5 курс / Пульмонология и фтизиатрия / Clinical_Manifestations_and_Assessment_of_Respiratory

frothy sputum production, WBC 21,000/mm3. On FIO2 1.0: pH 7.29, PaCO2 52, 25, PaO2 38, SaO2 67%. CXR: “White-out.”

A

•Pulmonary edema secondary to near wet drowning (frothy sputum).

•Acute ventilatory failure with severe hypoxemia (ABGs).

P Continue on FIO2 1.0 and bag-mask ventilate. Page physician stat. Obtain intubation

equipment and prepare to place patient on ventilator. Follow oximetry. Prepare to assist in placement of Swan-Ganz catheter.

The patient was intubated and paralyzed with succinylcholine. As soon as he was intubated, copious pink foam was aspirated from the endotracheal tube. He was alternately suctioned and ventilated with an Ambu bag. He was given 7 mg of morphine for sedation and was mechanically ventilated in continuous mechanical ventilation (CMV) mode at a rate of 10

breaths/min. On an FIO2 of 1.0 and PEEP of 10 cm H2O, his blood gases were pH 7.44, PaCO2 43 mm Hg, 22 mEq/L, PaO2 109 mm Hg, SaO2 98%. At this time, the respiratory therapist started to slowly decrease the patient's FIO2. Because

he was still fighting the ventilator, he was paralyzed with pancuronium.

After several hours, the lungs were clear, the secretions were no longer present, and his blood gas values returned to

normal on an FIO2 of 0.50 and PEEP of 10 cm H2O (pH 7.38, PaCO2 42 mm Hg, 24 mEq/L, PaO2 98 mm Hg, SaO2

97%). His hemodynamic status was normal. The chest radiograph revealed considerable clearing of the earlier noted bilateral pulmonary infiltrates. A pulmonary artery catheter was not placed, because clinical improvement was clearly occurring. The respiratory therapist entered the following assessment and plan.

Respiratory Assessment and Plan

S N/A (patient sedated, paralyzed).

O Lungs clear. No secretions. On FIO2 0.50 and +10 PEEP: pH 7.38, PaCO2 42, 24, PaO2 98, SaO2 97%. CXR: Considerable improvement in bilateral infiltrates. Swan-Ganz catheter not

inserted because patient is improving. A

•Considerable improvement on CMV and PEEP (general improvement of clinical indicators)

•Acceptable ventilation and oxygenation status on present ventilator settings (ABG)

•Frothy airway secretions no longer present (clear lungs and no secretions)

P Contact physician to wean from muscle relaxant. Wean from mechanically ventilated breaths, FIO2, and PEEP per Mechanical Ventilation Protocol. Change ventilator mode to synchronized

intermittent mandatory ventilation (SIMV).

The patient was weaned from the ventilator over a period of 6 hours, after which he was extubated. The following

morning, ABGs on an FIO2 0.28 Venturi oxygen mask were pH 7.42, PaCO2 35 mm Hg, 22 mEq/L, PaO2 158 mm Hg, and SaO2 98%. His chest radiograph was normal. An oxygen titration protocol was performed. He was discharged 2 days later.

Discussion

This case demonstrates initial worsening of the near wet drowning victim despite intensive respiratory care. The initial ABG values showed severe hypoxemia as a result of increased alveolar-capillary membrane thickness and alveolar flooding (see Fig. 44.1) and acute ventilatory failure and metabolic (probably lactic) acidosis. Bronchospasm never developed, and aggressive respiratory care prohibited the development of atelectasis and aspiration pneumonia.

When suctioning, supplemental oxygen, and bag ventilation were no longer successful, the patient was intubated and mechanical ventilation with PEEP was begun. Even on these modalities, the patient remained anxious and was ultimately paralyzed to allow better respiratory synchrony and diminish the chance of ventilatory-associated lung injury (barotrauma or volutrauma). Morphine was used for its sedative qualities and as a vascular afterload reducer. The fact that the patient was fighting the ventilator some time after succinylcholine had been administered reflects the fact that it is a very shortacting paralyzing agent. Pancuronium has a much longer half-life, and its use is standard in settings where longer effectiveness is required. Once the abnormal pathologic processes of the lungs associated with this case improved, the patient's cardiopulmonary status quickly returned to normal, and the respiratory therapist was able wean the patient from the ventilation in a relatively short time.

This case demonstrates the necessity for frequent reassessment of the patient and therapeutic adjustments to follow the findings so observed. Note that the therapist appropriately documented the reason that one of his suggestions (the SwanGanz catheter) was not placed. In the protocol-rich environment, such documentation is vital, if only for medical legal reasons.

Self-Assessment Questions

1.In the United States, drowning is the:

a.Leading cause of accidental death

b.Second leading cause of accidental death

c.Third leading cause of accidental death

d.Fourth leading cause of accidental death

2.According to the Centers for Disease Control and Prevention, about how many people drown each year in the United States?

a.500

b.1000

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C H A P T E R 4 5

Smoke Inhalation, Thermal Lung

Injuries, and Carbon Monoxide

Intoxication

CHAPTER OUTLINE

Anatomic Alterations of the Lungs

Thermal Injury

Smoke Inhalation Injury

Etiology and Epidemiology Body Surface Burns

Overview of the Cardiopulmonary Clinical Manifestations Associated With Smoke Inhalation and Thermal Injuries

General Management of Smoke Inhalation and Thermal Injuries

General Emergency Care Airway Management Bronchoscopy

Hyperbaric Oxygen Therapy Treatment for Cyanide Poisoning Pharmacologic Treatment Respiratory Care Treatment Protocols

Case Study: Smoke Inhalation and Thermal Lung Injury Self-Assessment Questions

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, thermal injuries, and carbon monoxide intoxication.

•List the cardiopulmonary clinical manifestations associated with smoke inhalation, thermal injuries, and carbon monoxide intoxication.

•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 end of chapter and Evolve.

KEY TERMS

Acute Respiratory Distress Syndrome (ARDS)

Body Surface Burns

Bronchiolitis Obliterans Organizing Pneumonia (BOOP)

Bronchospasm

Carbon Monoxide Poisoning

Carbonaceous Sputum

Carboxyhemoglobin

Chest Wall Burns

COHB Half-Life

CO-Oximetry

Cyanide Blood Level

Cyanide Poisoning

Cryptogenic Organizing Pneumonia (COP)

Eschar

Facial Burns

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First-Degree Burn

Hyperbaric Oxygenation (HBO) Therapy

Lactic Acidosis

Multiorgan Dysfunction Syndrome (MODS)

Noncardiogenic Pulmonary Edema

Parkland Formula (Fluid Resuscitation)

Pulmonary Embolism

Pyrolysis

Second-Degree Burn

Smoke Inhalation Injury

Steam Inhalation

Thermal Lung Injury

Third-Degree Burn

Anatomic Alterations of the Lungs

The inhalation of smoke, 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 Lung 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 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. 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 (Fig. 45.1).

FIGURE 45.1 Smoke inhalation and thermal injuries. BL, Airway blister; FWS, frothy white secretions (pulmonary edema); ME, mucosal edema; SM, smoke (toxic gas); TS, thick secretions.

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 (see Chapter 27).

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

In 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 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), (see Chapter 28), 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 in Fig. 45.1). In severe cases, ARDS 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 continue to be a problem. For example, 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 mucus plugging and atelectasis. In addition, the mucus 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 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 administration of narcotics, (3) immobility, (4) increased airway resistance, and (5) decreased lung and chest wall compliance.

Late Stage (5 Days and Longer After Inhalation)

Infections resulting from burn wounds on the body surface are the major concern during the late stage (5 days and longer after smoke inhalation). These infections often lead to sepsis and multiorgan dysfunction syndrome (MODS). Sepsisinduced MODS is the primary cause of death in seriously burned patients during this stage.

Pneumonia continues to be a major problem during this period. In addition, pulmonary embolism 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 is generally 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:

Thermal injury (upper airway—nasal cavity, oral cavity, and pharynx):

•Blistering

•Mucosal edema

•Vascular congestion

•Epithelial sloughing

•Thick secretions

•Acute UAO

Smoke inhalation injury (tracheobronchial tree and alveoli):

•Inflammation of the tracheobronchial tree

•Bronchospasm

•Excessive bronchial secretions and mucous plugging

•Decreased mucosal ciliary transport

•Atelectasis

•Alveolar edema and frothy secretions (noncardiogenic pulmonary edema)

•ARDS (severe cases)

•COP (also called bronchiolitis obliterans organizing pneumonia)

•Alveolar fibrosis, bronchial stenosis, bronchial polyps, bronchiolitis, and bronchiectasis (severe cases)

Pneumonia (see Chapter 18, Pneumonia, Lung Abscess Formation, and Important Fungal Diseases) and pulmonary embolism (see Chapter 21, Pulmonary Vascular Disease: Pulmonary Embolism and Pulmonary Hypertension) often complicate smoke inhalation injury.

Etiology and Epidemiology

According to the National Fire Protection Association (NFPA),1 more than 1.3 million fires were reported by fire departments in 2016, resulting in an estimated 3390 civilian deaths—the highest number of fatalities since 2008. The NFPA estimates that public fire departments in the United States responded to 1,342,000 fires during this period. In addition to the 3390 civilian deaths in 2016, there were an estimated 14,660 civilian fire injuries. NFPA estimates that the 1,342,000 fires in 2016 caused 10.6 billion dollars in property damage.

The prognosis of fire victims is usually determined by the (1) extent and duration of smoke exposure, (2) chemical composition of the smoke, (3) size and depth of body surface burns (Table 45.1), (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.

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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 Fig. 10.7), alveolar consolidation (see Fig. 10.8), increased alveolar-capillary membrane thickness (see Fig. 10.9), bronchospasm (see Fig. 10.10), and excessive bronchial secretions (see Fig. 10.11)—the major anatomic alterations of the lungs associated with smoke inhalation and thermal injuries (see Fig. 45.1).

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)

•Relationship of decreased lung compliance to increased ventilatory rate

•Stimulation of J receptors

•Pain, anxiety

•Fever (with infection)

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 therapist 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 or facial burns at admission.

Cyanosis

Cough and Sputum Production

When the patient experiences upper airway thermal injuries, abnormally thick and sometimes excessive secretions usually result. 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 production is common.

Chest Assessment Findings

•Normal breath sounds (early stage)

•Wheezing

•Crackles

Clinical Data Obtained From Laboratory Tests and Special Procedures

Pulmonary Function Test Findings

(Extrapolated Data for Instructional Purposes) (Primarily Restrictive Lung Pathophysiology)

Forced Expiratory Volume and Flow Rate Findings

Lung Volume and Capacity Findings

1↑ When airways are partially obstructed.

Decreased Diffusion Capacity (DLCO)

Arterial Blood Gases

Early Stages of Smoke Inhalation

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8CO, Cardiac output; CI, cardiac index; 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.

7When ARDS is present, noncardiogenic pulmonary edema findings may be present (see Chapter 28, Acute Respiratory Distress Syndrome).

In general, the hemodynamic profile 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 are usually normal during the intermediate stage.

Carbon Monoxide Poisoning

When a patient has been exposed to smoke, 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 greater. In other words, 40% or more of the hemoglobin oxygen transport system is then unavailable for oxygen transport.

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 SpO2 and pulse oximeter–based oxygen content measurements are misleading and unreliable in the presence

of COHb. ABG measurements (with CO-oximetry) provide important information regarding the presence of hypoxemia, widened alveolar-arterial oxygen gradient, acid-base status, and a correct measurement of both oxygen saturation (%) and COHb (%).

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. If available, hyperbaric oxygen (HBO) therapy is usually used at a COHb greater than 10%. Cigarette smokers may demonstrate COHb levels of 5% or greater to 7%; in cigar smokers levels can be as high as 15%.

Table 45.3 lists the clinical manifestations associated with CO poisoning.

TABLE 45.3

Blood Carboxyhemoglobin (COHb) Levels and Clinical Manifestations

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 and SpO2 are 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.

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Radiologic Findings

Chest Radiograph

•Usually normal (early stage)

•Pulmonary edema, ARDS (may be present during early 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 radiograph reveals dense, fluffy opacities and patchy or segmental infiltrates (Fig. 45.2).

FIGURE 45.2 (A) Radiograph of a young man admitted after accidentally setting his kitchen on fire while intoxicated. (B) Prompt recovery after 72 hours. (From Hansell, D. M., Lynch, D. A., McAdams, H. P., et al. [2010]. Imaging of diseases of the chest [5th ed.]. Philadelphia,

PA: Elsevier.)

General Management of Smoke Inhalation and Thermal Injuries

General Emergency Care

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, cardiovascular status, percentage of body burned, and depth of burns. An intravenous line should be started immediately to administer medications and fluids. Easily separated clothing should be removed, and 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 lactated Ringer 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 45.1) 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/h and a central venous pressure target of 2 to 6 mm Hg. Because this process may lead 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 are usually much greater under these conditions. What type of material was burning in the fire? Are the inhaled toxins known? Was CO or cyanide produced by the burning substances? Was the patient unconscious before entering the hospital? If the history warrants, tests for alcohol ingestion, poisoning, or drug overdose should be performed.

Airway Management

Early elective endotracheal intubation should be performed on the patient who has inhaled hot gases and demonstrates any signs of impending UAO (e.g., upper airway edema, blisters, inspiratory stridor, thick secretions). This is a medical emergency. Even though acute UAO is considered one of the most treatable complications of smoke inhalation, deaths still occur from UAO (hence the well-supported clinical guideline that states, “When in doubt, intubate.”).

Securing an endotracheal tube often is difficult in the presence of facial burns (typically wet wounds). Adhesive tape may cause further trauma to the burn wounds. Ingenuity and creativity may be required. Securing the endotracheal tube without traumatizing the patient has been successful with use of umbilical tape and a variety of helmets, halo traction devices, and Velcro straps.

Because of the infections associated with body surface burns and smoke inhalation, a tracheostomy should be reserved for patients in whom an airway cannot be established otherwise or who will require prolonged mechanical ventilation.

Bronchoscopy

Therapeutic bronchoscopy often is used to clear the airways of mucus plugs and eschar.2 In addition, early bronchoscopy often is performed for inspection and evaluation of the upper airways. Mucosal changes distal to the larynx serve as good predictors of subsequent respiratory problems.

Hyperbaric Oxygen Therapy

Hyperbaric oxygenation (HBO) therapy is useful in the rapid elimination of CO and the enhancement of skin graft viability. Its clinical utility, however, is still a matter of debate in the medical literature. Although a PaO2 greater than