CO , Toxin Inhalation and Thermal Lung Injury

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CO , Toxin Inhalation and Thermal Lung Injury

• SKH Pulmonary Critical Care Department
• Dr.CK Chang

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Introduction

• Smoke inhalation is a major cause of morbidity
  and mortality in fore-exposed persons
• High-water solubility ? proximal airway injury
• Low-water solubility ? distal airway injury
• Particle size lt 0.5um ? terminal bronchioles and
  alveoli injury
• Acid injury ? coagulation of underlying tissue
• Alkali injury ? liquification of mucosa ? deep
  penetration injury
• Reactive oxygen ? lipid peroxidation ? direct
  injury to cells

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Carbon Monoxide (CO)

• Odorless, colorless gas
• Mort dangerous gas in fire. Leading cause of
  death at scene and 24h after fire
• Affinity of CO for Hb gt210x than O2 ?shift
  dissociation curve to left ? tissue hypoxia
• CAD(), COHb 4.5 ? exercise tolerance
  decreased and MI increased
• CAD(), COHb 6 ?ventricular arrythmia
  increased during exercise ? death
• COHb 60-70 ? unconsciousness, convulsions, resp.
  failure and death

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CO

• S/S skin blisters, retinal hemorrhage, DIC,
  myonecrosis, hyperglycemia and DI
• Acute and chronic neurologic and psychologic
  sequelae

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CO -- Treatment

• Emergent 100 oxygen therapy
• 100 O2 ? COHb t1/2 80min
• 3 atm 100 O2 ? COHb t1/2 25min
• Metabolic acidosis should not be treated unless
  severe (lt7.2), since acidosis facilitates oxygen
  delivery by shifting the O2 dissociation curve to
  the right

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CO -- Treatment

• Mild poisoning (COHblt20) --- 100
  non-rebreathing mask until level falls lt5
• Moderate poisoning (COHb 20 40) without
  cardiac or neurologic dysfunction --- monitoring
  of acid-base status and 100 oxygen until level
  falls lt5
• Severe poisoning (COHbgt40) or with cardiac or
  neurologic symptoms--- hyperbaric oxygen therapy
• Admission is required for all with level gt25 or
  with cardiac and neurologic symptoms

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Hydrogen Cyanide

• Colorless with odor of bitter almond
• Interferes with cellular utilization of oxygen
  and inhibits cytochrome-c oxidase in mitochondria
• Causes anaerobic metabolism and lactic acidosis (
  increased anion gap)
• Blood level 0.5-1 mg/dL ? flushing and
  tachycardia
• Blood level gt2.5mg/dL ? severe poisoning ?
  hypotension, slow labored breathing, pupils
  dilate

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Hydrogen Cyanide

• Pink face and nail beds, bright venous vlood
  despite poor oxygen utilization
• HCN CO ? synergic effect to depress CNS
• T1/2 is about 1h difficult to detect in general
  hospitals
• Use cyanide antidote inhaled amylnitrite
  pearls(10 sodium nitrite 25 sodium
  thiosulfate solution) if toxication is highly
  suspected.

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Hydrogen Chloride

• Produced by burning of PVC
• React with H2O to become Hydrochloric acid
• Irritation of upper airway and mucosa

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Aldehydes

• Dermal and mucosal irritants
• Pulmonary edema and death
• Wood smoke and kerosene smoke

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THERMAL INHALATION LUNG INJURY

• High temperature may cause surface burns and
  thermal injury to airways
• Usually limited to upper airways
• Injury to lower airways be considered when
• Overwhelming heat exposure
• Inhalation of steam ? increased heat-carrying
  capacity
• Aspiration of hot liquids ? direct pulmonary
  injury
• Respiratory complications and lung infection are
  the leading cause of death.

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Pathophysiology of Acute Smoke Inhalation and
Inhalational Injury

• In burn patients
• Hypermetabolic state
• Increase in plasma levels of catecholamines,
  glucagons, cortisol, and growth hormone
• Increase in O2 consumption, body temperature,
  protein catabolism, and hyperglycemia

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Pathophysiology of Acute Smoke Inhalation and
Inhalational Injury

• Smoke and heat induced Lung Injury
• Direct coagulative necrosis
• Lipid peroxidation ? free radicals
• Mediators release and complement activation ?
  inflammation
• May occur in burn patients with only skin burns

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Effects of Acute Smoke Inhalation and Thermal
injury

• Impairment of mucociliary function ? infection
• Mucus hypersecretion
• Tissue inflammation with tracheobronchiolitis,
  bronchitis, laryngitis, pneumonitis
• Epithelial sloughing
• Biochemical alteration with surfactant
  inactivation
• Increases vascular permeability and lung edema
• Bronchiconstriction
• Initially large airway obstruction ? late small
  and large airways
• BAL ? granulocytes and macrophage

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Respiratory Tract Pathology

• Similar to Acute Lung Injury (ALI)
• Early exudative phase interstitial and alveolar
  edema, hemorrhage, granulocyte influx, and type I
  cell alternation
• Degenerative phase type I cell injury,
  denudation of basement membranes, tissue
  necrosis, and generation of hyaline membranes
• Proliferative and repair responses type II cell
  hyperplasia ?alveolar basement membrane
  reepithelialization ? evolve into type I cell,
  fibroblast proliferation and matrix production ?
  attempt to restore architectural integrity
• Survivors BO, atelectasis, coagulative necrosis
  of alveoli

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Spectrum of Clinical manifestation

• Acute Manifestations
• Upper airways s/s might appear 2-4 days after
  fluid resuscitation
• Acute pulmonary edema is not common and it is a
  marker of disease severity

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Spectrum of Clinical manifestation

• Subacute/Chronic Manifestation
• Delayed-onset upper airway obstruction ? after
  fluid resuscitation 3-4 days after injury ?
  airway inflammation and edema, epithelial injury,
  hyperreactivity of airway
• Delayed-onset pulmonary edema or resp. failure ?
• -- ARDS due to irritant gases
• -- Secondary hypotension
• -- Superimposed infection or diffuse
  pneumonia
• Most recovered without much sequelae

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Clinical Evaluation

• Expectoration of carbonaceous sputum, increased
  nasal and oral secretion
• Hemoptysis not common
• Hoarseness, change in voice quality,or painful
  swelling ? raise the possibility of severe upper
  airway injury
• Severe third degree burns of the chest wall ?
  limit respiratory excursion ? restrictive
  ventilatory defect.

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Assessment of Oxygenation/Ventilation

• V/Q mismatch with mild hypoxemia
• CO intoxication normal calculated SaO2 low
  measured SaO2 and arterial O2
• CXR normal in early phase
• Patients with smoke inhalation and thermal injury
  may manisfest focal and patchy lung infiltrates
  as late as 24-48hs after smoke inhalation
• Diffuse alveolar infiltrates may be seen as late
  as 96hs

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Physiologic Evaluation

• Obstructive ventilatory defect
• Restrictive defects pulmonary edema, pneumonia,
  atelectasis, major parenchymal abnormality, large
  surface burn
• Flow-volume curve variable extrathoracic
  obstruction fixed upper airway obstruction
  variable intrathoracic obstruction
• Saw-toothing of normal smooth curves ? upper
  airway instability
• Serial flow-volume curves ? detecting
  delayed-onset upper airway obstruction and
  late-onset subglottic stenosis

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Treatment

• Airway patency and ventilation ?intubated with
  100 oxygen beware of delayed upper airway
  obstruction
• Oxygen supply
• Bronchodilators
• Antibiotics empiric antibiotic therapy is not
  recommended

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Treatment

• Corticosteroids
• Is not indicated for fire victims with dermal
  burn and thermal inhalation injury
• Did not reduce pulmonary complications and
  mortality
• Increased risk (3-4x) of mortality due to
  infections
• Indications underlying asthma and severe
  bronshospasm BO upper airway edema who fail
  extubation

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