Copyright © 2006 by Mosby, Inc. Slide 1 Chapter 43 Smoke Inhalation and Thermal Injures Figure Smoke inhalation and thermal injuries. TS, Thick secretions; BL, airway blister; ME, mucosal edema; SM, smoke (toxic gas); FWS, frothy white secretions (pulmonary edema). AB FWS SM TS ME
Copyright © 2006 by Mosby, Inc. Slide 2 Anatomic Alterations of the Lungs: Thermal Injury Injury caused by the inhalation of hot gases Usually confined to upper airway Nasal cavity Oral cavity Nasopharynx Oropharynx Laryngopharynx
Copyright © 2006 by Mosby, Inc. Slide 3 Anatomic Alterations of the Lungs: Thermal Injury Distal airways—usually spared because of: Ability of upper airways to cool hot gases Reflex laryngospasm Glottic closure
Copyright © 2006 by Mosby, Inc. Slide 4 Anatomic Alterations of the Lungs: Thermal Injury Except for the rare instance of steam inhalation, direct thermal injuries do not usually occur below the level of the larynx Distal airway damage is usually caused by the harmful products found in SMOKE
Copyright © 2006 by Mosby, Inc. Slide 5 Anatomic Alterations of the Lungs: Smoke Inhalation Injury Early Stage (0 to 24 Hours Postinhalation) Injuries not apparent right away Pulmonary status changes over first 24 hours Tracheobronchial tree becomes inflamed Excessive airway secretions develop Bronchospasms develop
Copyright © 2006 by Mosby, Inc. Slide 6 Anatomic Alterations of the Lungs: Smoke Inhalation Injury Intermediate Stage (2 to 5 Days Postinhalation) Upper airways begin to improve, but the effects of smoke inhalation peak Excessive airway secretions Mucosa sloughing occurs Mucus plugging and atelectasis develop
Copyright © 2006 by Mosby, Inc. Slide 7 Anatomic Alterations of the Lungs: Smoke Inhalation Injury Intermediate Stage (2 to 5 Days Postinhalation) Bronchial colonization, bronchitis, and pneumonia frequently develop Gram-positive Staphylococcus aureus Staphylococcus aureus Gram-negative Klebsiella Klebsiella Enterobacter Enterobacter Escherichia coli Escherichia coli Pseudomonas Pseudomonas
Copyright © 2006 by Mosby, Inc. Slide 8 Anatomic Alterations of the Lungs: Smoke Inhalation Injury Intermediate Stage (2 to 5 Days Postinhalation) If not already present, the following may develop: Noncardiogenic pulmonary edema Acute respiratory distress syndrome When chest wall burns are present, the patient may not be able to breathe deeply and cough due to: Pain The use of narcotics Immobility Increased airway resistance Decreased lung and chest compliance
Copyright © 2006 by Mosby, Inc. Slide 9 Anatomic Alterations of the Lungs: Smoke Inhalation Injury Late Stage (5 or More Days Postinhalation) Infections resulting from burn wounds are the major concern during this period Sepsis-induced multiorgan failure is the primary cause of death during this stage Pneumonia continues to be a major problem Pulmonary embolism may develop
Copyright © 2006 by Mosby, Inc. Slide 10 Anatomic Alterations of the Lungs: Smoke Inhalation Injury Late Stage (5 or More Days Postinhalation) Finally, the long-term effects of smoke inhalation can result in either a restrictive or obstructive lung disorder Restrictive lung disorder Alveolar fibrosis Alveolar fibrosis Chronic atelectasis Chronic atelectasis Obstructive lung disorder Chronic bronchial secretions Chronic bronchial secretions Bronchial stenosis Bronchial stenosis Bronchial polyps Bronchial polyps Bronchiectasis Bronchiectasis Bronchiolitis Bronchiolitis
Copyright © 2006 by Mosby, Inc. Slide 11 Anatomic Alterations of the Lungs: Thermal Injury Blistering Mucosal edema Vascular congestion Epithelial sloughing Thick secretions Acute upper airway obstruction
Copyright © 2006 by Mosby, Inc. Slide 12 Anatomic Alterations of the Lungs: Smoke Inhalation Injury Inflammation of the bronchial airways Bronchospasm Excessive bronchial secretions and mucus plugging Decreased mucosal ciliary transport Atelectasis Alveolar edema (pulmonary edema)
Copyright © 2006 by Mosby, Inc. Slide 13 Anatomic Alterations of the Lungs: Smoke Inhalation Injury ARDS (severe cases) Bronchiolitis obliterans with organizing pneumonia (BOOP) Alveolar fibrosis, bronchial stenosis, bronchial polyps, and bronchiectasis
Copyright © 2006 by Mosby, Inc. Slide 14 Etiology Fire-related death is the third most common cause of accidental death in the United States It is estimated that thermal injury results in about 60,000 hospitalizations and about 6000 deaths annually Children account for about 50% of these deaths Scalding burns account for up to 80% of thermal injuries among children
Copyright © 2006 by Mosby, Inc. Slide 15 Etiology The prognosis of fire victims usually is determined by the: 1. Extent and duration of smoke exposure 2. Chemical composition of the smoke 3. Size and depth of body surface burns 4. Temperature of gases inhaled 5. Age (prognosis worsens in the very young and old) 6. Preexisting health status
Copyright © 2006 by Mosby, Inc. Slide 16 Table 43-1.
Copyright © 2006 by Mosby, Inc. Slide 17 Table 43-1., cont.
Copyright © 2006 by Mosby, Inc. Slide 18 Table 43-1., cont.
Copyright © 2006 by Mosby, Inc. Slide 19 Table 43-1., cont.
Copyright © 2006 by Mosby, Inc. Slide 20 Table 43-2.
Copyright © 2006 by Mosby, Inc. Slide 21 Etiology The severity and depth of burns usually are defined as follows: First degree Minimal depth in skin Minimal depth in skin Second degree Superficial to deep thickness of skin Superficial to deep thickness of skin Third degree Full thickness of skin including tissue beneath skin Full thickness of skin including tissue beneath skin
Copyright © 2006 by Mosby, Inc. Slide 22 Overview of the Cardiopulmonary Clinical Manifestations Associated with SMOKE INHALATION AND THERMAL INJURIES The following clinical manifestations result from the pathophysiologic mechanisms caused (or activated) by Atelectasis (see Figure 9-7), Alveolar Consolidation (see Figure 9-8), Increased Alveolar-Capillary Membrane Thickness (see Figure 9-9), Bronchospasm (see Figure 9-10), and Excessive Airway Secretions (see Figure 9-11)—the major anatomic alterations of the lungs associated with smoke inhalation and thermal injuries (see Figure 43-1)
Copyright © 2006 by Mosby, Inc. Slide 23 Figure 9-7. Atelectasis clinical scenario.
Copyright © 2006 by Mosby, Inc. Slide 24 Figure 9-8. Alveolar consolidation clinical scenario.
Copyright © 2006 by Mosby, Inc. Slide 25 Figure 9-9. Increased alveolar-capillary membrane thickness clinical scenario.
Copyright © 2006 by Mosby, Inc. Slide 26 Figure Bronchospasm clinical scenario (e.g., asthma).
Copyright © 2006 by Mosby, Inc. Slide 27 Figure Excessive bronchial secretions clinical scenario.
Copyright © 2006 by Mosby, Inc. Slide 28 Clinical Data Obtained at the Patient’s Bedside Vital signs Increased respiratory rate Increased heart rate, cardiac output, blood pressure
Copyright © 2006 by Mosby, Inc. Slide 29 Clinical Data Obtained at the Patient’s Bedside Assessment of acute upper airway obstruction (thermal injury) Obvious pharyngeal edema and swelling Inspiratory stridor Hoarseness Altered voice Painful swallowing
Copyright © 2006 by Mosby, Inc. Slide 30 Clinical Data Obtained at the Patient’s Bedside Cyanosis Cough and sputum production Chest assessment findings Usually normal breath sounds (early stage) Wheezing Crackles Rhonchi
Copyright © 2006 by Mosby, Inc. Slide 31 Clinical Data Obtained from Laboratory Tests and Special Procedures
Copyright © 2006 by Mosby, Inc. Slide 32 Pulmonary Function Study: Expiratory Maneuver Findings FVC FEV T FEF 25%-75% FEF N or N or N PEFR MVV FEF 50% FEV 1% N N or N N or FVC FEV T FEF 25%-75% FEF N or N or N PEFR MVV FEF 50% FEV 1% N N or N N or
Copyright © 2006 by Mosby, Inc. Slide 33 Pulmonary Function Study: Lung Volume and Capacity Findings V T RV* FRC* TLC N or VC IC ERV RV/TLC% N V T RV* FRC* TLC N or VC IC ERV RV/TLC% N * When airways are partially obstructed.
Copyright © 2006 by Mosby, Inc. Slide 34 Decreased Diffusion Capacity (DL CO )
Copyright © 2006 by Mosby, Inc. Slide 35 Arterial Blood Gases Early Stages of Smoke Inhalation Acute alveolar hyperventilation with hypoxemia pH Pa CO 2 HCO 3 - Pa O 2 (Slightly) /Normal pH Pa CO 2 HCO 3 - Pa O 2 (Slightly) /Normal
Copyright © 2006 by Mosby, Inc. Slide 36 Time and Progression of Disease Pa CO Alveolar Hyperventilation Point at which PaO 2 declines enough to stimulate peripheral oxygen receptors Pa O 2 Disease Onset Pa O 2 or Pa CO 2 Figure 4-2. PaO 2 and PaCO 2 trends during acute alveolar hyperventilation.
Copyright © 2006 by Mosby, Inc. Slide 37 Arterial Blood Gases Severe Smoke Inhalation and Burns with Metabolic Acidosis When carbon monoxide or cyanide poisoning is present, the patient may demonstrate the following: COHB pH* Pac O 2 HCO 3 - Pa O 2 Normal * Lactic acidemia. † But patient has tissue hypoxia.
Copyright © 2006 by Mosby, Inc. Slide 38 Arterial Blood Gases Late Stages of Smoke Inhalation Acute ventilatory failure with hypoxemia pH Pa CO 2 HCO 3 - Pa O 2 (Slightly)
Copyright © 2006 by Mosby, Inc. Slide 39 Oxygenation Indices DO 2 VO 2 C(a-v)O 2 O 2 ER SvO 2 Early and Intermediate Stages Late Stage. _ _
Copyright © 2006 by Mosby, Inc. Slide 40 Hemodynamic Indices (Cardiogenic Pulmonary Edema) Early Stage Intermediate Stage Late Stage CVP Normal RAP Normal PA Normal PCWP Normal CO Normal SV Normal SVI Normal CI Normal __
Copyright © 2006 by Mosby, Inc. Slide 41 Hemodynamic Indices, cont. RVSWI Normal LVSWI Normal PVRNormalNormal SVR Normal Early Stage Intermediate Stage Late Stage
Copyright © 2006 by Mosby, Inc. Slide 42 Carbon Monoxide Poisoning
Copyright © 2006 by Mosby, Inc. Slide 43 Table 43-3.
Copyright © 2006 by Mosby, Inc. Slide 44 Table 43-3., cont.
Copyright © 2006 by Mosby, Inc. Slide 45 Cyanide Poisoning
Copyright © 2006 by Mosby, Inc. Slide 46 Radiologic Findings Chest radiograph Usually normal (early stage) Pulmonary edema/ARDS (intermediate stage) Patchy or segmental infiltrates (late stage)
Copyright © 2006 by Mosby, Inc. Slide 47 Figure A, Radiograph of a young man admitted after accidentally setting his kitchen on fire while intoxicated. B, Prompt recovery after 72 hours. (Courtesy Dr. K. Simpkins, Leeds, England. From Armstrong P et al: Imaging of diseases of the chest, ed 2, St. Louis, 1995, Mosby.)
Copyright © 2006 by Mosby, Inc. Slide 48 General Management of Hot Gas and Smoke Inhalation General emergency care Airway management Bronchoscopy Hyperbaric oxygen Treatment for cyanide poisoning Antibiotic agents Expectorants Analgesic agents Prophylactic anticoagulants
Copyright © 2006 by Mosby, Inc. Slide 49 General Management of Hot Gas and Smoke Inhalation Respiratory care treatment protocols Oxygen therapy protocol Bronchopulmonary hygiene therapy protocol Hyperinflation therapy protocol Aerosolized medication protocol Mechanical ventilation protocol
Copyright © 2006 by Mosby, Inc. Slide 50 Classroom Discussion Case Study: Smoke Inhalation and Thermal Injury