Chapter 7 Body Systems - Kingwood Application Server
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Transcript Chapter 7 Body Systems - Kingwood Application Server
Chapter 43
Smoke Inhalation and
Thermal Injures
ME
AB
TS
SM
FWS
Figure 43-1. Smoke inhalation and thermal injuries. TS, Thick secretions; BL, airway blister;
ME, mucosal edema; SM, smoke (toxic gas); FWS, frothy white secretions (pulmonary edema).
Slide 1
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Anatomic Alterations of the Lungs:
Thermal Injury
Slide 2
Injury caused by the inhalation of hot gases
Usually confined to upper airway
Nasal cavity
Oral cavity
Nasopharynx
Oropharynx
Laryngopharynx
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Anatomic Alterations of the Lungs:
Thermal Injury
Slide 3
Distal airways—usually spared because of:
Ability of upper airways to cool hot gases
Reflex laryngospasm
Glottic closure
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Anatomic Alterations of the Lungs:
Thermal Injury
Slide 4
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
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Anatomic Alterations of the Lungs:
Smoke Inhalation Injury
Early Stage (0 to 24 Hours Postinhalation)
Slide 5
Injuries not apparent right away
Pulmonary status changes over first 24 hours
Tracheobronchial tree becomes inflamed
Excessive airway secretions develop
Bronchospasms develop
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Anatomic Alterations of the Lungs:
Smoke Inhalation Injury
Intermediate Stage (2 to 5 Days Postinhalation)
Slide 6
Upper airways begin to improve, but the effects
of smoke inhalation peak
Excessive airway secretions
Mucosa sloughing occurs
Mucus plugging and atelectasis develop
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Anatomic Alterations of the Lungs:
Smoke Inhalation Injury
Intermediate Stage (2 to 5 Days Postinhalation)
Slide 7
Bronchial colonization, bronchitis, and
pneumonia frequently develop
Gram-positive
• Staphylococcus aureus
Gram-negative
• Klebsiella
• Enterobacter
• Escherichia coli
• Pseudomonas
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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
Slide 8
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Anatomic Alterations of the Lungs:
Smoke Inhalation Injury
Late Stage (5 or More Days Postinhalation)
Slide 9
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
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Anatomic Alterations of the Lungs:
Smoke Inhalation Injury
Slide 10
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
• Chronic atelectasis
Obstructive lung disorder
• Chronic bronchial secretions
• Bronchial stenosis
• Bronchial polyps
• Bronchiectasis
• Bronchiolitis
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Anatomic Alterations of the Lungs:
Thermal Injury
Slide 11
Blistering
Mucosal edema
Vascular congestion
Epithelial sloughing
Thick secretions
Acute upper airway obstruction
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Anatomic Alterations of the Lungs:
Smoke Inhalation Injury
Slide 12
Inflammation of the bronchial airways
Bronchospasm
Excessive bronchial secretions and mucus
plugging
Decreased mucosal ciliary transport
Atelectasis
Alveolar edema (pulmonary edema)
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Anatomic Alterations of the Lungs:
Smoke Inhalation Injury
Slide 13
ARDS (severe cases)
Bronchiolitis obliterans with organizing
pneumonia (BOOP)
Alveolar fibrosis, bronchial stenosis,
bronchial polyps, and bronchiectasis
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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
Slide 14
Scalding burns account for up to 80% of thermal
injuries among children
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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
Slide 15
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Table 43-1.
Slide 16
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Table 43-1., cont.
Slide 17
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Table 43-1., cont.
Slide 18
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Table 43-1., cont.
Slide 19
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Table 43-2.
Slide 20
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Etiology
Slide 21
The severity and depth of burns usually are
defined as follows:
First degree
• Minimal depth in skin
Second degree
• Superficial to deep thickness of skin
Third degree
• Full thickness of skin including tissue beneath skin
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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)
Slide 22
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Figure 9-7. Atelectasis clinical scenario.
Slide 23
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Figure 9-8. Alveolar consolidation clinical scenario.
Slide 24
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Figure 9-9. Increased alveolar-capillary membrane thickness clinical scenario.
Slide 25
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Figure 9-10. Bronchospasm clinical scenario (e.g., asthma).
Slide 26
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Figure 9-11. Excessive bronchial secretions clinical scenario.
Slide 27
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Clinical Data Obtained at the
Patient’s Bedside
Vital signs
Slide 28
Increased respiratory rate
Increased heart rate, cardiac output,
blood pressure
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Clinical Data Obtained at the
Patient’s Bedside
Slide 29
Assessment of acute upper airway
obstruction (thermal injury)
Obvious pharyngeal edema and swelling
Inspiratory stridor
Hoarseness
Altered voice
Painful swallowing
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Clinical Data Obtained at the
Patient’s Bedside
Slide 30
Cyanosis
Cough and sputum production
Chest assessment findings
Usually normal breath sounds (early stage)
Wheezing
Crackles
Rhonchi
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Clinical Data Obtained from
Laboratory Tests and Special
Procedures
Slide 31
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Pulmonary Function Study:
Expiratory Maneuver Findings
FVC
FEVT
N or
FEF25%-75%
N or
FEF200-1200
N
PEFR
MVV
FEF50%
FEV1%
N
Slide 32
N or
N
N or
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Pulmonary Function Study:
Lung Volume and Capacity Findings
VT
N or
VC
RV*
FRC*
TLC
ERV
RV/TLC%
N
IC
* When airways are partially obstructed.
Slide 33
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Decreased Diffusion Capacity
(DLCO)
Slide 34
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Arterial Blood Gases
Early Stages of Smoke Inhalation
pH
Slide 35
Acute alveolar hyperventilation with
hypoxemia
PaCO2
HCO3 (Slightly)
PaO2
/Normal
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Time and Progression of Disease
Disease Onset
Alveolar Hyperventilation
100
90
PaO2 or PaCO2
80
Point at which PaO2
declines enough to
stimulate peripheral
oxygen receptors
70
60
PaO2
50
40
30
20
10
0
Figure 4-2. PaO2 and PaCO2 trends during acute alveolar hyperventilation.
Slide 36
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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*
PacO2
HCO3
PaO2
Normal
* Lactic acidemia.
† But patient has tissue hypoxia.
Slide 37
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Arterial Blood Gases
Late Stages of Smoke Inhalation
Slide 38
Acute ventilatory failure with hypoxemia
pH
PaCO2
HCO3 (Slightly)
PaO2
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Oxygenation Indices
Early and
Intermediate Stages
Late Stage
DO2
VO2
_
C(a-v)O2
O2ER
SvO2
.
_
Slide 39
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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
__
Slide 40
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Hemodynamic Indices, cont.
Slide 41
Early
Stage
Intermediate
Stage
Late
Stage
RVSWI
Normal
LVSWI
Normal
PVR
Normal
Normal
SVR
Normal
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Carbon Monoxide Poisoning
Slide 42
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Table 43-3.
Slide 43
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Table 43-3., cont.
Slide 44
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Cyanide Poisoning
Slide 45
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Radiologic Findings
Chest radiograph
Slide 46
Usually normal (early stage)
Pulmonary edema/ARDS (intermediate stage)
Patchy or segmental infiltrates (late stage)
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Figure 43-2. 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.)
Slide 47
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General Management of
Hot Gas and Smoke Inhalation
Slide 48
General emergency care
Airway management
Bronchoscopy
Hyperbaric oxygen
Treatment for cyanide poisoning
Antibiotic agents
Expectorants
Analgesic agents
Prophylactic anticoagulants
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General Management of
Hot Gas and Smoke Inhalation
Respiratory care treatment protocols
Slide 49
Oxygen therapy protocol
Bronchopulmonary hygiene therapy protocol
Hyperinflation therapy protocol
Aerosolized medication protocol
Mechanical ventilation protocol
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Classroom Discussion
Case Study:
Smoke Inhalation and Thermal Injury
Slide 50
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