Chapter 9: Smoke Inhalation Injury and Burns · § List the effects of smoke inhalation injury on...
Transcript of Chapter 9: Smoke Inhalation Injury and Burns · § List the effects of smoke inhalation injury on...
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Lecture Notes Chapter 9: Smoke Inhalation
Injury and Burns
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Objectives § List the factors that influence mortality rate § Describe the nature of smoke inhalation and the
fire environment § Recognize the pulmonary and systemic
changes that occur following smoke inhalation and burn injury
§ List the effects of smoke inhalation injury on the upper and lower airways
§ Identify methods to diagnose smoke inhalation injury and CO poisoning
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Objectives § Describe the methods used to determine the
type and extent of burn injury § Recognize the emergent treatment for smoke
inhalation injury and CO poisoning § Describe the airway and ventilatory support
strategies for smoke inhalation and burn injury § Describe the fluid, surgical, and nutritional
support used in the treatment of burn injuries
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Introduction § Fire is a major source of injury, death, and
economic loss § Burns rank third most common cause of serious
injury and death § 80% of deaths in residential fires § 5%–10% mortality due to asphyxiation, systemic
poisoning, and respiratory tract injury
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Introduction § Prevalence of smoke inhalation among burn
victims = 10%–35% § Pulmonary complications according to the
resuscitative phase § Early (first 24 hours)
§ Inhalation of toxic or hot gases § Fluid loss § Heavy sedation
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Introduction § Intermediate (2–7 days) post resuscitative
phase § Analgesic-related respiratory dysfunction § Secretion retention § Airway obstruction § Atelectasis § ARDS
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Introduction § Late (> 7 days)
§ Pneumonia § Sepsis § Multiple organ dysfunction § Pulmonary embolism § Chronic pulmonary disease
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Etiology § Fire – residential fires – most common § Superheated gases § Scalding liquids § Chemicals § Electrical currents
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Pathophysiology: Early Pulmonary and Systemic Changes § Within 24 hours post-burn
§ Carbon monoxide § Produced in fire environment, especially if
§ Oxygen levels are low § Combustion is incomplete
§ Rapidly absorbs into blood
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Pathophysiology: Early Pulmonary and Systemic Changes § Carbon monoxide
§ It converts HbO2 into HbCO § Normal HbCO: < 3% § Minor smoke inhalation: 10%–15% § Severe smoke inhalation: > 50%
§ Compromise of O2 transport § Inability of Hb to transport O2
§ The Hb conversion and inhibition of O2 release result in Functional anemia
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Pathophysiology: Early Pulmonary and Systemic Changes § Carbon monoxide
§ Skeletal and cardiac muscle dysfunction § Cerebral vasodilation § Rapid loss of consciousness and cerebral edema § Lethal CO poisoning typically occurs when COHb
> 50%–60%
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Pathophysiology: Early Pulmonary and Systemic Changes § Hydrogen cyanide (HCN)
§ Linked to early and late death in burned patients § Easily transported to tissues through circulatory
system; blocks tissue use of O2 § Shift to anaerobic metabolism and elevated lactic
acid production
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Pathophysiology: Early Pulmonary and Systemic Changes § Other considerations
Reduced oxygen transport Cellular metabolic dysfunction
Release of inflammatory mediators Vascular changes
Compromise of nervous system, cardiovascular
system, and skeletal muscle function (Causes of death)
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Pathophysiology: Early Pulmonary and Systemic Changes § Other considerations
§ Thermal injury to the respiratory tract § Typically confined to the face, oral and nasal
cavities, pharynx, and trachea § Blistering, edema, accumulation of thick saliva,
and glottic closure if severe
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Pathophysiology: Early Pulmonary and Systemic Changes § Other considerations
§ Chemical injury to the respiratory tract § Injuries extend into the lungs § Tracheobronchitis, bronchospasm, bronchorrhea,
mucosal sloughing, airway obstruction § Alveolar de-recruitment - atelectasis § Pulmonary edema in severe cases
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Pathophysiology: Early Pulmonary and Systemic Changes § Other considerations
§ Systemic changes are associated with § Decline in O2 transport § Metabolic derangement § Release of inflammatory mediators § Fluid loss
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Pathophysiology: Intermediate Pulmonary and Systemic § Changes (2–7 days post-burn)
§ Signs of respiratory distress often after 24–48 hours
§ PVR returns to normal § Hypermetabolic state continues
§ Increased O2 consumption and CO2 production
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Pathophysiology § Airway edema resolves between day 2 and 4 § Increased mucus production § Atelectasis, pleural effusion, acute lung injury
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Pathophysiology: Late Pulmonary and Systemic Changes
§ > 7 days post-burn § Hypermetabolic state for 1–3 wks § Infection is the most common complication in this
period § Staphylococcus aureus § MRSA § Pseudomona aeruginosa
§ Pulmonary embolism can develop within 2 weeks of burn injury
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Clinical Features § Brain and heart = first to show dysfunction § HbCO content is potential indicator of the dose
of smoked inhaled § SpO2 should not be used since HbO2 and
HbCO have similar light absorption
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Clinical Features § Upper respiratory manifestations
§ Stridor – Hoarseness § Difficulty speaking – Chest retractions
§ Severe form of inhalation injury § Cough – Dyspnea § Tachypnea – Cyanosis § Wheezing – Crackles § Rhonchi
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Clinical Features: Chest Radiograph § Frequently no signs in early period § CT scans may be more useful to determine
severity of pulmonary injury
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Clinical Features: Arterial Blood Gases § To trend the patient’s pulmonary insult § Reduced PaO2 and SaO2 § Reduced PaO2/FiO2 (ALI vs ARDS) § Respiratory alkalosis in early post-burn period § Metabolic acidosis and respiratory failure are
signs of life threatening injuries
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Clinical Features: Hemodynamic Monitoring § To optimize fluid resuscitation § Monitor
§ CVP § PAP § CO § Urine output
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Treatment § Goals of respiratory care in burn patient
§ Achieve a patent airway § Secretion removal § Maintenance of effective ventilation § Preservation of lung volume § Adequate oxygenation § Maintenance of acid–base balance
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Treatment: Airway § Monitor for airway closure § High Fowler’s position to reduce WOB § Intubation if airway closure is anticipated § Extubation if
§ Patient is improving § Maintain his/her own secretions § Cuff leak § Adequate ventilation
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Treatment: Carbon Monoxide Poisoning § Oxygen therapy: cornerstone of therapy (NRM) § High-flow mask CPAP 5–10 cm H2O if
§ Patient with minimal upper airway thermal injury § Increasing dyspnea § Increasing hypoxemia
§ Intubation if HbCO > 30%
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Treatment § Mechanical Ventilation if
§ Respiratory failure § Pneumonia § ALI/ARDS § Sedation and paralysis are necessary
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Treatment: Fluid Balance § To minimize development of
§ Shock § Renal failure § Pulmonary edema
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Treatment: Prevention of Burn Complications § Isolation technique § Room pressurization Front line of § Air filtration infection defense § Wound covering § Topical silver sulfadiazine § Prophylactic antibiotics