Inhalation Injuries

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Inhalation Injuries

• Resident Rounds
• January 30, 2003
• Roberto Newtoni Drummondi

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Overview

• Exposure to population vs individual
• types of inhalational exposure
• approach
• four cases to illustrate
• simple asphyxia
• smoke inhalation
• chemical asphyxia
• irritant gas exposure

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Sallier Papyrus 1650 BC
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1650 BC

• I do not see a sculptor on a missionor a
  goldsmith on the task of being dispatched (?)but
  I see the coppersmith at his toilat the mouth of
  his furnacehis fingers like crocodile skinhis
  stench worse than fish eggs

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• The mat-weaver (lives) inside the
  weaving-househe is worse off than a woman,with
  his knees up to his stomach,unable to breathe in
  any air

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1473 AD - Ellenbog

• The first treatise devoted solely to occupational
  health, "On the poisonous evil vapors" (Von den
  gifftigen besen Tempffen und Reuchen).This
  pamphlet describes inhalational hazards of coal
  smoke, mercury fume, and acid aerosols among
  goldsmiths

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Modern Era

• the use of poison gas in World War Ichlorine,
  phosgene, and mustard gases respiratory rather
  than systemic toxins.
• World War I also spurred heightened governmental
  interest in and funding for industrial
  hygiene

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Exposures that affect huge communities

• Bhopal chemical disaster200,000 people were
  exposed to a cloud of methyl isocyanate 6000
  deaths were caused by acute respiratory failure
• 2001 World Trade Center terrorist attack in New
  York City, inhalation injury was the most
  frequent reason medical attention
• Wartime use of chemical agents, such as mustard
  gas, resulted in severe inhalation injuries to
  combatants

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Individual Exposure harder to detect

• Hard to diagnose can be covert and indolentMay
  know only that a toxic release occurred without
  detailsmust take thorough occupational
  historydiagnosis of inhalation injury is
  largely clinical,
• Despite the array of possible toxic inhalants,
  identification of a specific inhalant is often
  unnecessary because therapy is based primarily
  on the clinical manifestations

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Table 1. Selected occupational irritants

• Agricultural workers....... Ammonia, nitrogen
  dioxide, hydrogen sulfide Custodians
  ................ . Ammonia, bleach
  (hypochlorite), chloramines Firefighters.........
  ..... Smoke, hazardous materials releases
  Food service workers........ Cooking vapors,
  cigarette smoke Health professionals ........
  Glutaraldehyde, formaldehyde Laboratory
  workers.................Solvent vapors, inorganic
  acid vapors/mists Military personnel.............
  ......Zinc chloride smoke Power plant and oil
  refinery workers..........
  Sulfur dioxide

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• Printers, painters...............Solvent vapors
  Pulp mill workers..............Chlorine,
  chlorine dioxide, hydrogen sulfide Railroad
  personnel, miners, truck drivers...............Die
  sel exhaust Refrigeration workers
  (commercial).........
  Ammonia Roofers, pavers...................
  Asphalt vapors, PAHsa Swimming pool service
  workers......................Chlorine
  (hypochlorite), hydrogen chloride Waste water
  treatment workers.....................Chlorine,
  hydrogen sulfide Welders...........metalic oxide
  fumes, nitrogen oxides, ozone
  Woodworkers...................Wood dust

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Common Inhaled Toxins Inhalant Source/use
Predominant class

• Acrolein.....................Combustion
  Irritant, highly soluble Ammonia
  Fertilizer.................combustion Irritant,
  highly soluble Carbon dioxide....................
  Fermentation, complete combustion, fire
  extinguisher Simple systemic effects Carbon
  monoxide...................... Incomplete
  combustion, methylene chloride Chemical
  Chloramine.........Mixed cleaning products
  (hypochlorite bleach and ammonia) Irritant,
  highly soluble Chlorine..................
  ..Swimming pool disinfectant, cleaning products
  Irritant, intermediate solubility
  Chlorobenzylidenemalononitrile/choroacetophenone
  ................Tear gas Irritant
  Ethane.................Natural gas, refrigerant
  Simple Hydrogen chloride.................Tanning
  and electroplating industry Irritant, highly
  soluble Hydrogen cyanide................Combustio
  n of plastics, acidification of cyanide salts
  (e.g., jewelry) Chemical

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• Hydrogen fluoride Hydrofluoric acid...............
  Irritant, highly soluble systemic effects
  Hydrogen sulfide ................Decaying
  organic matter, oil industry, mines, asphalt
  Chemical irritant, highly
  Methane........................
  .....Natural gas, swamp gas Simple
  Methylbromide.............Fumigant Chemical
  Nitrogen......................... Mines, scuba
  divers (nitrogen narcosis, decompression
  sickness) Nitrous oxide .....................Inha
  lant of abuse, whipping cream, racing fuel
  booster Simple Noble gases....................(e.
  g. helium) Industry, laboratories Oxides of
  nitrogen....................Silos, anesthetics,
  combustion Irritant, intermediate solubility
  Oxygen..................Medical use, hyperbaric
  conditions Irritant, free radical systemic
  effects Ozone......................
  Electrostatic energy Irritant, free radical
  Phosgene.......................Combustion of
  chlorinated hydrocarbons Irritant, poorly soluble
  Phosphine ...................Hydration of
  aluminum or zinc phosphide (fumigants) Chemical
  Smoke .......................(varying
  composition) Combustion Variable, but may include
  all classes Sulfur dioxide ......................
  ..Photochemical smog (fossil fuels) Irritant

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Occupational and Environmental Lung
DiseaseFatal Work-Related Inhalation of Harmful
Substances in the United States
Francesca Valent MDMARCH 2002 CHEST

• USA 1992 to 1998, a total of 523 workers died The
  overall mortality rate was
• 0.56 deaths per 1,000,000 worker-years
• women had lower mortality rates than men
• Worse if gt65
• Carbon monoxide was more frequently involved in
  fatal inhalations
• irritants, particularly chlorine gas the most
  common sources of emergency department visits
  not requiring hospitalization. Exposure to
  carbon monoxide was a major problem across
  industries
• result not of fires but of malfunctioning
  machines exposure to other substances was more
  industry specific
• CDC identified mining, agriculture, forestry,
  fishing, and construction as the industries with
  the highest rates fatal inhalations.
• auto and miscellaneous repair services to be an
  industry with increased inhalation mortality
  rate.
• one fourth of the victims were doing repair or
  maintenance.

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PHYSICAL AND CHEMICAL QUALITIES

• Gases formless state of matter can
  expand to occupy an available space
• Fumes condensing vapour in
  cooler air
• Dusts suspensions solid particles
  in air
• Smoke incomplete combustion of
  carbon containing material
• Mists airborne finely divided fluid
  droplets
• Aerosols very fine liquid droplets
  suspended in air prolonged time

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Mechanisms of toxicity

• common target airway epithelium.
• disruption of the integrity protective barrier.
• edema, inflammation, smooth muscle contraction,
  and stimulation of afferent neurons
• not always respiratory disorders (eg, lead
  poisoning from fume inhalation),
• converselyingested toxins effects on the lung
  paraquat and hydrocarbon
• irritants damage cells in a nonimmunologic
  fashion formation of an acid, alkali, or
  reactive oxygen species.
• tissue depletion of glutathione, a free radical
  scavenger
• direct thermal injury to cells and tissue (steam
  especially)

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Exposure level

• The intensity of the exposure
• Controlled industrial vs uncontrolled explosion
• Environment confined space vs outdoors
• The Occupational Health and Safety Administration
  (OSHA)
• permissible exposure limits for many chemical
  substances

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Water solubility

• Determines where inhaled gases deposit.
• mucus is a watery solution,
• gases that are highly water soluble (ammonia,
  sulfur dioxide, and hydrogen chloride),
• acute irritant injury to mucus membranes, ( eyes
  nose upper airway)
• spare the lower respiratory tract
• Unpleasant symptoms protective
• Gases of intermediate solubility( chlorine)
  widespread irritant effectst.
• less water-soluble( nitrogen dioxide and
  phosgene) travel distally
• result in delayed onset chemical pneumonitis

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Particle size

• smaller than 100 microns can enter the
  airwaysmaller than 10 microns can reach the
  lower respiratory tract,smaller than 5 microns
  can deposit in the lung parenchyma
• Host factors Patients with pre existing disease
  COPD etc

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Site of injury

• Upper airway
• Warns of exposure through protective
  mechanism Mucous, cough, sneeze, glottic
  closure, Modifies temperature and humidity
• From simple, transient irritation to airway
  compromise chronic rhinitis , sinusitis, nasal
  perforation Reactive Upper Airways dysfunction
  syndrome RUDS Vocal Cord Dysfunction chronic
  pharyngitis

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Conducting airway injury

• Damage to the epithelial cells and tight
  junctions increases mucosal permeability
  leads to inflammation and cellular damage.
• Results in bronchoconstriction,.
• irritant effects include tracheitis and
  bronchitis.
• exacerbates underlying reactive airway disease
• More intense exposures airway constriction, even
  in individuals without a history of reactive
  airways disease.
• Airway obstruction may worsen over the first 24
  hours after exposure as inflammation
  develops.
• reactive airways disease syndrome
• Classically, RADS develops after a single, high
  dose exposure, but it may also occur after
  repeated lower level exposure

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Injury to lower respiratory tract

• lower water solubility and particles less than 5
  microns
• Diffuse bronchiolar inflammation can occur
• Atelectasis may result from disruption of the
  pulmonary surfactant
• Pneumonitis is the most common acute
  manifestation dyspnea, cough, and hypoxemia
• pulmonary edema or ARDS.
• Chronic effects bronchiolitis obliterans,
  bronchiolitis obliterans organizing pneumonia
  (BOOP), and pulmonary fibrosis.
• Fixed airway obstruction granulation and
  interstitial fibrosis extending into small
  airways
• usually cytokine mediated, without obvious lung
  injury

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Systemic effects

• Inhalation of mercury vapor a toxic
  pneumonitis with pulmonary edema fever,
  tremors, and chest pain.
• Metal fume fever flu-like symptoms from metal
  oxides fumes, including zinc , copper, and
  magnesium oxides.
• Organic toxic dust syndrome agricultural workers
  after exposure to moldy grains flu-like
  syndrome cough, fever, myalgias and dyspnea
• Exposure to high doses of hydrofluoric acid
  hypocalcemia and hypomagnesemia

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PHYSIOLOGIC DERANGEMENTS

• Loss of airway patency secondary to mucosal edema
• Bronchospasm secondary to inhaled irritants
• Intrapulmonary shunting from small airway
  occlusion caused by mucosal edema and sloughed
  endobronchial debris
• Diminished compliance secondary to alveolar
  flooding and collapse
• Pneumonia and tracheobronchitis associated with
  loss of ciliary clearance
• Respiratory failure progressing to multiple-organ
  dysfunction

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Approach to the patient with inhalation
injury History

• what the individual was doing at the time of the
  exposure
• the substances involved and the intensity and
  duration of exposure.
• .
• If eye or upper airway mucus membrane irritation
  occurred, and when such
• irritation began provides information about the
  water solubility of a substance.
• The occurrence of symptoms in coworkers
• If material safety data sheets or container
  warnings

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• Other respiratory symptoms include cough, sputum
  production, wheezing, chest pain, and shortness
  of breath. taste sensations, central nervous
  system symptoms such as lightheadedness or
  dizziness, fever or malaise.
• The past medical history underlying lung disease
  such as asthma or COPD, whether the patient is a
  smoker,.

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Physical examination

• signs that indicate the severity of injury.
• Heart rate, respiratory rate, temperature, blood
  pressure and oxygen saturation may initially be
  normal, even in the setting of a significant
  inhalation injury.
• The skin, hair and nares, and oropharynx should
  be examined for signs of burns or chemical
  injury.
• It is important to remember that significant
  injury can occur without visible abnormalities in
  these structures.
• The presence of stridor. of wheezes or crackles.
  cyanosis, confusion, tachycardia, pulsus
  paradoxus, and fever.

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Laboratory examination

• pulse oximetry and an arterial blood gas
• If smoke inhalation is suspected, a
  carboxyhemoglobin level should be obtained. CBC
  lytes specific toxin mercury eg
• elevated plasma lactate levels may indicate
  cyanide toxicity
• If cyanide toxicity is suspected, a cyanide level
  should be drawn, but treatment should not be
  delayed if clinical suspicion is high.
• A chest radiograph may be normal early in the
  course of the event Bilateral patchy
  infiltrates suggest the development of
  pneumonitis, whereas air trapping suggests airway
  obstruction

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• laryngoscopy, or less commonly, bronchoscopy may
  be helpful looking for deposits of soot or edema
• indicates a higher risk for respiratory failure
  and a potential need for intubation.
• peak flow measurements and spirometryfull
  pulmonary function testing can help determine
  whether restrictive or obstructive pulmonary
  disease is present
• findings at the time of initial evaluation
  frequently do not correlate with the ultimate
  clinical course

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Treatment

• In general, treatment of inhalation injury is
  supportive.
• An exception is for exposures, such as
  hydrofluoric acid, that may benefit from
  treatment with a specific antidote.
• oxygen to ensure adequate oxygenation and to help
  displace carbon monoxide from hemoglobin
• smoke inhalation may require greater fluid
  resuscitation(no predictable guidelines)

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• Pulmonary toilet
• Intubation or tracheotomy may be necessary if
  there is significant upper airway compromise or
  respiratory failure
• The role of steroids in the treatment of
  inhalation injury is controversialIn patients
  with smoke inhalation, steroids have no benefit
• Several experimental treatments ascorbic acid
  infusions for treatment of inhalation injuries
• In an animal model, hyperbaric oxygen and free
  radical scavenging medications reduced the
  severity of smoke-induced pulmonary edema

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• intubation for standard indications, positive
  pressure ventilation, pulmonary toilet, and
  antibiotics for established infection.
• no value to prophylactic intubation, steroids, or
  antibiotics
• support such patients while they go through a
  predictable 7- to 21-day period of endobronchial
  slough, secondary failure of gas exchange and
  compliance, infection, and healing.
• Survivors are left with a variable degree of
  permanent lung dysfunction
• Death following burns and other forms of trauma
  is frequently the result of multiple organ system
  failure

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Disposition

• knowledge of the agent involved, and the
  intensity and duration of exposure
• Inhalation of certain agents, such as phosgene,
  can produce few initial symptoms, yet progress to
  significant pulmonary edema, ARDS, and
  respiratory failure within 12 to 24 hours of
  exposure.
• Indicators of poor prognosis include progressive
  respiratory difficulty, presence of rales on
  physical examination, burns to the face,
  hypoxemia, and altered mental status.

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Follow-up care

• often self-limited events,
• For mild exposures, a follow-up appointment
  should be made several days after the initial
  exposure, with clear instructions to the patient
  to seek medical care immediately if symptoms are
  worsening.
• serial spirometry
• methacholine challenge test
• psychological and social support to avoid
  post-traumatic stress disorder
• Social issues, related to returning to work and
  work restrictions, as well as workers
  compensation programs, may be present.
• consultation with an industrial hygienist or a
  regional occupational and environmental health
  center

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CASE

• Coal miner in bellevue underground mine4 miles
  to the coal facewent down into new seamcanary
  stopped singing found by partner at the end of
  shiftvery dead

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I TOT I TAW A PUDDY TAT... I DID, I DID TEE A
PUDDDDDD______
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Physical Asphyxiants

• any gas that displaces sufficient oxygen from the
  breathable air. produces tissue anoxia
• asymptomatic if the FiO2 is normalworkplace
  relatedNitrogen, carbon dioxide, ethane, methane
  all colourless odourless gasesless commonly
  encountered are the inert gases argon, neon, and
  heliumA consistent history, an appropriate
  spectrum of complaints, and rapid resolution on
  removal from exposure
• oxygenation, and supportive care.

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• the differential diagnosis is extensive
• scene investigation
• (interestingly deaths related to intentions
  inhalation of automotive exhaust result from
  simple asphyxiation and not CO)headache,
  hyperventilation, nausea, confusion, loss of
  consciousness, apnea, and death. At high
  concentrations of gas, unconsciousness may occur
  within minutes..Dyspnea is not an early finding
  because hypoxemia vs hypercarbiamost patients
  present with resolving symptoms.
• failure to improve may suggest complications of
  ischemia (e.g., seizures, coma, cardiac arrest)
  and is associated with a poor prognosis

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• Nitrogen gas clear, colorless gasindustrial
  processes, underground mines when accompanied
  by carbon dioxide in coal mines, black damp
• Carbon dioxide
• clear, odorless gas used in its gaseous, liquid,
  or solid form. textile, leather, wine, and
  chemical industries, in food preservation, in
  welding, as a fire extinguisher,

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• Methane and ethane low-molecular-weight
  hydrocarbons that are colorless and odorless.
  Mercaptan is usually added to methaneMethane is
  the principal component of natural gas (85)
  formed from decaying organic matter such as from
  swamps Ethane is a small component of natural
  gas (9) and is also used as a refrigerant.
  Methane is lighter than air
• Explosion may occur before death by
  asphyxiation. suicides with natural gas,.

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Case

• Firefighter whose respirator malfunctionedFound
  down in basement of styrofoam factoryunconsious
• singed nasal hairs soot in back of throat

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Smoke Inhalation

• 4000 persons die or are injured by residential
  fires in the United States Smoke inhalation
  injury is typically irritant in nature.
  Irritant toxins produced by the fire are adsorbed
  onto carbonaceous particlesdamage the mucosa
  acid generation and free radical formation,
  Early visualization of the airway is critical
  with early intubation if damage is present.
  Inhalation injury commonly accompanies burning
  and is a major determinant of length of intensive
  care unit stay
• air has such a low heat capacity that it rarely
  produces lower airway damage.

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• Smoke is always undefined and nonuniform very
  variableThe nature of the fuel determines the
  composition complex chemistry of heat
  decomposition and pyrolysisthe toxins of concern
  are formed de novo
• carbon monoxide and cyanide with smoke inhalation
  
• the onset of clinical symptomatology is highly
  variable can be delayedsinged nasal hairs and
  soot in the sputum suggest substantial exposure
  but are not sufficiently sensitive or specific to
  be practical.
• filtered smoke (e.g., in a different room) or to
  relatively smokeless combustion (e.g., engine
  exhaust) inhale predominantly CO, cyanide, and
  metabolic poisons and do not suffer irritant
  exposure.
• .

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• ongoing bacterial pneumonitis. Staphylococcus
  and pseudomonas
• bronchoalveolar lavage to assist with pulmonary
  toilet No lavage of carbonaceous material
• Corticosteroids, whether inhaled or systemic, are
  not indicated and potentially harmfullong-term
  morbidity, including the development of
  bronchiolitis obliterans and asthmaPatients
  with concerning clinical findings (e.g.,
  hoarseness, respiratory distress) and those with
  identifiers of substantial exposure (e.g.,
  closed-space exposure, carbonaceous sputum)
  should be admitted to a critical care unit or
  transferred to a burn center

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CHEMICAL ASPHYXIANTS

• tissue hypoxia from interference with oxygen
  delivery or utilization.
• Carbon monoxide combines with hemoglobin to form
  carboxyhemoglobinand interferes with oxygen
  delivery,
• hydrogen cyanide and hydrogen sulfide
• oxidative enzymes and impair oxygen utilization.

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THIRTEEN FACTS ABOUT CARBON MONOXIDE

• most common cause of acute poisoning death and
  the most common cause of fire-related death CO
  poisoning can be obscure and subacute with flu
  h/a symptomsincomplete combustion of virtually
  all carbon-containing products. interacts with
  deoxyhemoglobin to form carboxyhemoglobin (COHb),
  which cannot carry oxygen. (approximately 240
  times greater than for oxygen) be overcome by
  high tissue levels of oxygen. 4 to 6 hours on
  room air, 90 minutes with 100 oxygen at 1 atm,
  30 minutes on 100 oxygen at 3 atm of pressure.
  The affinity of fetal hemoglobin for CO is even
  greater, hcg on all women

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• affects myoglobin, and interferes with oxidative
  phophorylation through cytochromealtered mental
  status, including coma and seizures extremely
  abnormal vital signs, including hypotension and
  cardiac arrest and metabolic acidosis.cigarett
  es contains 3 to 6 carbon monoxide, or an
  average exposure of 400 ppm during inhalation.
  By comparison, the work-place standard allowed
  by OSHA is 50 ppm. cherry-red color is a
  postmortem findingThe ABG measurement cannot be
  used as a diagnostic test
• HBO therapy in patients with CO poisoning are
  controversialLevels .gt 25. 40Disposition
  Patients with no or mild symptoms (after
  exposure of less than 5 minutes) who become
  asymptomatic after a few hours of oxygen therapy
  and have a CO level below 10, normal findings on
  physical examination and on neurologic-cognitive
  examination, and normal ABG parameters, may be
  discharged but instructed to return if any signs
  of neurologic dysfunction arise. Patients with CO
  poisoning necessitating treatment need follow-up
  neuropsychiatric examination.

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Simultaneous Carbon Monoxide and Cyanide
Poisoning (Fire Victim

• a major factor in the mortality associated with
  exposure to fire smoke. Standard therapy with
  the nitrite in the cyanide antidote kit produces
  methemoglobinemia,
• worsens carcon monoxide poisoningSodium
  thiosulfate, administered alone is safe
• A standard dose of 12.5 g therapy in an HBO
  chamber may receive nitrite therapy while
  pressurized

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FIFTEEN FACTS About Hydrogen Cyanide

• Hydrogen cyanide is a colorless liquid or gas
• widespread industrial use,. Combustion of various
  plastics.... found in fruit pits,
  nitroprussideHydrogen cyanide is
  nonirritating...... odor of bitter apricot
  rapidly absorbed distributed to the
  oxygen-utilizing body tissues. Inhibition of
  oxidative metabolism by binding to complex IV of
  the electron transport chain within mitochondria
  occurs within secondsdepletes ATP high venous
  oxygen content aterialization of venous blood
  Fundal veins and arteries may appear equally
  red.

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• An increased anion gap metabolic acidosis should
  be present, and the serum lactate level should be
  elevated. A lactate level greater than 10 mmol/L
  in a fire victim is highly predictive of cyanide
  poisoning. stimulates chemoreceptors in the
  aorta and carotid artery, causing
  hyperpnea.acyanotic patient with respiratory
  and cns symptoms Contact with cyanide salts may
  also cause direct respiratory, mucous membrane,
  and skin irritation, as well as skin burns from
  the caustic solution. mild acute poisoning is
  uncommon high index of suspicion with rapid
  responsean appropriate history of exposure or
  ingestion.

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• Specific therapy the production of methemoglobin,
  inducing methemoglobinemia which competes with
  the cytochrome oxidase system for binding of
  cyanide. Cyanide has a high affinity for MetHb
  and readily leaves cytochrome oxidase to form
  cyanomethemoglobin
• inhaled Amyl nitrite followed by (IV) sodium
  nitrite more effecticvethiosulfate component,
  should be administered immediately
• The last part of the antidote kit is the
  sulfur-containing compound sodium thiosulfate.
  The adult dose is 12.5 gms. Cyanide and
  cyanomethemoglobin are detoxified by sulfur
  transferase sulfur donor
• The best results are attained when the kit is
  used in combination with aggressive
  resuscitation.

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Case

• Two men killed in manhole accidentPutting in
  wires for television companyWaiting over man
  hole hit by wave of gasHidden in the trees,
  around the bend of the river, was a lake of raw
  sewage created from the overflowing line. In all,
  there was about 2,750 feet of 18- and 15-inch
  pipe filled with septic sewage behind the plugs.
  It had been standing in the pipes for at least 40
  daysHe fell forward, paralyzed, directly into
  the channel of the nine-foot deep manhole. Head
  injuries from the fall alone would have killed
  himFriend went into hole to get him died also

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Hydrogen SulfideProduction and Uses

• Rapid tests for hydrogen sulfide are not
  available,
• Although not routinely available, blood sulfide
  levels can be measured.
• presence of blackened copper coins in the.pockets
• Hydrogen sulfide is a colorless gas heavier than
  air,accumulates at the bottom of a confined space
  with a characteristic rotten-egg odor
• low olfactory threshold, at 0.02 ppm,
• (olfactory fatigue can occur at concentrations of
  100 to 150 ppm,)
• Hydrogen sulfide is used industrially
• oil refineries decompostion of organic material
  mining
• potent cytotoxic asphyxiant, impairing cytochrome
  oxidase and cellular respiration

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• The treatment of hydrogen urgency as for
  hydrogen cyanide, and general supportive
  measures are similar.
• The formation of methemoglobin reverses the
  effects of hydrogen sulfide
• rapid cardiovascular collapse and death a
  mechanism identical to that for cyanide
  poisoning. Hydrogen sufide spontaneously
  dissociates from the mitochondria allowing
  patients to survive after exposure
• inhalation of amyl nitrite followed by infusion
  of 10 mL of a 3 solution of sodium nitrite over
  2 to 4 minutes.
• sodium thiosulfate not generally recommended.
  (hydrogen sulfide is not detoxified by rhodanese)
• A potential role for the use of HBO not uniformly
  acceptedfor delayed neuropsychiatric symptoms
• All patients with symptomatic cyanide or hydrogen
  sulfide admitted

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• Workers can experience a knockdown with one
  inhalation
• often fall away from gas exposure into fresh air
• three most common causes of death are
• a fall into water, into machinery, into a space
  with compromised airway
• antidotes are usually not useful because once the
  patient is removed from source recover quickly
• permanent damage is caused by hypoxic injury
• awaken suddenly spontaneously with overwhelming
  air hunger

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Case

• 128 people many of whom were childrenbrought in
  from pool in Tuebingen found to have irritated
  eyes, coughsome complaining of inability to
  smelltwo required intubation for
  hypoxiadefective bottle found in pump room

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IRRITANT GASES

• Irritant gases cause pulmonary damage by direct
  injury
• The severity of injury depends upon the duration
  of exposure, concentration of the irritant, and
  physical and chemical properties.
• More water-soluble irritants, such as ammonia,
  formaldehyde and chlorine, cause upper airway
  injury and burning and watery eyes or cough

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• Severe exposure may result in pulmonary edema,
  hypoxemia, and respiratory failure
• Anosmia may also result from chlorine gas
  exposure
• Pulmonary function studies may show an
  obstructive pattern bronchiolitis obliterans
• decline in pulmonary function over several years
• Repeated low level exposures may have cumulative
  effects

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Chlorine

• It is greenish-yellow in color and has a pungent
  odor low odor threshold and good warning
  properties. Industrial use
• Transported in pressurize containers as liquid
• Prolonged exposure chlorine is denser than air
  remains at ground level.
• industrial leaks, environmental releases
  occurring primarily in transport, water
  purification, swimming pool-related events, and
  household-cleaning product misadventures.

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Other Irritant Gases

• PhosgeneTen times as toxic as chlorine not water
  soluble so has its effect deep in the
  parenchymAmmoniaFrom fertiizer a base or
  alkaliLiquefactive necrosis full thickness
  tissue destructionBronchiectasis chronic
  restrictive and obstructive pulmonary
  changesNitrogen DioxideReddish brown
  gasoccupational exposure manufacture of nitric
  and sulfuric acids, explosives, fertilizers,
  cellulose compounds, and dyes. metal etching and
  photoengraving and the cleaning of copper and
  brass. Nitric oxide is produced in welding.

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• Ozone
• is a bluish gas pungent odor of photochemical
  smog Ozone is highly toxic to the respiratory
  tract. water purification, Sulfur dioxide
• Sulfur dioxide (SO2) gas is a byproduct of the
  combustion of sulfur-containing fossil fuels.
  major component of air pollution smog.

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• Hydrofluoric acid
• (hydrogen fluoride), irritant effects, clinically
  significant hypocalcemia A specific antidote,
  calcium gluconate, is available for topical use,
  and is also available in an inhaled form. Crowd
  control agents ("tear gasses)to incapacitate
  persons via immediate mucous membrane irritation
  chloroacetophenone ("mace"), and
  orthochlorobenzamalonitrile lower respiratory
  injury with high-intensity exposure

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Inhalations With Systemic Effects

• Cadmium, Mercury, and Other Toxic
  MetalsInhalation of certain metal fumes or
  vapors causes acute pneumonitisMetal Fume
  Fever, Polymer Fume Fever, and Organic Dust Toxic
  Syndromehallmark is chills, fever, malaise, and
  myalgia with onset 4 to 8 hours after Metal fume
  fever is associated with zinc oxide inhalation
  from welding galvanized metal or brass working

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Take Home Points

• Inhalation injury most common form of industrial
  accident
• Identify agent with occupational history
• Inhalation injury caused by four mechanisms,
  simple asphyxiation, chemical asphyxiation,
  irritant exposure and systemic effects
• Carbon Monoxide is the most common inhalational
  agent
• Think cyanide poisoning in smoke inhalation
• There is a three stage antidote kit for cyanide
  and hydrogen sulfide poisoning
• Say your prayers when the canary stops singing!!!

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