5 курс / Пульмонология и фтизиатрия / Clinical_Manifestations_and_Assessment_of_Respiratory

Severe Acute Respiratory Syndrome

In 2002, China reported the first case of severe acute respiratory syndrome (SARS). Shortly after this report, the disease was documented in numerous countries, including Vietnam, Singapore, and Indonesia. Both the United States and Canada have reported imported cases. Health officials believe that the cause of SARS is a newly recognized virus strain called a coronavirus. Other viruses, however, are still under investigation as potential causes. Coronaviruses are a group of viruses that have a halo-like or corona-like appearance when observed under an electron microscope. Known forms of coronavirus cause common colds and upper respiratory tract infections. SARS is highly contagious on close personal contact with infected individuals. It spreads through droplet transmission by coughing and sneezing. SARS might be transmitted through the air or from objects that have become contaminated.

The incubation period for SARS is typically 2 to 7 days. Initially, the patient usually develops a fever (>100.4°F [>38.0°C]), followed by chills, headaches, general feeling of discomfort, and body aches. Toward the end of the incubation period, the patient with SARS usually develops a dry, nonproductive cough, shortness of breath, and malaise. In severe cases, hypoxemia develops. According to the Centers for Disease Control and Prevention (CDC), 10% to 20% of patients with SARS require mechanical ventilation. In spite of this fact, death from SARS is rare. No specific treatment recommendations exist at this time. The CDC, however, recommends that patients with SARS receive the same treatment used for any patient with serious community-acquired atypical pneumonia of unknown cause.

Lipoid Pneumonitis

The aspiration of mineral oil, used medically as a lubricant, has been known to cause pneumonitis—lipoid pneumonitis. The severity of the pneumonia depends on the type of oil aspirated. Oils from animal fats cause the most serious reaction, whereas oils of vegetable origin are relatively inert. When mineral oil is inhaled in an aerosolized form, an intense pulmonary tissue reaction occurs.

Avian Influenza A

Avian influenza A (also called bird flu and H5N1) is a subtype of the A strain virus and is highly contagious in birds. Historically, bird flu has not been known to infect humans. However, in Hong Kong in 1997 the first avian influenza virus to infect humans directly was reported. This outbreak was linked to chickens and classified as avian influenza A (H5N1). Since the Hong Kong outbreak, the bird flu virus has been reported in parts of Europe, Turkey, Romania, the Near East, and Africa. Many of the infected patients have died. Experts are concerned that if the avian flu virus continues to spread, a worldwide pandemic outbreak could occur. People with bird flu may develop life-threatening complications, such as viral pneumonia and ARDS (the most common cause of bird flu–related deaths).

Necrotizing Pneumonia and Lung Abscess

Necrotizing pneumonia refers to a pneumonia that causes the death of lung tissue cells within the infected pulmonary parenchyma. It is often characterized as a localized area of pus and tissue necrosis. In severe cases, necrotizing pneumonia can result in a lung abscess. A lung abscess (also known as necrotizing pneumonia or lung gangrene) is characterized as a localized airand fluid-filled cavity, which is a collection of purulent exudate that is composed of liquefied white blood cell remains, proteins, and tissue debris. The airand fluid-filled cavity is encapsulated in a so-called pyogenic membrane that consists of a layer of fibrin, inflammatory cells, and granulation tissue.

During the early stages of a lung abscess, the pathologic findings are indistinguishable from those of any acute pneumonia. Polymorphonuclear leukocytes and macrophages move into the infected area to engulf any invading organisms. This action causes the pulmonary capillaries to dilate, the interstitial space to fill with fluid, and the alveolar epithelium to swell from the edema fluid. In response to this inflammatory reaction, the alveoli in the infected area become consolidated (Fig. 18.11).

FIGURE 18.11 Lung abscess. (A) Cross-sectional view of lung abscess. (B) Consolidation. (C) Excessive bronchial secretions are common secondary anatomic alterations of the lungs. AFC, Air-fluid cavity; EDA, early development of abscess; PM, pyogenic membrane; RB, ruptured bronchus (and drainage of the liquefied contents of the cavity).

As the inflammatory process progresses, tissue necrosis occurs. In severe cases the tissue necrosis can rupture into adjacent bronchi, which in turn allows a partial or total drainage of the liquefied contents from the cavity to flow into the bronchi. In addition, an airand fluid-filled cavity also may rupture into the intrapleural space and cause pleural effusion and empyema (see Chapter 24, Pleural Effusion and Empyema). This may lead to inflammation of the parietal pleura, pleuritic chest pain, decreased chest expansion, and atelectasis. After a time, fibrosis and calcification of the tissues around the cavity encapsulate the abscess (see Fig. 18.11).

The major pathologic or structural changes associated with a lung abscess are as follows:

• Alveolar consolidation

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•Alveolar-capillary tissue and bronchial wall destruction

•Tissue necrosis

•Cavity formation

•Fibrosis and calcification of the lung parenchyma

•Bronchopleural fistulas and empyema

•Atelectasis

•Excessive airway secretions

Lung abscesses most commonly occur as a complication of aspiration pneumonia—that is, the pathologic events that follow shortly after aspirating either (1) acidic gastric fluids or (2) a variety of organisms (both anaerobic and aerobic) that are normally found in oropharyngeal secretions. The aspiration of acidic gastric fluids is associated with immediate injury to the tracheobronchial tree and lung parenchyma—often likened to a flash burn. Box 18.3 provides a summary of organisms known to cause lung abscess. Such organisms commonly colonize and multiply in the small grooves, gingival crevices, and spaces between the teeth and gums in patients with poor oral hygiene. For example, anaerobic organisms are frequently found in patients with gingivitis and dead or abscessed teeth.

Box 18.3

Organisms Known to Cause Lung Abscess

Common Organisms Associated With Aspiration

•Anaerobic gram-positive cocci

•Peptostreptococci

•Peptococci

•Anaerobic gram-negative bacilli

•Bacteroides fragilis

•Prevotella melaninogenica

•Fusobacterium spp.

Less Common Organisms

•Klebsiella

•Staphylococci

•Mycobacterium tuberculosis (plus atypical organisms Mycobacterium kansasii and Mycobacterium avium)

•Histoplasma capsulatum

•Coccidioides immitis

•Blastomyces

•Aspergillus fumigatus

Parasites

•Paragonimus westermani

•Echinococcus

•Entamoeba histolytica

Rare Causes

•Streptococcus pneumoniae

•Pseudomonas aeruginosa

•Legionella pneumophila

Aspiration often occurs in the patient with a decreased level of consciousness. Predisposing factors include (1) alcohol abuse, (2) seizure disorders, (3) general anesthesia, (4) head trauma, (5) cerebrovascular accidents, and (6) swallowing disorders. Anatomically, lung abscesses most commonly develop in lung regions that are dependent in the recumbent position (e.g., the posterior segments of the upper lobes or the superior segments of the lower lobes). The right lung is more commonly involved than the left.

Finally, a lung abscess may also develop as a result of (1) bronchial obstruction with secondary cavitating infection (e.g., distal to bronchogenic carcinoma or an aspirated foreign body), (2) vascular obstruction with tissue infarction (e.g., septic embolism, vasculitis), (3) interstitial lung disease with cavity formation (e.g., pneumoconiosis [silicosis], Wegener granulomatosis, and rheumatoid nodules), (4) bullae or cysts that become infected (e.g., congenital or bronchogenic cysts), or (5) penetrating chest wounds that lead to an infection (e.g., bullet wound).

Overview of the Cardiopulmonary Clinical Manifestations Associated With Pneumonia

The following clinical manifestations result from the pathologic mechanisms caused (or activated) by alveolar consolidation (see Fig. 10.8), increased alveolar-capillary membrane thickness (see Fig. 10.9), and atelectasis (see Fig. 10.7)—the major anatomic alterations of the lungs associated with pneumonia (see Fig. 18.1).

During the resolution stage of pneumonia, excessive bronchial secretions (see Fig. 10.11) may also play a part in the clinical presentation.

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 lung compliance to increased ventilatory rate

•Stimulation of J receptors

•Pain, anxiety, fever

Increased Temperature (Bacterial >101°F and Viral <101°F)

Increased Heart Rate (Pulse) and Blood Pressure

Chest Pain (Pleuritic) and Decreased Chest Expansion

Cyanosis

Cough, Sputum Production, and Hemoptysis

Initially the patient with pneumonia usually has a nonproductive barking or hacking cough. As the disease progresses, however, the cough becomes productive. When the disease progresses to this point, the patient often expectorates small amounts of purulent, blood-streaked, or rusty sputum. This is caused by fluid moving from the pulmonary capillaries into the alveoli in response to the inflammatory process. As fluid crosses into the alveoli, some RBCs may also move into the alveoli and produce the blood-streaked or rusty appearance of the fluid (see Fig. 18.1). Some of the fluid that moves in the alveoli also may work its way into the bronchioles and bronchi. As the fluid accumulates in the bronchial tree, the subepithelial receptors in the trachea, bronchi, and bronchioles are stimulated and initiate a cough reflex. Because the bronchioles and the smaller bronchi are deep in the lung parenchyma, the patient with pneumonia initially has a dry, hacking cough, and fluid cannot be easily expectorated until secretions reach the larger bronchi.

Chest Assessment Findings

•Increased tactile and vocal fremitus

•Dull percussion note

•Bronchial breath sounds

•Crackles

•Pleural friction rub (if process extends to pleural surface)

•Whispered pectoriloquy

Clinical Data Obtained from Laboratory Tests and Special Procedures

Pulmonary Function Test Findings

(Restrictive Lung Pathophysiology)1

Forced Expiratory Volume and Flow Rate Findings2

Lung Volume and Capacity Findings

1The pulmonary function tests (PFTs) here are for a typical case of interstitial or alveolar-filling pneumonia, not complicated with excessive airway secretions, bronchospasm, etc.

2The decreased forced expiratory volumes and flow rate findings are primarily caused by the low vital capacity associated with the disorder.

Arterial Blood Gases

Mild to Moderate Stages

Acute Alveolar Hyperventilation With Hypoxemia3 (Acute Respiratory Alkalosis)

Severe Stage

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Acute Ventilatory Failure With Hypoxemia4 (Acute Respiratory Acidosis)

3See Fig. 5.2 and Table 5.4 and related discussion for the acute pH, PaCO2, and changes associated with acute alveolar hyperventilation.

4See Fig. 5.2 and Table 5.5 and related discussion for the acute pH, PaCO2, and changes associated with acute ventilatory failure.

5When tissue hypoxia is severe enough to produce lactic acid, the pH and values will be lower than expected for a particular PaCO2 level.

Oxygenation Indices6

7The DO2 may be normal in patients who have compensated to the decreased oxygenation status with (1) an increased cardiac output, (2) an increased hemoglobin level, or (3) a combination of both. When the DO2 is normal, the O2ER is usually normal.

8May be increased in the patient with a fever caused by bacterial pneumonia.

6, Arterial-venous oxygen difference; DO2, total oxygen delivery; O2ER, oxygen extraction ratio; QS/QT, pulmonary shunt fraction; , mixed venous oxygen saturation; VO2, oxygen consumption.

Abnormal Laboratory Test and Procedure Results

Sputum examination findings (see discussion of etiology in this chapter, Box 18.2)

Radiologic Findings

Chest Radiograph

•Increased density (from consolidation and atelectasis)

•Air bronchograms

•Lung abscess and/or airand fluid-filled cavity

•Pleural effusions/empyema

The radiographic signs vary considerably depending on the causative agent and the stage of the pneumonia process. In general, pneumonia (alveolar consolidation) appears as an area of increased density that may involve a small lung segment, a lobe, or one or both lungs (Figs. 18.3 and 18.12). The process may appear patchy or uniform throughout the area. As the alveolar consolidation intensifies, alveolar density increases and air bronchograms may be seen (Fig. 18.13). A lung abscess—or airand fluid-filled cavity—appears on the radiograph as a circular radiolucency that contains an air-fluid level, surrounded by a dense wall of lung parenchyma (Fig. 18.14).

FIGURE 18.12 Chest radiograph of a 20-year-old woman with severe pneumonia of the left lung and patchy pneumonia in the right middle and lower lobes.

FIGURE 18.13 Air bronchogram (shown in chest radiograph). The branching linear lucencies within the consolidation in the right lower lobe are particularly well demonstrated (arrow) in this example of staphylococcal pneumonia. (From Hansell, D. M., Lynch, D. A.,

McAdams, H. P., et al. [2010]. Imaging of diseases of the chest [5th ed.]. Philadelphia, PA: Elsevier.)

FIGURE 18.14 A large cavitary lesion containing an air-fluid level in the right lower lobe (see arrow). Smaller cavitary lesions are also seen in other lobes (see arrows). (From Hansell, D. M., Armstrong, P., Lynch, D. A., McAdams, H. P. [Eds.]. [2005]. Imaging of diseases of the

chest [4th ed.]. Philadelphia, PA: Elsevier.)

During the early stages of many pulmonary fungal infections, localized infiltration and consolidation with or without lymph node involvement are commonly seen (Fig. 18.15). Single or numerous spherical nodules may be seen (Fig. 18.16). During the advanced stages, bilateral cavities in the apical and posterior segments of the upper lobes are often seen (Fig. 18.17). A pleural effusion may be identified on the chest radiograph (see Chapter 24, Pleural Effusion and Empyema).

FIGURE 18.15 Acute inhalational histoplasmosis in an otherwise healthy patient. This young man developed fever and cough after tearing down an old barn. The radiograph shows bilateral hilar adenopathy and diffuse nodular opacities. (From Hansell, D. M.,

Lynch, D. A., McAdams, H. P., et al. [2010]. Imaging of diseases of the chest [5th ed.]. Philadelphia, PA: Elsevier.)

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hospitalization may be required. The following is an overview of the treatments used for pneumonia.

The general management of lung abscess varies based on the severity of the pneumonia and the severity of the lung abscess. Treatment includes appropriate (usually intravenous) antimicrobial therapy coupled with prompt drainage and surgical debridement. When it is treated properly, most patients with a lung abscess show improvement. In acute cases, the size of the abscess quickly decreases and eventually closes altogether. In severe or chronic cases, the patient's improvement may be slow or insignificant, even with appropriate therapy.

The standard treatment for a lung abscess caused by an anaerobic pathogen is clindamycin. Other drugs that may be used are any combination of beta-lactam–beta-lactamase inhibitors (e.g., ampicillin-sulbactam), penicillin plus metronidazole, or a carbapenem. When the lung abscess is caused by MRSA, linezolid is recommended. An alternative to linezolid is vancomycin; followed by ceftaroline, trimethoprim-sulfamethoxazole, and telavancin.

Respiratory Care Treatment Protocols

Oxygen Therapy Protocol

Oxygen therapy is used to treat hypoxemia, decrease the work of breathing, and decrease myocardial work. Because of the hypoxemia associated with pneumonia, supplemental oxygen may be required. The hypoxemia that develops in pneumonia is most commonly caused by alveolar consolidation and capillary shunting associated with the disorder. Hypoxemia caused by capillary shunting is often at least partially refractory to oxygen therapy (see Oxygen Therapy Protocol, Protocol 10.1).

Lung Expansion Therapy Protocol

Lung expansion therapy may be administered to attempt to offset the atelectasis associated with some pneumonias, but its effects are not consistently good (see Lung Expansion Therapy Protocol, Protocol 10.3).

Airway Clearance Therapy Protocol

Because secretion accumulation is associated with severe pneumonias and lung abscess, a number of airway clearance therapies may be used to enhance the mobilization of bronchial secretions (see Airway Clearance Therapy Protocol, Protocol 10.2). A 1- or 2-day trial of chest physiotherapy modalities is not contraindicated in the otherwise stable patient.

Thoracentesis

Diagnostic and therapeutically, thoracentesis may be used if a pleural effusion is present (see Chapter 24). From a diagnostic standpoint, fluid samples may be examined for the following:

•Color

•Odor

•RBC count

•Protein

•Glucose

•Lactic dehydrogenase (LDH)

•Amylase

•pH

•Wright, Gram, and acid-fast bacillus (AFB) stains

•Aerobic, anaerobic, tuberculosis, and fungal cultures

•Cytology

Therapeutic thoracentesis may be used to encourage lung reexpansion when atelectasis is part of the clinical presentation.

Case Study Pneumonia

Admitting History and Physical Examination

A 47-year-old man spent a week deer hunting in northern Michigan with some friends. They spent considerable time outdoors in inclement weather and indulged freely in alcoholic beverages during the afternoons and evenings. Previously the man had been essentially healthy. He smoked one pack of cigarettes a day.

Returning home, he felt listless and thought that he was “coming down with a cold.” That night, he noticed a mild, nonproductive cough. He had a headache and some pain in the right side of his chest on deep inspiration and noticed that he was somewhat short of breath when he climbed one flight of stairs. During the night, he woke up and felt very chilled, then very warm. His wife put her hand on his forehead and was certain that he had a “high fever.” Because he felt miserable, they went to the emergency department of the nearest hospital.

On physical examination, his vital signs were blood pressure 150/88, pulse 116 beats/min, respiratory rate 28 breaths/min, and temperature (oral) 39.9°C. He was in moderate respiratory distress. Percussion of the chest revealed dullness on the right lower side, and on inspiration there were fine crackles heard in that area. The breath sounds were described as “bronchial.” The chest radiograph showed pneumonic consolidation of the right lower lung field. On room air,

his arterial blood gas (ABG) values were pH 7.53, PaCO2 27 mm Hg, 21 mEq/L, PaO2 62 mm Hg, and SaO2 93%. The respiratory therapist assigned to assess and treat the patient recorded the following SOAP note.

Respiratory Assessment and Plan

S Mild dyspnea (patient stated he was “short of breath”)

O Alert, cooperative, acutely ill. Mild nonproductive cough. Vital signs T 39.9°C, BP 150/88, P 116, RR 28. Dull to percussion over RLL, along with crackles and bronchial breath sounds.

CXR: Pneumonic consolidation RLL. ABG on room air pH 7.53, PaCO2 27, 21, PaO2 62, and SaO2 93%.

A

•RLL consolidation (pneumonia presumed)

•Acute alveolar hyperventilation with mild hypoxemia (ABG)

P Oxygen Therapy Protocol: Monitor SpO2. (Titrate O2 per NC as needed to keep SpO2 >90%.)

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4.Mendelson syndrome is associated with which of the following?

a.Lipoid pneumonitis

b.Rubella

c.Varicella

d.Aspiration pneumonia

5.Which of the following is the most common viral pulmonary complication of AIDS?

a.Aspergillus

b.Cryptococcus

c.Pneumocystis jirovecii\

d.Cytomegalovirus

6.Which of the following infects almost all children by age 2?

a.Klebsiella

b.Haemophilus influenzae type B

c.Respiratory syncytial virus

d.Pseudomonas aeruginosa

7.Which of the following is almost always the cause of acute epiglottitis?

a.Haemophilus influenzae type B

b.Klebsiella

c.Streptococcus

d.Mycoplasma pneumoniae

8.Which of the following is related to mumps, rubella, and RSV?

a.Streptococcus

b.Parainfluenza virus

c.Mycoplasma pneumoniae

d.Adenovirus

9.In the absence of a secondary bacterial infection, lung inflammation caused by the aspiration of gastric fluids usually becomes insignificant in approximately how many days?

a.2 days

b.3 days

c.5 days

d.7 days

10.Which of the following findings is/are associated with pneumonia?

1.Decreased tactile and vocal fremitus

2.Increased

3.Decreased functional residual capacity

4.Increased vital capacity

a.1 only

b.3 only

c.2 and 4 only

d.1 and 3 only

11.Which of the following is the most common fungal infection in the United States?

a.Coccidioidomycosis

b.Histoplasmosis

c.San Joaquin Valley disease

d.Blastomycosis

12.Which of the following is(are) anaerobic organisms?

1.Blastomyces

2.Peptococcus

3.Coccidioides immitis

4.Bacteroides

a.1 and 2 only

b.2 and 4 only

c.3 and 4 only

d.2, 3, and 4 only

13.Anatomically, a lung abscess most commonly forms in which part(s) of the lung? 1. Posterior segment of the upper lobe

2.Lateral basal segment of the lower lobe

3.Anterior segment of the upper lobe

4.Superior segment of the lower lobe

a.1 only

b.3 only

c.1 and 4 only

d.2 and 3 only

14.Incidence of histoplasmosis is especially high in which of the following area(s)?

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