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Contains the following key public domain (not copyrighted) U.S. Government publication(s) on one CD-ROM in both Microsoft PowerPoint and Adobe Acrobat PDF file formats:
TITLE:
TOXIC INHALANTS, 87 pages
SLIDE TOPICS, SUBTOPICS and CONTENTS:
TOXIC INHALATIONS CDR MIKE PENNY Case 1 As a town lies sleeping a storage tank at a major industrial complex ruptures releasing tons of an unknown substance into the night air Close to the plant hundreds die in their beds At farther distances they collapse in the streets and are trampled in the swelling panic Case 2 23y/o Army Ranger suffers multiple traumatic injuries and subsequent smoke inhalation while being extricated from a burning C-130 Initial BP is 80/30 which responds rapidly to NS Pt is intubated in the ED and placement is confirmed by CXR He is taken to the OR where he has a splenectomy and operative management of pelvic and open tibia fractures Objectives Overview of pulmonary toxins encountered in ED practice Considerations and management of general classes of toxic gases A brief look at the mechanism of toxicity and management of carbon monoxide A brief look at the mechanism of toxicity and management of cyanide
FACTS Inhalational injuries are common: -Fire is the most frequent cause of inhalational injury --Cyanide is a common combustion product of synthetic material -CO is the most frequent cause of mortality related to inhalational injuries Concerns have been raised about TICS and TIMS and their vulnerability to terrorists
Definitions What Are TICs? -Toxic Industrial Chemicals What Are TIMs? - Toxic Industrial Materials
Don’t believe the hype these terms are essentially referring to the same thing Common Industrial Chemicals Ammonia 4,901 Ammonium Nitrate 1,143 Benzene 854 Butadiene 238 Chlorine 1,096 Ethylene 3,390 Hydrochloric Acid 166 Nitric Acid 1,085 Polyethylene 2,643 Polystyrene 203 Propylene 888 Sodium Chlorate 1,110 Sodium Hydroxide 1,097 Sulfuric Acid 3,719 Toluene 216 Urea 3,797 Xylenes 322
Historical Relevance 1984 methyl isocyanate release in Bhopal India causes 2000 deaths and 250,000 injuries 1986 release of toxic gases (HS and CO2) from Lake Nyos in Cameroon lead to 2000 deaths 2004 Dalton Georgia MFB Chemical INC -Allyl Alcohol release -100 families evacuated ->154 people deconned and txed in ED 1980-2001 >167 reactive accidents >100 fatalities
MILITARY RELEVANCE Gas (chlorine) is first used at Ypres Belgium WWI WWII Nazis develop Nerve Agents Cold War Brits/Soviets discover VX at the same time 1980’s and Halabjah 1990’s and Bosnia
Military Relevance Other nations (South Africa, Chad, Cambodia etc.) are alleged to have used chemical agents against insurgents in the 80’s and the 90’s Soviet Unions collapses leads many of their former chemical experts to seek paying jobs TICs vs CWA TICs -industrial use -stored in large quanities -stored near population centers -easy access in US -variable speed of effect CWA -limited industrial use -difficult access in US -rapid effect
History 1988 NATO ITF-25 -Analyzes the threat of TICs&TIMs to NATO forces -Determined hazard criteria for more than 100 common industrial chemicals -created a list categorizing these chemicals as high, medium or low risk EPA -EPCRA (Emergency Planning Community Right to know Act) 2001 Chemical Security Act Comprehensive Homeland Security Act of 2003 Hazard Index Ranks chemicals according to: -production -transportation -storage -toxicity -vapor pressure Agency for Toxic Substances and Disease Registry Ten Step Procedure 1. Identify, assess and prioritize threats 2. Identify local sources of chemicals that may be used by terrorists 3. Evaluate potential exposure pathways 4. Identify potential acute and chronic health impacts 5. Estimate potential impacts on infrastructure and the environment 6. Identify health risk communication needs 7. Identify methods to mitigate potential hazards 8. Identify specific steps to prevent the use of these TIMs as improvised weapons 9. Incorporate the threat assessment, mitigation, and prevention information into emergency response plans 10. Conduct training exercises to address the health threats USACHPPM TICs Info Card General Pathophysiology of TIMs CNS toxicity - i.e. organophosphates or carbamates
Interference with oxygenation -pretty much everything else TICS Disrupt Respiration By: Diminished respiratory drive Decreased O2 concentration Interruption of airway integrity Interference with Oxygen transport (CO) Interference with Oxygen delivery (CO) Interference with O2 utilization (CN)
Etiology of Common Toxic Inhalants Ammonia CO CO2 Chloramine Chlorine Ethane HCL Hydrogen cyanide Hydrogen sulfide Methane Nitrogen Oxides of nitrogen Fertilizer/refrigeration/combustion Incomplete combustion/methylene chloride Fermentation/natural springs/combustion Cleaning products Swimming pools/cleaning/refrigeration Natural gas/refrigeration Tanning/electroplating Combustion/acid + cyanide salts Decaying organic matter/oil&mining industry/asphalt Swamp gas Mines Silos/anesthetics/combustion Diminished respiratory drive Diminished respiratory drive Hypoventilation Hypercapnea/Hypoxia
Examples: -inhalational anesthetics -hydrocarbons Decreased O2 concentration Simple asphyxiants are gases which produce hypoxemia by displacing oxygen
Toxicity will not occur as long as the FIO2(fraction of inspired oxygen) is adequate Asphyxiation Normal FIO2= 21% FIO2 12-16%: tachycardia, tachypnea,headache, incoordination FIO2 10-14%: exhaustion FIO2 6-10%: nausea, vomiting, lethargy FIO2 <6%: Death Examples of Simple Asphyxiants Methane Nitrogen Helium CO2 Ethane Hydrogen Argon Tx of Simple Asphyxiant Remove from exposure (beware of manure pits) ABC’s and supportive care 100% O2 Sx’s resolve rapidly if no end organ damage If sx’s don’t resolve rapidly think again (CO, CN, coingestant, trauma, associated conditions) Case Study Union Carbide Plant ILL. 1998 ethylene oxide production facility -2 workers enter open pipe to inspect it -ambient light interferes so they instruct 2 workers to hold a tarp over the entrance. -workers holding tarp check on them :15 later - workers are down -1 dead, 1 brain damaged from Nitrogen accumulation and hypoxia
Clinical Approach ABC’s(assess need for intubation), High flow O2, IV, monitor, VS History of: location (garbage pit, mine, bilge?) circumstance (known gas leak?) combustion (CO, CN?) odors (hay, almonds?) number of victims identity of agents …..aid in treatment and immediate actions Considerations in Treatment of Specific Agents Asphyxiants: -The clinical course of asphyxiants is determined by duration of exposure -Short exposures without end organ damage recover rapidly with extrication, O2 and airway maintenance Halogenated/aromatic hydrocarbons: - sensitize the heart to catecholamines dysrhythmias - care should be taken if catecholamines are used in ACLS protocols with these agents Case Study Chlorine poisoning in Sri Lanka A case of chlorine poisoning in a 37-year-old mechanical supervisor at a water purification plant in Sri Lanka is described. Manipulating the main cylinder valve, he was exposed to chlorine fumes for a few seconds as he was running in and out to stop the gas flow. He started to have an intense feeling of suffocation and tightness of chest, coughing, intolerable irritation of eyes and mouth, headache and stomach problems. He still had symptoms 27 days after the incident. Case Study A massive chlorine release as a result of a tank leak in a car carrying chlorine took place in Norway. A total of 85 people, from 6 months to 82 years of age were hospitalized, and out of those 3 died. approximately 7-8 tons of chlorine gas formed a 10 km long cloud which covered the valley Pulmonary Irritants A wide variety of agents which share the ability to react with water in the lung mucosa and generate toxic intermediates Pathophysiology: pulmonary irritants interfere with gas exchange by: laryngospasm bronchospasm noncardiogenic pulmonary edema Examples of Pulmonary Irritants Cl2 + H2O 2HCl + O Chlorine Hydrochloric acid and an oxygen radical NH3 + H2O NH4OH Ammonia Ammonia hydroxide SO2 + H2O H2SO4 Sulphur dioxide Sulphuric acid COCl2 + H2O 2HCl + CO2 Phosgene Hydrochloric acid and Carbon dioxide Clinical Effects Determined by: water solubility the rate of reaction with H2O time of exposure
Highly Water Soluble Agents Result in immediate irritation, lacrimation, nasal burning and cough Primary action is on the mucous membranes of the upper airways and face Pungent odor and immediate discomfort usually limit exposure Exceedingly high concentrations or long exposures laryngeal edema/spasm and NCPE Examples: Ammonia, chloramine, HCL, and sulphur dioxide Gases With Low H2O Solubility No warning of toxicity -little if any immediate irritation -no effect on the upper airway Odor may be pleasant Example: Phosgene – newly mown hay Mild to moderate exposure NCPE in 2-24 hours Example: the oxidation and disruption of pulmonary lipid membranes by ozone Gases with Intermediate Water Solubility Clinical effects are intermediate to high and low water soluble gases Lower airway effects (bronchospasm/NCPE) predominate over upper airway effects Example: chlorine CHLORINE Greenish-yellow gas with a pungent odor heavier than air (the cloud formed spreads along the ground) 1 part per million (ppm) = limit of odor detection. At 15 ppm irritation of the mucous membranes of the eyes and nose, and especially of the throat and lungs occurs. At 100-150 ppm with an exposure duration of 5-10 minutes chlorine causes fatalities. 300 ppm for 30 minutesfatal 1000 ppm for a few breathsfatal
Clinical Approach ABC’s(assess need for intubation), High flow O2, IV, monitor, VS History of: location (garbage pit, mine, bilge?) circumstance (known gas leak?) combustion (CO, CN?) odors (hay, almonds?) number of victims identity of agents …..aid in treatment and immediate actions Examination Airway: signs of upper airway injury (stridor, larygospasm, bronchospasm) suspicion of thermal/irritant injury intubation if immediate airway control is necessary or assessment with fiberoptic endoscope and guided intubation if significant edema or injury is noted. Carbonaceous sputum and facial burns should raise suspicion for airway burns but correlate poorly with their presence Care should be taken to evaluate even asymptomatic patients because of the significant risk of rapid progression to airway obstruction Examination Pulmonary: Wheezing/rales/rhonchi = obstruction or NCPE CV: sinus tachycardia Neuro: Ranges from coma to subtle findings such as memory deficit and perceptual difficulties Skin: Irritation of skin and conjunctivairritant gases “Chocolate Cyanosis” MetHb “Cherry red color” CO/CN Bullae may be seen in CO Ancillary Tests ABG: -pH, pCO2 and pO2 measured -sats are derived from plotting measured pO2 on an O2 Hb dissociation curve -cannot account for abnormal Hb (COHb/MetHb) Cooximetry: -uses spectrophotometry to measure Hb, oxyHb, deoxyHb, COHb, MetHb and total oxygen content of the blood
Ancillary Studies CXR: assess for NCPE EKG: to assess for CO related myocardial ischemia Loke advocates ventilation scans with radiolabeled xenon gas as a predictor of lower airway injury -abnormal gas retention at 90 seconds CXR Tx of Pulmonary Irritants Lanryngospasm - corticosteroids of theoretical benefeit - early intubation for definitive airway management Bronchospasm - standard bronchodilators -avoid parenteral agents if aromatic or halogenated hydrocarbons are involved -steroids again have theoretical benefit -nebulized sodium bicarbonate for symptomatic relief in Cl and HCl gas exposure Noncardiogenic pulmonary edema -PEEP/CPAP
Complications of Inhalational Injury Acute:(Onset minutes to hours) -primarily related to hypoxic effects on CNS and CV systems or primary respiratory injury Subacute:(onset 4-48 hours) -noncardiogenic pulmonary edema -NCPE defined as diffuse pulmonary alveolar infiltrates with pO2<60 on 50% O2 in the absence of CHF Case 2 Patient did well post-operatively,…at first 24 hours later: -Pt becomes agitated and RR increases to 30 -Minute ventilation increases from 8.5 to 20 liters/minute -airway pressure increases from18 to 65 cm H2O -ABG shows pO2 of 35mm Toxic Inhalations Break Interference with Oxygen transport (CO) CO is released by the combustion of carbon containing compounds or exposure to methylene chloride The affinity of Hb for CO is 230-260 times that of O2 (even greater for fetal Hb) For this reason it is possible to accumulate carboxyhemoglobin (COHb) in environments with very low [CO] “Soaking” Carbon Monoxide Colorless, odorless Greater than 10,000 cases per year > 3500 deaths per year Case Study 2 year old twins found down after 12- 18 hours exposure in a house with a faulty heater. COHb levels at 1 hour were 10% and 4.8 % at 1 hour respectively Both require intubation and extended ICU stays for multi-system organ failure. Both show severe CNS involvement COHb T1/2 At 1ATA and 21%O2 : 4-6 hours
At 1ATA and 100%O2 : 90 minutes
At 3ATA and 100%O2: 30 minutes CO Effects COHb 10% No effect COHb 10-20% Headache, fatigue, nausea,AMS COHb 20% LOC, Coma, Death Effects A carboxyhemoglobin of 50% can be thought of as acute loss of 50% of Hb by hemorrhage. This oversimplifies the effect of CO which generally causes CV collapse at 50% COHb COHb additionally interferes with O2 delivery/utilization at a cellular level Interference with oxygen delivery (CO) Shifts O2 dissociation curve left Binds and reduces myoglobin and cytochrome c diminishing O2 extraction and O2 stores Additional Effects of CO Binds cytochrome a-a3 interfering with cellular oxidative metabolism Causes lipid peroxidation and associated free radical damage of CNS microvascular endothelium Increased intracellular glutamate Ca2+ release and cell death Guanylate cyclase activation and displacement of NO from platelets hypotension syncope (poor prognostic sign) Presenting Features Earliest symptoms = H/A and nausea/vomiting -leads to frequent misdiagnosis of flu, food poisoning, gastroenteritis Longer exposures lead to DOE and symptoms of cardiac ischemia Neurological effects range from dizziness and ataxia at lower levels (15-20%) to syncope/seizure/coma at high levels Things to remember about CO COHgb levels Normal 0-5 Smoker 5-10 -may demonstrate an acute exposure, but are not predictive of syncope, symptoms or outcome Metabolic acidosis from high lactate is associated with severe toxicity Syncope is associated with delayed neurologic sequelae Considerations in the Tx of CO Exposure CO interferes with the binding and unloading of Hb and O2 and utilization at the cellular level COHb levels do not correlate well with toxicity Fetal Hb binds CO even more avidly than adult Hb Serum T1/2 of CO is dependent on pO2 Case Patient 1 recovers over the following 6 months but continues to have persistent muscle weakness and spasticity requiring intensive therapy to walk. Patient 2 recovers over 1 month without neurological deficit Clinical Approach ABC’s(assess need for intubation), High flow O2, IV, monitor, VS History of: location (garbage pit, mine, bilge?) circumstance (known gas leak?) combustion (CO, CN?) odors (hay, almonds?) number of victims identity of agents …..aid in treatment and immediate actions Tx Triage (dependent on situation/number/severity) O2 and intubation if necessary Monitor IV and “standard blood work” advocated by Hoffman ABG with cooximetry VBG if CN is a possibility Hx and PE guide the decision to perform bronchoscopy and ventilation scanning
Ancillary Studies CXR: assess for NCPE EKG: to assess for CO related myocardial ischemia Loke advocates ventilation scans with radiolabeled xenon gas as a predictor of lower airway injury -abnormal gas retention at 90 seconds Tx of CO Mainstay of Tx is 100% O2 - increased pO2 leads to increase in dissolved O2 with a minor effect on O2 delivery - increased pO2 decreased COHb T1/2
Hyperbaric Oxygen in CO Indications: -neuropsychiatric symptoms -CV instability -COHb level of 25% (15% in pregnancy) HBO most effective within 6 hours -may necessitate the need for rapid transfer to HBO facility - deterioration during transfer to HBO is rare -Those that do deteriorate have a uniformly poor outcome if HBO is withheld Sloan EP et al Complications and protocol considerations in CO poisoned patients who require HBO therapy, Ann Emerg Med 18:629 1989 -It all comes down to documentation HBO Tx
HBO: -TT5 -high ppO2 further decreases COHb T1/2 -Increases dissolved O2 in the blood by a magnitude of 10 -shown to prevent lipid peroxidation in rat brains after LOC -may decrease WBC adherence to CNS microvascular endothelium and accelerate cytochrome oxidase regeneration limiting reperfusion injury
Interference with O2 utilization (CN) CN and H2S are considered tissue asphyxiants because of their ability to produce anoxia at normal pO2
CN is a clear or pale blue liquid or gas +/- odor of burnt almonds
The e- transport system–Synthesis of ATP ATP is synthesized in mitochondria and released to be used by the cell. NADH and FADH2 carry H atoms into e- transport system. Enzymes and Cytochromes (proteins) in cristae separate H into H+ and e-. Electrons are transported step by step thru the system, each step releasing free energy that drives the synthesis of ATP by ATP synthetase enzyme complex . Each NADH can produce 3 ATP; each FADH2 can produce 2 ATP. At the end, H2O is formed by a terminal cytochrome, which reduces O2 with e- and H+ from NADH and FADH2 (only step requiring oxygen).
Cyanide Poisoning Picture Rosens Third edition Vol 3 page 2677 (fig142-2) CN (and H2S/CO) bind to cytochrome a-a3 on the electron transport chain and prevent the formation of H2O. Build up of TCA intermediates inhibits TCA cycle through a feedback loop resulting in a lack of ATP and lactic acidosis from conversion of pyruvate to lactate in an effort to preserve anaerobic glycolysis. CN Poisoning CN binds to Fe3+ in Cytochrome a-a3 complex poisoning the use of O2 to produce energy and causing lactic acidosis Tx of CN poisoning is the 3 piece Lilly Cyanide Antidote Kit -Amyl Nitrite (inhaled) -Sodium Nitrite (IV) -Sodium Thiosulfate Each kit can treat 2 adults Acceptable Levels Odor threshold- 0.58 PPM NIOSH- 4.7 PPM OSHA- 10 PPM PEL Mild to Moderate CN Poisoning Rapid (fast) breathing. Restlessness and decreased ability to settle down to tasks like watching TV or reading. Dizziness. Weakness. Headache. Eye irritation (itching, burning). Nausea (feeling sick to your stomach) and vomiting (throwing up). Rapid heartbeat Large Amounts of CN Convulsions Severe Bradycardia Loss of consciousness. Your breathing will stop Cyanide LCt50 Exposure time (min.) LC50 (mg/m3) O.5 4O64 l 34O4 3 l466 lO 6O7 30 688 Clinical Approach ABC’s(assess need for intubation), High flow O2, IV, monitor, VS History of: location (garbage pit, mine, bilge?) circumstance (known gas leak?) combustion (CO, CN?) odors (hay, almonds?) number of victims identity of agents …..aid in treatment and immediate actions Blood Gases ABG with cooximetry VBG: -May aid in the Dx of suspected CN and H2S poisonings -Inability of the cells to extract O2 due to these toxins should show minimal change in pO2 when VBG and ABG are compared CN Antidotes Amyl Nitrite/ Sodium Nitrite: - drives the formation of MetHb which acts as an alternative source of ferric ions and frees cytochrome a-a3 MetHb + CN cyanomethemoglobin (cannot measure) -amyl nitrite is for immediate use only while an IV is started -sodium nitrite dosage: -Adults 10ml of 3% solution in adults over 2-4 minutes -Children 0.2ml/kg over 2-4 minutes Successful Tx 25% MetHb (generally tolerated){Rosen 8%} Potential complications: -hypotension -worsened tissue hypoxia if concomitant CO poisoning CN Antidotes Sodium Thiosulfate -acts as a sulfur donor to detoxify cyanomethemoglobin -availability of sulfur substrate is the rate limiting factor in this reaction Rhodanese -cyanomethemoglobin + sodium thiosulfate thiocyanate + MetHb -thiocyanate is eliminated in urine Hydroxycobalamin: - under study -would replace and avoid the complications of the nitrites -Hydroxycobalamin + CN cyanocobalamin (B12) Pit falls in Tx of CN Poisoning Frequently combustion produces CO and CN in the same incident Tx of CO toxicity with HBO is inadequate if CN is also involved Tx of CN with nitrites may worsen CO toxicity by producing MetHb and further diminishing oxyhemoglobin Recommendations in Mixed CN/CO Poisoning ABC’s with high flow 100% O2, monitor and IV access Initial labs should include ABG/VBG and cooximetry Sodium thiosulfate will be initiated immediately If COHb is low give sodium nitrite at standard dose If COHb is elevated HBO and administer the sodium nitrite when patient is at depth HallAH, et al Increasing survival in acute CN poisoning. Emerg Med Rep 9:129, 1988 Repeat sodium thiosulfate if sodium nitrite is administered at depth Patient Disposition Admit all pts with: respiratory arrest, CN/H2S and symptomatic CO exposures, laryngeal spasm/edema In irritant exposure: Low solubility agents: hospitalize High solubility: Asymptomatic D/C at 6 hours Symptomatic Tx as RAD Social admissions if CO exposure without identified source Bibliography Emergency Medicine Concepts and Clinical Practice Third ED Rosen Peter Editor Chapter 142 P.2673- 2684 HallAH, et al Increasing survival in acute CN poisoning. Emerg Med Rep 9:129, 1988 Moon, Christopher, Case Report, Case 98-03, WWW.CME 1998 Sloan EP et al Complications and protocol considerations in CO poisoned patients who require HBO therapy, Ann Emerg Med 18:629 1989 Toxicologic Emergencies Sixth Ed, Golfrank L R Editor Chapters 94-97 P.1523-1585 Weaver L.K. et al Hyperbaric Oxygen for Acute Carbon Monoxide Poisoning New England Jouurnal of Medicine OCT 2002 Vol 347 P. 1057-1067
Resources Helpful References Include : the North American Emergency Response Guide Book (http://hazmat.dot.gov/gydebook.htm) toxicological profiles, chemical fact sheets, Case Studies in Environmental Medicine, and Medical Management Guidelines published by ATSDR (1-888-422-8737, http://www.atsdr.cdc.gov/) fact sheets from the U.S. Environmental Protection Agency (http://www.epa.gov) material safety data sheets from academia http://www.chem.utah.edu/MSDS) commercial hazardous substances databases such as TOMES by Micromedix.
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