Smoke Inhalation and Thermal Injuries



Smoke Inhalation and Thermal Injuries



Chapter Objectives


After reading this chapter, you will be able to:


• List the anatomic alterations of the lungs associated with smoke inhalation and thermal injuries.


• Describe the causes of smoke inhalation and thermal injuries.


• List the cardiopulmonary clinical manifestations associated with smoke inhalation and thermal injuries.


• Describe the general management of smoke inhalation and thermal injuries.


• Describe the clinical strategies and rationales of the SOAPs presented in the case study.


• Define key terms and complete self-assessment questions at the end of the chapter and on Evolve.



Key Terms





















Anatomic Alterations of the Lungs


The inhalation of smoke and hot gases and body surface burns—in any combination—continue to be a major cause of morbidity and mortality among fire victims and firefighters. In general, fire-related pulmonary injuries can be divided into thermal and smoke (toxic gases) injuries.



Thermal Injury


Thermal injury refers to injury caused by the inhalation of hot gases. Thermal injuries are usually confined to the upper airway—the nasal cavity, oral cavity, nasopharynx, oropharynx, and larynx. The distal airways and the alveoli are usually spared serious injury because of (1) the remarkable ability of the upper airways to cool hot gases, (2) reflex laryngospasm, and (3) glottic closure. The upper airway is an extremely efficient “heat sink.” In fact, in 1945, Moritz and associates demonstrated that the inhalation of hot gases alone did not produce significant damage to the lung. Anesthetized dogs were forced to breathe air heated to 500° C through an insulated endotracheal tube. The researchers’ results showed that the air temperature dropped to 50° C by the time it reached the level of the carina. No histologic damage was noticed in the lower trachea or lungs.


Even though thermal injury may occur with or without surface burns, the presence of facial burns is a classic predictor of thermal injury. Thermal injury to the upper airway results in blistering, mucosal edema, vascular congestion, epithelial sloughing, and accumulation of thick secretions. An acute upper airway obstruction (UAO) occurs in about 20% to 30% of hospitalized patients with thermal injury and is usually most marked in the supraglottic structures. When body surface burns require the rapid administration of resuscitative fluids, a UAO may develop rapidly (see Figure 41-1).


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FIGURE 41-1 Smoke inhalation and thermal injuries. BL, Airway blister; FWS, frothy white secretions (pulmonary edema); ME, mucosal edema; SM, smoke (toxic gas); TS, thick secretions.

It should be noted that the inhalation of steam at 100° C or greater usually results in severe damage at all levels of the respiratory tract. This damage occurs because steam has about 500 times the heat energy content of dry gas at the same temperature. Thermal injury to the distal airways results in mucosal edema, vascular congestion, epithelial sloughing, cryptogenic organizing pneumonia (COP)—also known as bronchiolitis obliterans organizing pneumonia (BOOP)—atelectasis, and pulmonary edema.


Therefore, direct thermal injuries usually do not occur below the level of the larynx, except in the rare instance of steam inhalation. Damage to the distal airways is mostly caused by a variety of harmful products found in smoke.



Smoke Inhalation Injury


The pathologic changes in the distal airways and alveoli are mainly caused by the irritating and toxic gases, suspended soot particles, and vapors associated with incomplete combustion and smoke. Many of the substances found in smoke are extremely caustic to the tracheobronchial tree and poisonous to the body. The progression of injuries that develop from smoke inhalation and burns is described as the early stage, intermediate stage, and late stage.



Early Stage (0 to 24 Hours after Inhalation)


The injuries associated with smoke inhalation do not always appear right away, even when extensive body surface burns are evident. During the first 24 hours—the early stage (0 to 24 hours after smoke inhalation)—however, the patient’s pulmonary status often changes markedly. Initially, the tracheobronchial tree becomes more inflamed, resulting in bronchospasm. This process causes an overabundance of bronchial secretions to move into the airways, resulting in further airway obstruction. In addition, the toxic effects of smoke often slow the activity of the mucosal ciliary transport mechanism, causing further retention of mucus.


Smoke inhalation also may cause acute respiratory distress syndrome (ARDS), noncardiogenic high-permeability pulmonary edema—commonly referred to in smoke inhalation cases as “leaky alveoli.” Noncardiogenic pulmonary edema also may be caused by overhydration resulting from overzealous fluid resuscitation (see insert panel in Figure 41-1). In severe cases, ARDS also may occur early in the course of the pathology.



Intermediate Stage (2 to 5 Days after Inhalation)


Whereas upper airway thermal injuries usually begin to improve during the intermediate stage (2 to 5 days after smoke inhalation), the pathologic changes deep in the lungs associated with smoke inhalation usually peak. Production of mucus continues to increase, whereas mucosal ciliary transport activity continues to decrease. The mucosa of the tracheobronchial tree frequently becomes necrotic and sloughs (usually at 3 to 4 days). The necrotic debris, excessive production of mucus, and retention of mucus lead to mucous plugging and atelectasis. In addition, the mucous accumulation often leads to bacterial colonization, bronchitis, and pneumonia. Organisms commonly cultured include gram-positive Staphylococcus aureus and gram-negative Klebsiella, Enterobacter, Escherichia coli, and Pseudomonas. If not already present, ARDS may develop at any time during this period.


When chest wall (thorax) burns are present, the situation may be further aggravated by the patient’s inability to breathe deeply and cough as a result of (1) pain, (2) the use of narcotics, (3) immobility, (4) increased airway resistance, and (5) decreased lung and chest compliance.



Late Stage (5 or More Days after Inhalation)


Infections resulting from burn wounds on the body surface are the major concern during the late stage (5 or more days after smoke inhalation). These infections often lead to sepsis and multiorgan failure. Sepsis-induced multiorgan failure is the primary cause of death in seriously burned patients during this stage.


Pneumonia continues to be a major problem during this period. Pulmonary embolism also may develop within 2 weeks after serious body surface burns. Pulmonary embolism may develop from deep venous thrombosis secondary to a hypercoagulable state and prolonged immobility.


Finally, the long-term effects of smoke inhalation can result in restrictive and obstructive lung disorders. In general, a restrictive lung disorder develops from alveolar fibrosis and chronic atelectasis. An obstructive lung disorder generally is caused by increased and chronic bronchial secretions, bronchial stenosis, bronchial polyps, bronchiectasis, and bronchiolitis.


The major pathologic and structural changes of the respiratory system caused by thermal or smoke inhalation injuries are as follows:



Pneumonia (Chapter 15) and pulmonary embolism (Chapter 20) often complicate smoke inhalation injury.



Etiology and Epidemiology


According to the National Fire Protection Association (NFPA), public fire departments responded to an estimated 1,557,500 fires in the United States in 2007. There were about 530,500 structure fires (85% were residential fires), 258,000 vehicle fires, and 769,000 outside and other fires. This means that every 20 seconds a fire department responded to a fire somewhere in the nation. A fire occurs in a structure at the rate of once every 59 seconds, and in particular, a residential fire occurs every 76 seconds. Fires occur in vehicles at the rate of 1 every 122 seconds, and there is a fire in an outside property every 41 seconds. In addition, there were 3430 civilian fire deaths (1 every 153 minutes) and 17,675 civilian injuries (1 every 30 minutes) according to the NFPA in 2007. The NFPA estimated that more than 14 billion dollars in property damage occurred as a result of fires in 2007.


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 (the prognosis worsens in the very young or old), and (6) preexisting health status. When smoke inhalation injury is accompanied by a full-thickness or third-degree skin burn, the mortality rate almost doubles.


Smoke can result from either pyrolysis (smoldering in a low-oxygen environment) or combustion (burning, with visible flame, in an adequate-oxygen environment). Smoke is composed of a complex mixture of particulates, toxic gases, and vapors. The composition of smoke varies according to the chemical makeup of the material that is burning and the amount of oxygen being consumed by the fire. Table 41-1 lists some of the more common toxic substances produced by burning products that frequently are found in office, industrial, and residential buildings.



Although in some instances the toxic components of the smoke may be obvious, in most cases the precise identification of the inhaled toxins is not feasible. In general, the inhalation of smoke with toxic agents that have high water solubility (e.g., ammonia, sulfur dioxide, and hydrogen fluoride) affects the structures of the upper airway. In contrast, the inhalation of toxic agents that have a low water solubility (e.g., hydrogen chloride, chlorine, phosgene, and oxides of nitrogen) affects the distal airways and alveoli. Many of the substances in smoke are caustic and can cause significant injury to the tracheobronchial tree (e.g., aldehydes [especially acrolein], hydrochloride, and oxides of sulfur).



Body Surface Burns


Because the amount and severity of body surface burns play a major role in the patient’s risk of mortality and morbidity, an approximate estimate of the percentage of the body surface area burned is important. Table 41-2 lists the approximate percentage of surface area for various body regions of adults and infants. The severity and depth of burns usually are defined as follows:




First degree (minimal depth in skin): Superficial burn, damage limited to the outer layer of epidermis. This burn is characterized by reddened skin, tenderness, and pain. Blisters are not present. Healing time is about 6 to 10 days. The result of healing is normal skin.


Second degree (superficial to deep thickness of skin): Burns in which damage extends through the epidermis and into the dermis but is not of sufficient extent to interfere with regeneration of epidermis. If secondary infection results, the damage from a second-degree burn may be equivalent to that of a third-degree burn. Blisters usually are present. Healing time is 7 to 21 days. The result of healing ranges from normal to a hairless and depigmented skin with a texture that is normal, pitted, flat, or shiny.


Third degree (full thickness of skin including tissue beneath skin): Burns in which both epidermis and dermis are destroyed, with damage extending into underlying tissues. Tissue may be charred or coagulated. Healing may occur after 21 days or may never occur without skin grafting if the burned area is large. The resultant damage heals with hypertrophic scars (keloids) and chronic granulation.



image OVERVIEW of the Cardiopulmonary Clinical Manifestations Associated with Smoke Inhalation and Thermal Injuries


The following clinical manifestations result from the pathologic mechanisms caused (or activated) by Atelectasis (see Figure 9-8), Alveolar Consolidation (see Figure 9-9), Increased Alveolar-Capillary Membrane Thickness (see Figure 9-10), Bronchospasm (see Figure 9-11), and Excessive Bronchial Secretions (see Figure 9-12)—the major anatomic alterations of the lungs associated with smoke inhalation and thermal injuries (see Figure 41-1).


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Jun 11, 2016 | Posted by in RESPIRATORY | Comments Off on Smoke Inhalation and Thermal Injuries

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