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).

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.

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:

 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).

CLINICAL DATA OBTAINED AT THE PATIENT’S BEDSIDE

The Physical Examination

Vital Signs

Increased Respiratory Rate (Tachypnea)

Several pathophysiologic mechanisms operating simultaneously may lead to an increased ventilatory rate:

• Stimulation of peripheral chemoreceptors (hypoxemia)

• Decreased lung compliance–increased ventilatory rate relationship

• Stimulation of J receptors

• Pain, anxiety

Increased Heart Rate (Pulse) and Blood Pressure

Assessment of Acute Upper Airway Obstruction (Thermal Injury)

• Obvious pharyngeal edema and swelling

• Inspiratory stridor

• Hoarseness

• Altered voice

• Painful swallowing

Because the inhalation of hot gases often results in severe upper airway edema, the respiratory care practitioner always should be alert for any clinical manifestations of acute upper airway obstruction, even when the patient shows no remarkable upper airway problems or upper body burns at admission.

Cyanosis

Cough and Sputum Production

When the patient experiences upper airway thermal injuries, an excessive amount of thick secretions usually is present. During the early stage of recovery from smoke inhalation, the patient generally expectorates a small amount of black, sooty sputum (carbonaceous sputum). During the intermediate stage the patient may produce moderate to large amounts of frothy secretions. During the late stage, purulent mucus is common.

Chest Assessment Findings

• Usually normal breath sounds (early stage)

• Wheezing

• Crackles

• Rhonchi

CLINICAL DATA OBTAINED FROM LABORATORY TESTS AND SPECIAL PROCEDURES

Pulmonary Function Test Findings (Extrapolated Data for Instructional Purposes) (Primarily Restrictive Lung Pathophysiology)

FORCED EXPIRATORY FLOW RATE FINDINGS

FVC	FEVT	FEV1/FVC ratio	FEF25%-75%
↓	N or ↓	N or ↑	N or ↓
FEF50%	FEF200-1200	PEFR	MVV
N or ↓	N or ↓	N or ↓	N or ↓

LUNG VOLUME AND CAPACITY FINDINGS

VT	IRV	ERV	RV*
N or ↓	↓	↓	↓
VC	IC	FRC*	TLC	RV/TLC ratio
↓	↓	↓	↓	N

^*↑ when airways are partially obstructed.

DECREASED DIFFUSION CAPACITY (Dlco)

Arterial Blood Gases

EARLY STAGES OF SMOKE INHALATION

Acute Alveolar Hyperventilation with Hypoxemia (Acute Respiratory Alkalosis)

pH	Paco2		Pao2
↑	↓	↓ (slightly)	↓ or Normal

SEVERE SMOKE INHALATION AND BURNS WITH METABOLIC ACIDOSIS

COHb†	pH*	Paco2	*	Pao2
↑	↓ (lactic acidemia)	↓	↓	↓ or N (but tissue hypoxemia)

^*When tissue hypoxia is severe enough to produce lactic acid, the pH and values will be lower than expected for a particular Paco₂ level.

^†Carboxyhemoglobin.

When carbon monoxide or cyanide poisoning is present, the pH may be decreased during the early stages of smoke inhalation. This decrease in pH occurs because patients with severe carbon monoxide or cyanide poisoning commonly have lactic acidemia as a result of tissue hypoxia—even in the presence of a normal Pao₂. Therefore when carbon monoxide or cyanide poisoning is present, the patient may demonstrate the following arterial blood gas values.

SEVERE SMOKE INHALATION AND BURNS WITH METABOLIC ACIDOSIS

Acute Ventilatory Failure with Hypoxemia (Acute Respiratory Acidosis)

pH*	Paco2	*	Pao2
↓	↑	↑ (slightly)	↓

^*When tissue hypoxia is severe enough to produce lactic acid, the pH and values will be lower than expected for a particular Paco₂ level.

Oxygenation Indices

Smoke Inhalation and Burns

	Early and Intermediate Stages	Late Stage
Do2	↓	↓
	↑	↓
	↑	↓
O2ER	↑	↓
	↓	↓

When carbon monoxide or cyanide poisoning is present, the oxygenation indices are unreliable because the Pao₂ often is normal in the presence of carbon monoxide poisoning, and when cyanide poisoning is present, the tissue cells are prevented from consuming oxygen. Both of these conditions cause false oximeter readings. For example, when carbon monoxide is present, a normal Do₂ value may be calculated when, in reality, the patient’s oxygen transport status is extremely low. When cyanide poisoning is present, the patient’s may appear normal or increased when in actuality the tissue cells are extremely hypoxic. Typically these problems are not present during the intermediate and late stages in the presence of appropriate treatment.

Hemodynamic Indices*

Cardiogenic Pulmonary Edema

	Early Stage	Intermediate Stage	Late Stage
CVP	↓	Normal	↓
RAP	↓	Normal	↓
	↓	Normal	↓
PCWP	↓	Normal	↓
CO	↓	Normal	↓
SV	↓	Normal	↓
SVI	↓	Normal	↓
CL	↓	Normal	↓
RVSWI	↓	Normal	↓
LVSWI	↓	Normal	↓
PVR	Normal	Normal	↑
SVR	↑	Normal	↑

---

^*CO, Cardiac output; CVP, central venous pressure; LVSWI, left ventricular stroke work index; , mean pulmonary artery pressure; PCWP, pulmonary capillary wedge pressure; PVR, pulmonary vascular resistance; RAP, right atrial pressure; RVSWI, right ventricular stroke work index; SV, stroke volume; SVI, stroke volume index; SVR, systemic vascular resistance.

In general, the hemodynamic profile seen in patients with body surface burns relates to the amount of intravascular volume loss (hypovolemia) that occurs as a result of third-space fluid shifts. For example, during the early stage, the decreased values shown for the CVP, RAP, , CWP, CO, SV, SVI, CI, RVSWI, and LVSWI reflect the reduction in pulmonary intravascular and cardiac filling volumes. Hypovolemia causes a generalized peripheral vasoconstriction, which is reflected in an elevated SVR. When appropriate fluid resuscitation is administered, the patient’s hemodynamic indices usually are normal during the intermediate stage.

CARBON MONOXIDE POISONING

When a patient has been exposed to smoke, carbon monoxide (CO) poisoning must be assumed. Although CO has no direct injurious effect on the lungs, it can greatly reduce the patient’s oxygen transport because CO has an affinity for hemoglobin that is about 210 times greater than that of oxygen. CO attached to hemoglobin is called carboxyhemoglobin (COHb). Breathing CO at a partial pressure of less than 2 mm Hg can result in a COHb of 40% or more. In other words, 40% or more of the oxygen transport system is inactivated.

In addition, high concentrations of COHb cause the oxyhemoglobin dissociation curve to move markedly to the left, which makes it more difficult for oxygen to leave the hemoglobin at the tissue sites. In essence, the tissue cells are better oxygenated when 40% of the hemoglobin is absent (anemia) than when a COHb of 40% is present. Thus, it should be stressed that Pao₂ and SpO₂ measurements are misleading and unreliable in the presence of COHb. Arterial blood gas measurements, however, do provide important information regarding the presence of hypoxemia, widened alveolar-arterial oxygen gradient, and acid-base status.

A COHb level in excess of 20% is usually considered CO poisoning, and a COHb level of 40% or greater is considered severe. A COHb level in excess of 50% may cause irreversible damage to the central nervous system (CNS). If available, hyperbaric oxygen (HBO) therapy is usually used at a COHb >10%.

Table 41-3 lists the clinical manifestations associated with carbon monoxide poisoning.

TABLE 41-3

Blood Carboxyhemoglobin (COHb) Levels and Clinical Manifestations

COHb (%)	Clinical Manifestations
0-10	Usually no symptoms
10-20	Mild headache, dilation of cutaneous blood vessels
	Cherry red skin—but not always
20-30	Throbbing headache, nausea, vomiting, impaired judgment
30-50	Throbbing headache, possible syncope, increased respiratory and pulse rates
50-60	Syncope, increased respiratory and pulse rates, coma, convulsions, Cheyne-Stokes respiration
60-70	Coma, convulsions, cardiovascular and respiratory depression, and possible death
70-80	Cardiopulmonary failure and death

CYANIDE POISONING

When smoke contains cyanide, oxygen transport may be further impaired. Cyanide poisoning should be suspected in comatose patients who have inhaled fumes from burning plastic (polyurethane) or other synthetic materials. Inhaled cyanide is easily transported in the blood to the tissue cells, where it bonds to the cytochrome oxidase enzymes of the mitochondria. This inhibits the metabolism of oxygen and causes the tissue cells to shift to an inefficient anaerobic form of metabolism. The end product of anaerobic metabolism is lactic acid. Cyanide poisoning may result in lactic acidemia, which is caused by an inadequate tissue oxygen level, even though the Pao₂ is normal or above normal. Clinically, cyanide concentrations are easily measured with commercially available kits. A cyanide blood level in excess of 1 mg/L usually is fatal.

RADIOLOGIC FINDINGS

Chest Radiograph

• Usually normal (early stage)

• Pulmonary edema, acute respiratory distress syndrome (ARDS) (intermediate stage)

• Patchy or segmental infiltrates (late stage)

During the early stage, the radiograph is generally normal. Signs of pulmonary edema and ARDS may be seen during the intermediate and late stages. The chest x-ray film reveals dense, fluffy opacities and patchy or segmental infiltrates (Figure 41-2).

The principal goals in the initial care of patients with smoke inhalation injury and burns include the immediate assessment of the patient’s airway, respiratory status, and cardiovascular status, the percentage of body burned, and the depth of burns. An intravenous line should be started immediately to administer medications and fluids. Easily separated clothing should be removed. Any remaining clothing should be soaked thoroughly before removing. When present, burn wounds should be covered to prevent shock, fluid loss, heat loss, and pain. Infection control includes isolation, room pressurization, air filtration, and wound coverings.

Fluid resuscitation with Ringer’s lactate solution is usually initiated according to the Parkland Formula—4 mL/kg of body weight for each percent of body surface area burned (see Table 41-2) over a 24-hour period. The patient’s hemodynamic status will usually remain stable at this fluid replacement rate, with an average urine output target of 30 to 50 mL/hr and a central venous pressure (CVP) target of 2 to 6 mm Hg. Because this process often leads to overhydration and acute UAO and pulmonary edema, the patient’s fluid and electrolyte status (weight, input and output, and laboratory values) must be monitored carefully.

Finally, knowledge of the exposure characteristics of the fire-related accident may be helpful in assessing the potential clinical complications. For example, did the accident involve a closed-space setting or entrapment? The amount and concentration of smoke usually are much greater under these conditions. What type of material was burning in the fire? Are the inhaled toxins known? Was carbon monoxide (CO) or cyanide produced by the burning substances? Was the patient unconscious before entering the hospital?

A 21-year-old man, after smoking marijuana and falling asleep, suffered second- and third-degree burns on his face, chest, and abdomen as a result of his bed catching fire. The extent of second- and third-degree burns was only 6% to 8% of his total body surface area. He had previously been in excellent health.

Shortly after admission, he developed respiratory distress and pulmonary edema. His blood pressure was 110/60, pulse 100 bpm, and respiratory rate 30/min. His oral temperature was 98.8° F. Bilateral crackles, rhonchi, and occasional wheezing were present. Spontaneous cough produced large amounts of thick, whitish-grey sputum. The chest radiograph revealed bilateral patchy infiltrates and consolidation. On 4 L/min oxygen, his arterial blood gas values were pH 7.51, Paco₂ 28, 21, and Pao₂ 45. A COHb level was not obtained.

The patient was treated conservatively. He was placed on a oxygen mask, and the pulmonary edema progressively cleared over the next 48 hours. However, the respiratory distress and hypoxemia persisted, even on 60% oxygen by high-flow oxygen enrichment (HAFOE) mask. Three days after his admission, the patient’s condition was worsening. The patient was agitated and he complained of a productive cough, worsening shortness of breath, and substernal chest pain with deep breathing and coughing. Thick whitish-grey secretions were noted. Auscultation revealed bilateral crackles, rhonchi, and expiratory wheezing. His vital signs were as follows: temperature 98.6° F (rectal), blood pressure 120/65, pulse 119 (regular sinus rhythm), respiratory rate 35/min. On an Fio₂ of 0.60 his ABG values were as follows: pH 7.54, Paco₂ 25, 20, and Pao₂ 38. His chest x-ray showed patchy infiltrates and some segmental consolidation. Fiberoptic bronchoscopy revealed extensive thermal damage and eschar in the trachea and large bronchi. At that time, the following respiratory assessment was documented.

Respiratory Assessment and Plan

The patient was intubated and started on intravenously administered steroids. He was ventilated with an Fio₂ of 0.60, rate of 12, and PEEP of +10 cm H₂O. Because of the upper body burns, chest physical therapy and postural drainage were prohibited. The bronchial secretions, however, were loosened and mobilized adequately with an in-line ultrasonic nebulizer and frequent endotracheal suctioning. In-line aerosolized steroids also were administered at this time.

The patient’s vital signs and blood gas values improved on this regimen. After 12 days of respiratory care, he was weaned to room air and extubated. He continued to complain of exertional dyspnea with transfer activities but denied dyspnea at rest. Crackles were improved but still easily auscultated throughout all lung fields when the patient took deep breaths. Occasional expiratory wheezes also were heard.

Three days after extubation, on an Fio₂ of 0.35 via a HAFOE mask, his pH was 7.46, Paco₂ 38, 24, and Pao₂ 63. On exercise, the Spo₂ fell to 85%. His peak expiratory flow rate (PEFR) was 40% of predicted. The infiltrates previously noted on chest x-ray were much improved. At that time, the respiratory therapist recorded the following assessment in the patient’s chart.

Respiratory Assessment and Plan

Pulmonary function studies showed severely reduced expiratory flows and a sharply decreased diffusion capacity. Chest x-rays taken at regular intervals thereafter began to show emphysematous changes. The diaphragms were flattened, and bilateral coarse reticular infiltrates were evident. In spite of vigorous therapy over the next 6 weeks, the patient’s cardiopulmonary status continued to worsen. The patient died on day 59, 2 months after his original thermal and inhalational injury. The postmortem diagnosis at autopsy was cryptogenic organizing pneumonia (COP)—also known as bronchiolitis obliterans organizing pneumonia (BOOP).

Discussion

At the time of the first assessment, the patient demonstrated most of the pathophysiologic correlates of smoke inhalation and thermal injuries to the lung. His dyspnea reflected the increased work of breathing associated with Bronchospasm (see Figure 9-11), Increased Alveolar-Capillary Membrane Thickness (see Figure 9-10), and Excessive Bronchial Secretions (see Figure 9-12). The bronchospasm was treated with the vigorous use of both bronchodilator (albuterol) and decongestant (epinephrine) aerosols. The excessive bronchial secretions were treated with ultrasonic bland aerosols and airway suctioning. No specific treatment was available for the changes that occurred in the alveolar-capillary membrane

This interesting case is instructive for these reasons. The first is that all patients with burns of the upper chest, neck, or face should have a careful oropharyngeal examination to determine whether burns have indeed occurred in the upper airway. The presence of soot or eschar in the oropharynx is diagnostic of this problem; respiratory distress almost certainly will ensue if such findings are present, although this does not happen immediately. A 24- to 72-hour lag may occur between the burn and clinical obstruction of the airway. Second, a dreaded complication of smoke and heat inhalation is COP, which developed in this patient and ultimately was responsible for his demise.

Today, this patient might be considered a candidate for lung transplantation. This case study should remind the respiratory care practitioner that immediate intubation over the diagnostic bronchoscope may be necessary and that he or she should prepare accordingly.