine Hemodialysis in renal failure Sodium thiosulfate 12.5 g (50 ml of 25% sodium thiosulfate)

    28. October 28, 2003 Gases and Toxic Inhalation 28 Hydrogen sulfide Colorless gas with sweet odor Intermediate water solubility Product of bacterial decomposition of protein Industries at risk: Liquid manure & fertilizer, fishing, brewers, tanning, natural gas & oil exploration, sewer construction

    29. October 28, 2003 Gases and Toxic Inhalation 29 Inhalation Irritation of upper and lower respiratory system No bioaccumulation Detoxification within 1 hour Thiosulfate formation and renal excretion Inhibits cytochrome oxidase a3 Inhibits aerobic metabolism Hydrogen sulfide poisoning

    30. October 28, 2003 Gases and Toxic Inhalation 30

    31. October 28, 2003 Gases and Toxic Inhalation 31 Odor threshold 1 ppm characteristic sweet, rotten egg odor Olfactory fatigue within 10 minutes with 100 ppm; ‘loss of warning properties’ Low level: 10 ppm muscle fatigue on chronic exposure 50 ppm: Rapid onset of upper respiratory mucosal irritation: ocular pain, keratitis, cough, sore throat, corneal ulceration Hydrogen sulfide poisoning

    32. October 28, 2003 Gases and Toxic Inhalation 32 250 ppm: systemic effects of cellular anoxia Dyspnea, cough, tachypnea, chest pain Headache, dizziness, lethargy, confusion, delirium, seizures, coma Hypotension, tachycardia, myocardial ischemia and infarction, arrhythmias 1000 ppm: immediate death from respiratory depression and respiratory paralysis Hydrogen sulfide poisoning

    33. October 28, 2003 Gases and Toxic Inhalation 33 No specific laboratory from biological sample History, clinical manifestations, metabolic acidosis and environmental sampling Environmental sampling: ambient hydrogen sulfide level Hydrogen sulfide poisoning

    34. October 28, 2003 Gases and Toxic Inhalation 34 Removal from exposure 100% oxygen Do not perform mouth to mouth resuscitation Amyl nitrite and sodium nitrite for cases with manifestations of cellular hypoxia Methemoglobin binds with hydrogen sulfide into sulfmethemoglobin Hydrogen sulfide poisoning

    35. October 28, 2003 Gases and Toxic Inhalation 35 Irritant gases Large variety of chemicals Final common pathway: destruction of the integrity of respiratory mucosal barrier

    36. October 28, 2003 Gases and Toxic Inhalation 36 Rapid onset of symptoms (seconds to minutes) Signal to escape the exposure Oral, nasal and pharyngeal pain Mucosal edema, cough, stridor Conjunctival injection, chemosis, skin irritation Gases with good water solubility Upper airway obstruction Irritant gases: Clinical manifestations Short exposure

    37. October 28, 2003 Gases and Toxic Inhalation 37 Irritant gases: Clinical manifestations Prolonged exposure Gases without rapid onset of manifestation Entry into lower respiratory tract Tracheobronchitis, bronchiolitis, bronchospasm Acute lung injury, non-cardiogenic pulmonary edema Dyspnea, chest tightness, cough, frothy sputum, wheezing, crackles CXR: alveolar infiltration Arterial hypoxemia

    38. October 28, 2003 Gases and Toxic Inhalation 38 Irritant gases: highly water-soluble gases Ammonia Common industrial (plastic, fertilizer, refrigeration, explosives, cleaning agents) and household gases Characteristic odor Dissolution: NH4OH Chloramine (NH2Cl) Mixture of hypochlorite and ammonia Dissolution: hypochlorous acid, ammonia, oxygen radicals

    39. October 28, 2003 Gases and Toxic Inhalation 39 Hydrogen chloride Industrial acid, combustion product of vinyl chloride Dissolution: hydrochloric acid Hydrogen fluoride Glassware and semiconductor industry Hydrofluoric acid Upper and lower airway irritation, systemic hypocalcemia Irritant gases: highly water-soluble gases

    40. October 28, 2003 Gases and Toxic Inhalation 40 Sulfur dioxide Smelting and oil refining Warning properties: odor Dissolution: sulfurous and sulfuric acids Irritant gases: highly water-soluble gases

    41. October 28, 2003 Gases and Toxic Inhalation 41 Chlorine Exposure: mixing hypochlorite with acid, aged hypochlorite tablet, compressed chlorine gas for water chlorination Dissolution: Hypochlorous acid Mild initial upper respiratory symptoms Delayed symptoms of lower respiratory tract injury for hours Irritant gases: intermediate water-soluble gases

    42. October 28, 2003 Gases and Toxic Inhalation 42 Phosgene Colorless gas, heavier than air Musty odor exposure Combustion products of polyvinyl or isocyanate compounds Chemical warfare Irritant gases: poorly water-soluble gases

    43. October 28, 2003 Gases and Toxic Inhalation 43 Phosgene Slowly dissolves into hydrochloric acid Prolonged exposure Upper and lower respiratory tract irritation Delayed non-cardiogenic pulmonary edema up to 72 hours

    44. October 28, 2003 Gases and Toxic Inhalation 44 Nitrogen dioxide Reddish-brown color Water insoluble Heavier than air Sources Silos: grains Combustion: nitrocellulose in films and bed mattress Irritant gases: poorly water-soluble gases

    45. October 28, 2003 Gases and Toxic Inhalation 45 Nitrogen dioxide Mild upper airway irritation Dissolution into nitric and nitrous acids in bronchiole, terminal bronchiole and alveoli Acute non-cardiogenic pulmonary edema Pulmonary inflammation and bronchiolitis obliterans 2-6 after the exposure

    46. October 28, 2003 Gases and Toxic Inhalation 46 Nitrogen dioxide 1-3 ppm odor 15 ppm minimal irritation 50-150 ppm mild irritation LD50 for 1 hour exposure = 175 ppm Acute phase: Mucosal irritation (may last up to 2 weeks), methemoglobinemia

    47. October 28, 2003 Gases and Toxic Inhalation 47 Delayed: 3-36 hours Fever dyspnea rales hypoxemia cyanosis Perihilar infiltration on CXR Nitrogen dioxide

    48. October 28, 2003 Gases and Toxic Inhalation 48 Decontamination: Removal from gas exposure Airway management & intubation Oxygenation and PEEP Bronchodilator for bronchospasm Monitor ECG for patients with hydrocarbon exposure who receive bronchodilator Irritant gases: management

    49. October 28, 2003 Gases and Toxic Inhalation 49 Patient with hydrogen fluoride inhalation Nebulization of 2.5% calcium gluconate solution (1.5 mL of 10% calcium gluconate with 4.5 ml or NSS or water) Prevent fluoride induced hypocalcemia

    50. October 28, 2003 Gases and Toxic Inhalation 50 Smoke inhalation Another major mortality factor for patients with burns Half of all fire-related deaths are due to smoke inhalation Risk for smoke inhalation Closed-space fire Decreased mentation: overdose, alcohol intoxication, drug abuse, head injury

    51. October 28, 2003 Gases and Toxic Inhalation 51 Combustion or pyrolysis: the rapid decomposition or oxidation of a substance by heat Flame (light), heat, smoke Components of smoke are unpredictable: composition of the fuels, oxygen availability, heat Components of exposure from smoke inhalation Particulate matters, fumes, aerosols, vapors Toxic gases Smoke inhalation

    52. October 28, 2003 Gases and Toxic Inhalation 52 Heat: Thermal injury Thermal injury occurs only at upper airway levels Quick onset and rapid progression Injury below vocal cord occur only in cases of steam inhalation Smoke inhalation

    53. October 28, 2003 Gases and Toxic Inhalation 53 Particulate matters: Diameter less than 0.5 micrometer Products of incomplete combustion of organic materials Bronchospasm Edema of mucosa from upper respiratory system down to terminal bronchiole Onset of edema may be delayed up to 24 hours Smoke inhalation

    54. October 28, 2003 Gases and Toxic Inhalation 54 Toxic gases from smoke Carbon monoxide: incomplete combustion of organic substance Hydrogen cyanide: Combustion of nitrogen-containing organic substances: wool, silk, polyurethane, vinyl Smoke inhalation

    55. October 28, 2003 Gases and Toxic Inhalation 55 Examples of combustion products from common household materials

    56. October 28, 2003 Gases and Toxic Inhalation 56 Clues for diagnosis of smoke inhalation History of closed-space fire Physical signs facial burns, singed nasal hair, soot in the nose and throat, hoarseness, carbonaceous sputum, wheezing Carboxyhemoglobin level as a document of exposure to incomplete combustion in a enclosed space Chest x-ray may be normal at early stages Smoke inhalation

    57. October 28, 2003 Gases and Toxic Inhalation 57 Treatment should start before the definite diagnosis is made Early intubation may be needed to maintain airway: Indications for early intubation Full-thickness burns of the face or perioral region Circumferential neck burns Progressive hoarseness supraglottic edema or inflammation 100% humidified oxygen Carboxyhemoglobin level Smoke inhalation

    58. October 28, 2003 Gases and Toxic Inhalation 58 Empirical treatment for cyanide poisoning A patient with elevated carboxyhemoglobin Suspected cyanide poisoning:history, comatose, lactic acidosis Administration of sodium nitrite may worsen impaired oxygen transport IV Sodium thiosulfate alone

    59. October 28, 2003 Gases and Toxic Inhalation 59 Arsine A colorless, non-irritating gas Heavier than air Garlic-like odor Semiconductor industry: production of gallium arsenide Reaction of acids with arsenical compounds

    60. October 28, 2003 Gases and Toxic Inhalation 60 Arsine depletes RBC glutathione RBC cell membrane instability Intravascular hemolysis Absorbed into the body and is oxidized to trivalent arsenic compounds and cause chronic arsenic poisoning Arsine

    61. October 28, 2003 Gases and Toxic Inhalation 61 Acute inhalation of level 250 ppm or more can cause death Long term exposure of level 10-50 ppm can cause acute symptoms Chronic low level exposure may cause arsenic poisoning Arsine

    62. October 28, 2003 Gases and Toxic Inhalation 62 Intravascular hemolysis Headache, dizziness, malaise & weakness Nausea and vomiting, abdominal pain Dark-red ‘Cola color urine’ in 4-6 hours Jaundice in 24-48 Acute (nephrotoxic) tubular necrosis: secondary to deposition of RBC breakdown products Arsine

    63. October 28, 2003 Gases and Toxic Inhalation 63 Chronic arsenic poisoning Malaise, nausea, headache Painful peripheral neuropathy Hepatitis Bone marrow suppression Mee’s line Skin changes: hyper keratosis and hyper pigmentation, Bowen’s disease Arsine

    64. October 28, 2003 Gases and Toxic Inhalation 64 History of exposure, cluster of cases Abdominal pain Intravascular hemolysis Garlic-like odor Arsine

    65. October 28, 2003 Gases and Toxic Inhalation 65 Acute cases: Transient elevation of urine arsenic levels Acute anemia with decreased haptoglobin Negative Coomb’s test Hemoglobinuria without hematuria Hyperkalemia Acute renal failure Chronic cases: Elevation of urine arsenic level Arsine

    66. October 28, 2003 Gases and Toxic Inhalation 66 Arsine : Treatment Decontamination: Removal from exposure ABC: 100% oxygen Supportive care: Blood transfusion in case of severe anemia Urine alkalinization and maintain urine flow Hemodialysis

    67. October 28, 2003 Gases and Toxic Inhalation 67 No enhancement of elimination Chelation therapy: No indications in acute cases May be indicated for chronic exposure with persistent elevation of urine arsenic level Follow up Until stable hemolysis ceases and stable hematocrit Subacute and long-term follow up for renal function and chronic arsenic poisoning Asymptomatic exposed person should be observed for at least 6 hours

    68. October 28, 2003 Gases and Toxic Inhalation 68 Thank you Do you have any question?

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