Lung Abscess

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Lung Abscess

Chapter Objectives

After reading this chapter, you will be able to:

• List the anatomic alterations of the lungs associated with lung abscess.

• Describe the causes of lung abscess.

• List the cardiopulmonary clinical manifestations associated with lung abscess.

• Describe the general management of lung abscess.

• 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.

Anatomic Alterations of the Lungs

A lung abscess is defined as a necrosis of lung tissue that in severe cases leads to a localized air- and fluid-filled cavity. The fluid in the cavity is a collection of purulent exudate that is composed of liquefied white blood cell remains, proteins, and tissue debris. The air- and 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 pathology is indistinguishable from that 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 interstitium 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 (see Figure 15-1).

As the inflammatory process progresses, tissue necrosis involving all the lung structures occurs. In severe cases the tissue necrosis ruptures into a bronchus and allows a partial or total drainage of the liquefied contents into the cavity. An air- and fluid-filled cavity also may rupture into the intrapleural space via a bronchopleural fistula and cause pleural effusion and empyema (see Chapter 23, Pleural Diseases). This may lead to inflammation of the parietal pleura, chest pain, atelectasis, and decreased chest expansion. After a period of time, fibrosis and calcification of the tissues around the cavity encapsulate the abscess (see Figure 16-1).

FIGURE 16-1 Lung abscess. A, Cross-sectional view of lung abscess. B, Consolidation and **(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).

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

• Alveolar consolidation

• Alveolar-capillary and bronchial wall destruction

• Tissue necrosis

• Cavity formation

• Fibrosis and calcification of the lung parenchyma

• Bronchopleural fistulas and empyema

• Atelectasis

• Excessive airway secretions

Etiology and Epidemiology

A lung abscess is commonly associated with the aspiration of gastric and oral fluids. Aspiration can cause either (1) chemical pneumonia, (2) anaerobic bacterial pneumonia, or (3) a combination of both (see Chapter 15). The aspiration of acidic gastric fluids is associated with immediate injury to the tracheobronchial tree and lung parenchyma—often likened to a flash burn. Common anaerobic organisms found in the normal flora of the mouth, upper respiratory tract, and gastrointestinal tract include the following:

• Anaerobic gram-positive cocci

• Peptococci

• Peptostreptococci

• Anaerobic gram-negative bacilli

• Bacteroides fragilis

• Prevotella melaninogenica

• Fusobacterium species

Anaerobic organisms often colonize in the small grooves and spaces between the teeth and gums in patients with poor oral hygiene; anaerobic organisms are frequently associated with gingivitis and dead or abscessed teeth. 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. The incidence of lung abscesses caused by anaerobic organisms is also high in patients with poor oral hygiene. Anaerobic organisms are cultured in 62% to 87% of cases of aspiration pneumonia, in 85% to 93% of lung abscess cases, in 62% to 76% of patients with empyema, and as many as 94% of patients with exacerbations of bronchiectasis.

Other organisms known to cause a lung abscess are Klebsiella, Staphylococcus, Mycobacterium tuberculosis (including the atypical organisms Mycobacterium kansasii and Mycobacterium avium), Histoplasma capsulatum, Coccidioides immitis, Blastomyces, and Aspergillus fumigatus. Some parasites such as Paragonimus westermani, Echinococcus, and Entamoeba histolytica may also cause lung abscess formation. On rare occasions a lung abscess may also be caused by Streptococcus pneumoniae, Pseudomonas aeruginosa, or Legionella pneumophila. Typically, more than one type of bacterium is involved, as in an infection with anaerobic organisms mixed with aerobic ones.

Finally, a lung abscess may 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’s 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).

Anatomically, a lung abscess most commonly forms in the superior segments of the lower lobes and the posterior segments of the upper lobes. The tendency for an abscess to form in these areas is because of the effect of gravity and the dependent position of the tracheobronchial tree at the time of aspiration, which commonly occurs while the patient is in the supine position. The right lung is more commonly involved than the left.

Box 16-1 on p. 247 summarizes organisms known to cause lung abscess.

OVERVIEW of the Cardiopulmonary Clinical Manifestations Associated with Lung Abscess

The following clinical manifestations result from the pathologic mechanisms caused (or activated) by Alveolar Consolidation (see Figure 9-9) and, when the abscess is draining, by Excessive Bronchial Secretions (see Figure 9-12)—the major anatomic alterations of the lungs associated with lung abscess (see Figure 16-1).

CLINICAL DATA OBTAINED AT THE PATIENT’S BESIDE

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, fever

Increased Heart Rate (Pulse) and Blood Pressure

Chest Pain, Decreased Chest Expansion

Cyanosis

Cough, Sputum Production, and Hemoptysis

During the early stages, when the lung abscess is in the inflammatory pneumonia-like phase, the patient generally has a nonproductive barking or hacking cough. If the abscess progresses into an air- and fluid-filled cavity and ruptures through a bronchus, the patient may suddenly cough up large amounts of sputum. Foul-smelling brown or gray sputum indicates a putrid infection that is caused by numerous organisms, including anaerobes. An odorless green or yellow sputum indicates a nonputrid infection caused by a single aerobic organism. Blood-streaked sputum is common in patients with a lung abscess. Occasionally, frank hemoptysis is seen.

Chest Assessment Findings

• Increased tactile and vocal fremitus

• Crackles and rhonchi

The following may be noted directly over the abscess:

• Dull percussion note

• Bronchial breath sounds

• Diminished breath sounds

• Whispered pectoriloquy

• Pleural friction rub (if abscess is near pleural surface)

CLINICAL DATA OBTAINED FROM LABORATORY TESTS AND SPECIAL PROCEDURES

Pulmonary Function Test Findings Severe and Extensive Cases (Restrictive Lung Pathophysiology)

FORCED EXPIRATORY FLOW RATE FINDINGS

FVC	FEV_T	FEV₁/FVC ratio	FEF_25%-75%
↓	N or ↓	N or ↑*	N or ↓
FEF_50%	FEF_200-1200	PEFR	MVV
N or ↓	N or ↓	N or ↓	N or ↓

^*May be down in when airway obstruction is present.

Lung Volume and Capacity Findings

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

Arterial Blood Gases

MILD TO MODERATE LUNG ABSCESS

Acute Alveolar Hyperventilation with Hypoxemia (Acute Respiratory Alkalosis)

pH	Paco₂		Pao₂
↑	↓	↓ (slightly)	↓

SEVERE LUNG ABSCESS

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 *

	Do₂^†		C(a-)o₂	O₂ER
↑	↓	N	N	↑	↓

^†The 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.

^*C(a-)O₂, Arterial-venous oxygen difference; DO₂, total oxygen delivery; O₂ER, oxygen extraction ratio; , pulmonary shunt fraction; mixed venous oxygen saturation; oxygen consumption.

ABNORMAL LABORATORY TEST AND PROCEDURE RESULTS

Sputum Examination—Most Common Organisms (See Discussion of Etiology)

Anaerobic Organisms

Anaerobic Gram-Positive Cocci

• Peptococci

• Peptostreptococci

Anaerobic Gram-Negative Bacilli

• Bacteroides fragilis

• Prevotella melaninogenica

• Fusobacterium species

• Cavities with air-fluid levels

• Fibrosis and calcification

• Pleural effusion

The chest radiograph typically reveals localized consolidation during the early stages of lung abscess formation. Later, the characteristic radiographic appearance of a lung abscess appears after (1) the infection ruptures into a bronchus, (2) tissue destruction and necrosis have occurred, and (3) partial evacuation of the purulent contents has occurred. The abscess usually appears on the radiograph as a circular radiolucency that contains an air-fluid level surrounded by a dense wall of lung parenchyma (Figure 16-2).

FIGURE 16-2 Reactivation tuberculosis with a large cavitary lesion containing an air-fluid level in the right lower lobe. Smaller cavitary lesions are also seen in other lobes. (From Hansell DM, Armstrong P, Lynch DA, McAdams HP, eds: *Imaging of diseases of the chest,* ed 4, Philadelphia, 2005, Elsevier.)

General Management of Lung Abscess

Treatment varies based on the severity of the pneumonia and lung abscess. Treatment includes appropriate antimicrobial therapy coupled with prompt drainage and surgical debridement. When 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.

Medications and Procedures Commonly Prescribed by the Physician

Antibiotics

Antibiotics are the primary treatment for a lung abscess. For example, oropharyngeal anaerobic infections are treated with penicillin G. For anaerobic coverage, metronidazole (Flagyl) or clindamycin may be used. Because most of the problems associated with aspiration pneumonia are secondary to the inhaled acidic gastric contents—which in turn cause a chemical pneumonia—quinolones and penicillins are also used. When Klebsiella is the causative agent, the following may be administered: third- and/or fourth-generation cephalosporins (cefotaxime, ceftriaxone) plus aminoglycosides, antipseudomonal penicillins, monobactam (aztreonam), or quinolones.

When lung abscesses are caused by methicillin-susceptible strains of Staphylococcus aureus, nafcillin or oxacillin (with or without rifampin) may be used. In the case of methicillin-resistant strains of S. aureus, vancomycin (with or without rifampin) is commonly administered. Good alternative choices are cephalosporins and clindamycin. (See Appendix III, Antibiotics.)

Respiratory Care Treatment Protocols

CASE STUDY

Lung Abscess

Admitting History and Physical Examination

This 64-year-old unemployed man sought medical attention because of an increasingly severe cough that produced moderate amounts of foul-smelling sputum. He had undergone splenectomy for removal of a ruptured spleen 1 year ago. He reported that on several occasions recently he had a slight fever and that his appetite was poor; he had lost about 6 pounds. For the past 3 days he had noticed some right-sided chest pain, and his cough had become very productive. The patient denied cigarette smoking.

Physical examination showed a small and poorly nourished male in moderate distress, coughing throughout the interview. The patient’s vital signs were blood pressure 160/90, heart rate 120/min, respiratory rate 22/min, and oral temperature 100.6° F. There was brawny discoloration of the legs below the knees. His teeth were in deplorable condition, and he had marked halitosis. Examination of the chest revealed dullness to percussion, crackles, rhonchi, and bronchial breath sounds in the right lower lobe.

His frequent cough produced large amounts of foul-smelling brown and gray sputum. His cough was strong. The chest x-ray film showed a 4-cm diameter cavity in the right lower lobe with a clear air-fluid level. Patches of alveolar consolidation surrounded the cavity. There was no evidence of air trapping. Sputum for a culture and sensitivity study was obtained, but the results were still pending. His arterial blood gas values were as follows: pH 7.51, Paco₂ 29, 22, and Pao₂ 61 on room air. Intravenous antibiotic therapy was begun. The respiratory care practitioner assigned to his case recorded the following.

Respiratory Assessment and Plan

S “I can’t stop coughing.” Complains of low-grade fever, loss of appetite, weight loss (6 lb).

O Cachectic. BP 160/90, HR 120, RR 22, T 100.6° F orally. Teeth carious. Flat to percussion over RLL. Crackles, rhonchi, and bronchial breath sounds over RLL. CXR: 4-cm diameter cavity with fluid level and consolidation RLL. ABGs: pH 7.51, Paco₂ 29, 22, and Pao₂ 61. Excessive amount of foul-smelling, thick brown and gray sputum.

• Acute infection (fever)

• Malnourished (inspection)

• Lung abscess and consolidation, RLL (CXR)

• Acute alveolar hyperventilation with mild hypoxemia (ABG)

• Excessive and thick airway secretions (sputum, rhonchi)

• Good ability to mobilize secretions (strong cough)

P Oxygen Therapy Protocol: 2 L/min per nasal cannula. Spo₂ spot check to verify appropriateness of O₂ therapy. O₂ titration if necessary. Bronchopulmonary Hygiene Therapy Protocol: Deep breathe and cough, with postural drainage to right lower lobe q6h. Aerosolized Medication Protocol: Trial period of med nebs: 2.0 cc acetylcysteine with 0.5 mL albuterol hour before postural drainage q6h × 3 days, then reevaluate.

After reviewing the results of sputum culture sensitivity studies, the physician adjusted the patient’s antibiotic therapy. Over the next 5 days, the patient’s general condition improved. His cough and sputum production decreased remarkably but not completely. The sputum produced was no longer thick. His Pao₂ increased to 86 mm Hg, and he no longer had acute alveolar hyperventilation. A chest radiograph revealed that his lung abscess was slightly reduced in size compared with the chest radiograph taken on the day of his admission, and his pneumonia had improved significantly. A complete pulmonary function test (PFT) study revealed a mild reduction in lung volumes, capacities, and expiratory flow rates. Social Service worked with him on two occasions during his hospitalization and scheduled a follow-up appointment at his home 4 weeks after discharge. An oral surgery consultation was obtained and extraction of the patient’s carious teeth was scheduled. The patient was instructed on deep-breathing and coughing techniques and general bronchial hygiene and was discharged on the morning of the sixth day. He was discharged on a month-long course of oral antibiotics.

This case illustrates some of the classic clinical manifestations of a lung abscess. For example, the Alveolar Consolidation (see Figure 9-9), which was identified on the chest x-ray film, surrounding the abscess likely played a role in producing the patient’s fever and increased heart rate, blood pressure, and respiratory rate. In addition, the pneumonic consolidation also contributed to the patient’s alveolar hyperventilation and hypoxemia, the bronchial breath sounds, and the reduced lung volumes and capacities and flow rates identified on his PFT.

In addition, the clinical manifestations associated with Excessive Bronchial Secretions (see Figure 9-12) also were seen in this case. Not only did the excessive airway secretions contribute to the patient’s hypoxemia, secondary to the decreased ratio and pulmonary shunting, but they also contributed to the increased airway resistance (caused by the secretions) that resulted in the rhonchi, sputum production, and reduced air-flow rates seen in the PFT.