Streptococcus pneumoniae accounts for more than 80% of all the bacterial pneumonias. The organism is a gram-positive, nonmotile coccus that is found singly, in pairs (called diplococci), and in short chains (Figure 15-2). The cocci are enclosed in a smooth, thick polysaccharide capsule that is essential for virulence. There are more than 80 different types of S. pneumoniae. Serotype 3 organisms are the most virulent. Streptococci are generally transmitted by aerosol from a cough or sneeze of an infected individual. Most strains of S. pneumoniae are sensitive to penicillin and its derivatives. S. pneumoniae also is commonly cultured from the sputum of patients having an acute exacerbation of chronic bronchitis.

FIGURE 15-2 The *Streptococcus* organism is a gram-positive, nonmotile bacterium that occurs singly, in pairs, and in short chains.

Staphylococcal pneumonia

There are two major groups of Staphylococcus: (1) Staphylococcus aureus, which is responsible for most “staph” infections in humans, and (2) Staphylococcus albus and Staphylococcus epidermidis, which are part of the normal skin flora. The staphylococci are gram-positive cocci found singly, in pairs (called diplococci), and in irregular clusters (Figure 15-3). Staphylococcal pneumonia often follows a predisposing virus infection and is seen most often in children and immunosuppressed adults. S. aureus is commonly transmitted by aerosol from a cough or sneeze of an infected individual and indirectly via contact with contaminated floors, bedding, clothes, and the like. Staphylococci are a common cause of hospital-acquired pneumonia and are becoming increasingly antibiotic resistant—thus the term multiple drug–resistant S. aureus (MDRSA) organisms (some centers shorten this acronym to MRSA).

FIGURE 15-3 The *Staphylococcus* organism is a gram-positive, nonmotile coccus that is found singly, in pairs, and in irregular clusters.

Atypical Organisms

Mycoplasma pneumoniae

M. pneumoniae is a common cause of mild pneumonia. These organisms cause symptoms similar to both bacterial and viral pneumonia, although the symptoms develop more gradually and are often milder. A common symptom of mycoplasma pneumonia is a cough that tends to come in violent attacks, producing only a small amount of white mucus. Chills and fever are early symptoms. Some patients experience nausea or vomiting. Some patients may experience a profound weakness that lasts for a long time.

The mycoplasma are tiny, cell wall–deficient organisms. They are smaller than bacteria but larger than viruses. The pneumonia caused by the mycoplasmal organism is described as primary atypical pneumonia—atypical because the organism escapes identification by standard bacteriologic tests. M. pneumoniae is most frequently seen in people younger than 40 years of age during the late summer and early fall months. This type of pneumonia spreads easily in areas where people congregate, such as child-care centers, schools, and homeless shelters. Patients with M. pneumoniae often are said to have “walking pneumonia” because the condition is mild (i.e., slight fever, fatigue, and a characteristic dry, hacking cough) and the patient is usually ambulatory.

Legionella pneumophila

In July 1976, a severe pneumonia-like disease outbreak occurred at an American Legion convention in Philadelphia. The causative agent eluded identification for many months, despite the concerted efforts of the nation’s top epidemiologic experts. When the organism finally was recovered from a patient, it was found to be an unusual and fastidious gram-negative bacillus with atypical concentrations of certain branched-chain lipids. The initial isolate was designated as Legionella pneumophila. More than 20 Legionella species have now been identified.

Most of the species are free-living in soil and water, where they act as decomposer organisms. The organism also multiplies in standing water such as contaminated mud puddles, large air-conditioning systems, and water tanks. The organism is transmitted when it becomes airborne and enters the patient’s lungs as an aerosol. No convincing evidence suggests that the organism is transmitted from person to person. The organism can be detected in pleural fluid, sputum, or lung tissue by direct fluorescent antibody microscopy. Although it is rarely found outside the lungs, the organism may be found in other tissues. The disease is most commonly seen in middle-aged men who smoke.

Chlamydia psittaci (Psittacosis)

C. psittaci is a small gram-negative bacterium in the respiratory tract and feces of a variety of birds (e.g., parrots, parakeets, lorikeets, cockatoos, chickens, pigeons, ducks, pheasants, turkeys). C. psittaci is transmitted from birds to humans by aerosol or direct contact. The clinical manifestations of C. psittaci closely resemble those caused by M. pneumoniae.

Chlamydia pneumoniae

C. pneumoniae recently has been identified as a cause of pneumonia in adults. It has been detected in schools, military institutions, and families. It is associated with meningoencephalitis, myocarditis, endocarditis, coronary artery disease, and Guillain-Barré syndrome.

Anaerobic Bacterial Infections

The major anaerobic organisms associated with pneumonia are Peptostreptococcus species, Bacteroides melaninogenicus, Fusobacterium necrophorum, Bacteroides asaccharolyticus, Porphyromonas endodontalis, and Porphyromonas gingivalis. Aspiration of oropharyngeal secretions and gastric fluids are the major causes of anaerobic lung infections. Predisposing risk factors of aspiration include a decreased level of consciousness, impaired swallowing, poor dental hygiene, and gastrointestinal abnormalities. Aspiration pneumonia is often multimicrobial.

Viral Causes

Approximately half of all pneumonias are caused by viruses. More and more viruses are being identified as the cause of respiratory infections. Although most viruses attack the upper airways, some can produce pneumonia. Most of these pneumonias are not life threatening and last only a short time. Viral pneumonia tends to start with flulike signs and symptoms. The early symptoms are a dry (nonproductive) cough, headache, fever, muscle pain, and fatigue. As the disease progresses, the patient may become short of breath, cough, and produce a small amount of clear or white sputum. Viral pneumonia always carries the risk of development of a secondary bacterial pneumonia.

Viruses are minute organisms not visible by ordinary light microscopy. They are parasitic and depend on nutrients inside cells for their metabolic and reproductive needs. Approximately 90% of acute upper respiratory tract infections and 50% of lower respiratory tract infections are caused by viruses. Respiratory viruses are the most common cause of pneumonia in young children, peaking between the ages of 2 and 3. By school age, M. pneumoniae become more prevalent (see previous section). The most common viruses that cause respiratory infections are described in the following paragraphs.

Influenza Virus

Although the influenza virus has several subtypes, influenza A and B are the most common causes of viral respiratory tract infections. In the United States, influenza A and B commonly occur in epidemics during the winter months. Children, young adults, and older individuals are most at risk. Influenza is transmitted from person to person by aerosol droplets. Often the first sign of an epidemic is an increase in school absenteeism. The virus survives well in conditions of low temperatures and low humidity. It also has been found in horses, swine, and birds. Influenza viruses have an incubation period of 1 to 3 days and usually cause upper respiratory tract infections. Epidemiologists fear a pandemic of influenza, stating it is an issue of “when” and “where” rather than “if.” The recent epidemic of H1N1 (“swine flu”) is a case in point.

Respiratory Syncytial Virus

The respiratory syncytial virus (RSV) (see Chapter 36) is a member of the paramyxovirus group. Parainfluenza, mumps, and rubella viruses also belong to this group. RSV is most often seen in children less than 12 months of age and in older adults with underlying heart or pulmonary disease. Almost all children will be infected with RSV by their second birthday. The infection is rarely fatal in infants. RSV often goes unrecognized but may play an important role as a forerunner to bacterial infections. Early attempts to develop an RSV vaccine have been unsuccessful. The virus is transmitted by aerosol and by direct contact with infected individuals. RSV infections are most commonly seen in patients during the late fall, winter, or early spring months. Many times the virus is misdiagnosed in older children, who are given antibiotics that do not work.

Parainfluenza Virus

The parainfluenza viruses also are members of the paramyxovirus group and therefore are related to mumps, rubella, and RSV. There are five types of parainfluenza viruses: types 1, 2, 3, 4A, and 4B. Types 1, 2, and 3 are the major causes of infections in humans. Type 1 is considered a croup type of virus. Types 2 and 3 are associated with severe infections. Although type 3 is seen in persons of all ages, it usually is seen in infants younger than 2 months of age; types 1 and 2 are seen most often in children between the ages of 6 months and 5 years. Types 1 and 2 typically occur in the fall, whereas type 3 infection most often is seen in the late spring and summer. Parainfluenza viruses are transmitted by aerosol droplets and by direct person-to-person contact. The parainfluenza viruses are known for their ability to spread rapidly among members of the same family.

Adenoviruses

There are more than 30 adenovirus subgroups. Serotypes 4, 7, 14, and 21 cause viral infections and pneumonia in all age groups. Serotype 7 has been related to fatal cases of pneumonia in children. Adenoviruses are transmitted by aerosol. Pneumonia caused by adenoviruses generally occurs during the fall, winter, and spring.

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 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 typically is 2 to 7 days. Initially, the patient usually develops a fever (>100.4° F or >38.0° C), followed by chills, headaches, general feeling of discomfort, and body aches. Toward the end of the incubation period, the SARS patient usually develops a dry, nonproductive cough, shortness of breath, and malaise. In severe causes, hypoxemia develops. According to the Centers for Disease Control and Prevention (CDC), 10% to 20% of SARS patients 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 SARS patients receive the same treatment used for any patient with serious community-acquired atypical pneumonia of unknown cause.

Other Causes

Rickettsiae

Rickettsiae are small, pleomorphic coccobacilli. Most rickettsiae are intracellular parasites possessing both ribonucleic acid (RNA) and deoxyribonucleic acid (DNA). There are several pathogenic members of the Rickettsia family: Rickettsia rickettsii (Rocky Mountain spotted fever), Rickettsia akari (rickettsialpox), Rickettsia prowazekii (typhus), and Rickettsia burnetii, also called Coxiella burnetii (Q fever).

All species of the genus Rickettsia are unstable outside of cells except for R. burnetii (Q fever), which is extremely resistant to heat and light. Q fever can cause pneumonia as well as a prolonged febrile illness, an influenza-like illness, and endocarditis. The organism is commonly transmitted by arthropods (lice, fleas, ticks, mites). It also may be transmitted by cattle, sheep, and goats and possibly in raw milk.

Varicella (Chickenpox)

The varicella virus usually causes a benign disease in children aged 2 to 8 years, and complications of varicella are not common. In some cases, however, varicella has been noted to spread to the lungs and cause a serious secondary pneumonitis. The mortality rate of varicella pneumonia is about 20%.

Rubella (Measles)

Measles virus spreads from person to person by the respiratory route. Respiratory complications often are encountered in measles because of the widespread involvement of the mucosa of the respiratory tract (e.g., excessive bronchial secretions and infection).

Aspiration Pneumonitis

Aspiration of gastric fluid with a pH of 2.5 or less causes a serious and often fatal form of pneumonia. Aspiration of oropharyngeal secretions and gastric fluids are the major causes of anaerobic lung infections (see discussion of anaerobic bacterial infections, earlier). Aspiration pneumonitis is commonly missed because acute inflammatory reactions may not begin until several hours after aspiration of the gastric fluid. The inflammatory reaction generally increases in severity for 12 to 26 hours and may progress to acute respiratory distress syndrome (ARDS), which includes interstitial and intraalveolar edema, intraalveolar hyaline membrane formation, and atelectasis. In the absence of a secondary bacterial infection, the inflammation usually becomes clinically insignificant in approximately 72 hours. In 1946 Mendelson first described the clinical manifestations of tachycardia, dyspnea, and cyanosis associated with the aspiration of acid stomach contents. The clinical picture he described is now known as Mendelson’s syndrome and is usually confined to aspiration pneumonitis in pregnant women.

Aspiration pneumonia is broadly defined as the pulmonary result of the entry of material from the stomach or upper respiratory tract into the lower airways. There are at least three distinctive forms of aspiration pneumonia, classified according to the nature of the aspirate, the clinical presentation, and management guidelines, as follows:

1. Toxic injury to the lung (such as that caused by gastric acid)

2. Obstruction (by foreign body or fluids)

3. Infection

Aspiration is the presumed cause of nearly all cases of anaerobic pulmonary infections. Studies suggest that anaerobic bacteria are the most common causative agents of lung abscesses; they are also commonly isolated in cases of empyema.

There is a difference between the aspiration of gastric contents and the aspiration of food. Aspiration of gastric contents causes initial hypoxemia regardless of the aspirate’s pH level. Consequently, oximetry is a good measurement if aspiration is suspected. If the aspirate’s pH is relatively high (greater than 5.9), the initial injury is rapidly reversible. Such aspiration occurs in patients who receive antacids or proton pump inhibitors (PPIs). If the pH is low (pH of unbuffered gastric contents normally ranges from 1 to 1.5), parenchymal damage may occur, with inflammation, edema, and hemorrhage. When food is aspirated, obliterative bronchiolitis with subsequent granuloma formation occurs.

Gastroesophageal reflux disease (GERD) is the regurgitation of stomach contents into the esophagus. GERD causes disruption in nerve-mediated reflexes in the distal esophagus, resulting in alteration of the primary and secondary peristaltic wave and reflux. Therefore “to-and-fro” peristalsis can result from spasticity at the distal esophageal sphincter and retropulsion of middle and upper esophageal contents. This may result in aspiration, although not necessarily.

GERD is three times more prevalent in patients with asthma than in other patients. In other words, GERD is a frequently unrecognized cause of asthma. Presumably, acid reflux into the esophagus causes vagal stimulation, resulting in a reflexive increase in bronchial tone in patients with asthma. Recent literature suggests that asymptomatic reflux does not contribute to worsening lung function. Nevertheless, GERD does cause chronic cough in 10% to 20% of patients.

Normal swallowing mechanics has four phases, as follows:

The first two phases are considered voluntary stages (cerebral). These phases occur as the food or liquid is prepared for entry to the pharynx and esophagus. The airway is open while food is prepared in the oral cavity. Adequate tongue function is important for the manipulation and propulsion of the prepared food or liquid (called a bolus) into the pharynx. Spillage of liquid into the pharynx during the chewing of food is usually not a problem in patients with good airway protection.

The pharyngeal phase (involuntary brain stem function) of swallowing involves numerous physiologic actions that direct the bolus into the esophagus:

• Elevation and retraction of the velopharyngeal port (velum closure)

• Pharyngeal muscle contraction

• Elevation and forward excursion of the larynx (epiglottic closure)

• Closure of the laryngeal vestibule, false vocal folds, and true vocal folds (laryngeal closure)

• Relaxation of the upper esophageal sphincter (UES)

Airway closure progresses inferiorly to superiorly in the larynx as the food bolus is directed laterally around the airway and into the esophagus.

Respiration is halted during the pharyngeal phase for an approximately 1-second apneic period, although duration varies with bolus volume and viscosity. Bolus transit in the esophageal phase (under both brain stem and intrinsic neural control) lasts 8 to 20 seconds. In this phase the UES relaxes to receive the bolus with a peristaltic wave from the pharyngeal superior constrictor muscles, forcing the bolus through the relaxed UES. The primary peristalsis propels the bolus through the esophagus and lower esophageal sphincter and into the stomach.

Six cranial nerves carry motor signals generated by cerebral and brain stem swallowing centers:

• V (trigeminal)

• VII (facial)

• IX (glossopharyngeal)

• X (vagus)

• XI (spinal accessory [minor involvement])

• XII (hypoglossal)

The relationship between respiration and swallowing is not random. Expiration before and after the pharyngeal phase in normal swallowing is believed to serve as an inherent closure and clearance mechanism against penetration of food or liquids into the airway entrance.

Dysphagia is the result of an abnormal swallow that can involve the oral, pharyngeal, and esophageal phases. Penetration into the laryngeal vestibule occurs when food or liquid (or both) enters the larynx but does not pass through the vocal cords into the trachea. Aspiration is the passage of food or liquid into the trachea via the vocal cords.

Diagnostic tests for dysphagia include the modified barium swallow (MBS), videofluoroscopy, videofiberoptic endoscopy, and the modified Evan’s blue dye test. Evan’s blue dye test involves instilling a deep blue dye into the gastrointestinal tract and seeing if it can be suctioned from the trachea. If it can, it suggests a communication between the two structures, such as a fistula. The MBS and videofluoroscopy tests are most definitive for identification of the particular phase of the swallow that is dysfunctional. The modified Evan’s blue dye test can be unreliable (as much as 40% of the time) as a test suggesting aspiration in a tracheostomized patient. Both false-positive and false-negative test results occur.

A compromised respiratory system can cause dysphagia, and conversely, dysphagia may cause respiratory complications. COPD can result in a slowed oral and pharyngeal transit time, reduced coordination and strength of the oral and pharyngeal musculature, and reduced airway clearance by coughing.

Treatment of dysphagia is specific to the nature of the disorder. Varied methods of presentation of foods and liquids, bolus volumes and consistency, postural movements, and food temperature can affect the dynamics of the relation between respiration and swallowing. Large volumes of liquid requiring uninterrupted swallowing result in longer apneic periods and can be difficult for patients with shortness of breath and dyspnea. Small-volume bites and swallows make sense in this setting.

Unilateral cerebrovascular accidents (strokes) and hemorrhage tend to cause hypopharyngeal hemiparesis. Difficulty in swallowing (with impairment of the oral phase) and aspiration of thin fluids therefore may follow. The facial and tongue weakness can result in poor bolus control in the oral cavity.

Silent aspiration is defined as aspiration that does not evoke clinically observable adverse symptoms such as coughing, choking, and immediate respiratory distress. Some patients have silent aspiration after a stroke. Evidence also suggests that some sequelae of stroke include laryngopharyngeal sensory deficits with no subjective or objective evidence of dysphagia, such as choking, gagging, or cough.

Some patients with severe and bilateral sensory deficits develop aspiration pneumonia. The clinical findings of dysphonia, dysarthria, abnormal gag reflex, abnormal volitional cough, cough after swallow, and voice change after swallow all significantly relate to aspiration and are predictors of silent aspiration. Conversely, a normal reflex cough after a stroke indicates an intact laryngeal cough reflex, a protected airway, and low risk for developing aspiration pneumonia with oral feeding. The cough reflex is significantly reduced in older patients.

Tracheostomized patients are at high risk for silent aspiration. Perhaps 55% to 70% of intubated or tracheostomized patients aspirate. A tracheostomy tube has a direct effect on the pharyngeal phase of a swallow because of the alteration of normal respiratory function (exhalation timing) as well as the anatomic alteration and the physical resistance imposed by the tracheostomy tube itself. Laryngeal elevation is reduced, particularly with the cuff inflated, which leads to inadequate airway closure and increased pharyngeal residue.

Poor sensory response to material entering the larynx contributes to the slowing of an uncoordinated laryngeal closure. The protective cough may be lessened because of the impaired laryngeal sensation. Subglottic air pressure (coordinated exhalation with swallow) helps prevent entry of material into the trachea and is reduced in patients with a tracheostomy. An inflated cuffed tracheostomy can cause complications that can anchor the larynx to the anterior wall of the neck and desensitize the pharynx. Delayed triggering of the swallowing response and increased pharyngeal residue are prevalent.

Recommendations for oral feeding include considerations of dietary consistency, specifically defined for solids and liquids; skilled supervision with oral intake; safe swallowing strategies; positioning requirements; cuff deflation; and tracheal occlusion issues. It may be necessary to coordinate mealtime with ventilator weaning attempts to optimize more positive pressure generation to aid in expelling laryngeal residue and creating subglottic pressure.

Partial or complete endotracheal cuff deflation during meals promotes laryngeal elevation, allows expectoration of secretions, reduces the effect of friction on the tracheoesophageal wall, and enhances the senses of taste and smell. If an uncuffed tracheostomy is in place, possible placement of a Passey-Muir valve or capping of a fenestrated tracheostomy tube will aid in subglottic negative pressure and assist in an effective swallow.

The dynamic changes a patient may experience clinically necessitate a coordinated team approach, including physical, occupational, and respiratory therapists; a speech-language pathologist; registered dietitian; and nurse. This approach allows for effective management of tracheostomized and nontracheostomized patients and avoidance of aspiration.

Lipoid Pneumonitis

The aspiration of mineral oil, used medically as a lubricant, also 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.

Pneumocystis carinii Pneumonia

P. jiroveci is an opportunistic, often fatal, form of pneumonia seen in profoundly immunosuppressed patients. Although the Pneumocystis organism has been identified as a protozoan, recent information suggests that it is more closely related to fungi. Pneumocystis normally can be found in the lungs of humans, but it does not cause disease in healthy hosts, only in individuals whose immune systems are critically impaired. Currently, Pneumocystis pneumonia is the major pulmonary infection seen in patients with acquired immunodeficiency syndrome (AIDS) and HIV infection.

In vulnerable hosts the disease spreads rapidly throughout the lungs. Before AIDS, P. carinii pneumonia was seen primarily in patients with malignancy, in organ transplant recipients, and in patients with diseases requiring treatment with large doses of immunosuppressive agents. Today, most cases of P. carinii pneumonia are seen in patients with AIDS. The early clinical manifestations of Pneumocystis in patients with AIDS are indistinguishable from those of any other pneumonia. Typical signs and symptoms include progressive exertional dyspnea, a dry cough that may or may not produce mucoid sputum, difficulty in taking a deep breath (not caused by pleurisy), and fever with or without sweats. The therapist may hear normal breath sounds on auscultation or end-inspiratory crackles. The chest x-ray film may be normal at first; later it will show bilateral interstitial infiltrates, which may progress to alveolar filling and “white out” of the chest x-ray film.

Cytomegalovirus

Cytomegalovirus (CMV), a member of the herpesvirus family, is the most common viral pulmonary complication of AIDS. CMV infection commonly coexists with P. carinii infection.

Tuberculosis

Tuberculosis (see Chapter 17) is an infectious disease caused by Mycobacterium tuberculosis. M. tuberculosis is a slender, rod-shaped aerobic organism. Predisposing factors of tuberculosis include homelessness, drug abuse, and AIDS. The initial response of the lung is an inflammatory reaction that is similar to any acute pneumonia (see Chapter 17).

Fungal Infections

Because most fungi are aerobes, the lung is a prime site for fungal infections (see Chapter 18). Primary fungal pathogens include Histoplasma capsulatum, Coccidioides immitis, and Blastomyces dermatitidis. In addition, the opportunistic yeast pathogens Candida albicans, Cryptococcus neoformans, and Aspergillus also may cause pneumonia in certain patients. For example, C. albicans, which occurs as normal flora in the oral cavity, genitalia, and large intestine, is rarely seen in the tracheobronchial tree or lung parenchyma. In patients with AIDS, however, C. albicans commonly causes an infection of the mouth, pharynx, esophagus, vagina, skin, and lungs. A C. albicans infection of the mouth is called thrush; it is characterized by a white, adherent, patchy infection of the membranes of the mouth, gums, cheeks, and throat.

C. neoformans proliferates in pigeon droppings, which have a high nitrogen content, and readily scatters into the air and dust. Today, the highest rate of cryptococcosis occurs among patients with AIDS and persons undergoing steroid therapy. The molds of the genus Aspergillus may be the most pervasive of all fungi—especially Aspergillus fumigatus. Aspergillus is found in soil, vegetation, leaf detritus, food, and compost heaps. Persons who breathe the air of granaries, barns, and silos are at the greatest risk. Aspergillus infection usually occurs in the lungs. Aspergillus is almost always an opportunistic infection and lately has posed a serious threat to patients with AIDS. When fungal organisms are inhaled, the initial response of the lung is an inflammatory reaction similar to that produced by any acute pneumonia (see Chapter 18).

Avian Influenza A

Avian influenza A (also called bird flu and H5N1) is a subype 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 people 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).

Acquired Pneumonia Classifications

Pneumonia is often classified according to the location or method of exposure. Common acquired pneumonia classifications are community-acquired pneumonia (CAP), hospital-acquired pneumonia, ventilator-associated pneumonia (VAP), and nursing home–acquired pneumonia.

Community-Acquired Pneumonia

Community-acquired pneumonia is defined as a lower respiratory tract infection that is acquired outside of the hospital or during the first 48 hours of hospitalization. More than 4 million adults are diagnosed with CAP each year in the United States. The most common cause of CAP is Streptococcus. Other organisms associated with CAP include M. pneumoniae, H. influenzae, C. pneumoniae, L. pneumophila, S. aureus, and M. tuberculosis.

Hospital-Acquired Pneumonia

Hospital-acquired pneumonia (also called nosocomial pneumonia) is defined as a pneumonia that develops 48 hours or longer after admission to the hospital. Nosocomial pneumonia is estimated to account for more than 15% of all respiratory infections. Nosocomial infections include P. aeruginosa; S. aureus, including MDRSA; S. pneumoniae; Enterobacter; E. coli; Klebsiella; and oral anaerobes (aspiration).

Ventilator-Acquired Pneumonia

Ventilator-acquired pneumonia (also called ventilator-associated pneumonia) is defined as a pneumonia that develops more than 48 to 72 hours after endotracheal intubation. Common ventilator-associated infections include P. aeruginosa, Enterobacter, Klebsiella, Stenotrophomonas maltophilia, and S. aureus. Concern that the occurrence of VAP is preventable lies as the root of possible reimbursement penalties for hospitals in which it occurs.

Nursing Home–Acquired Pneumonia

Nursing home–acquired pneumonia is defined as a respiratory tract infection that develops in a long-term care facility. Common nursing home–acquired infections include mixed aerobic and anaerobic mouth flora, S. aureus, enteric gram-negative bacilli, influenza, and M. tuberculosis.

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 Figure 9-9), Increased Alveolar-Capillary Membrane Thickness (see Figure 9-10), and Atelectasis (see Figure 9-8)—the major anatomic alterations of the lungs associated with pneumonia (see Figure 15-1).

During the resolution stage of pneumonia, Excessive Bronchial Secretions (see Figure 9-12) also may 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)

• Decreased lung compliance–increased ventilatory rate relationship

• Stimulation of J receptors

• Pain, anxiety, fever

Increased Heart Rate (Pulse) and Blood Pressure

Chest Pain 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 red blood cells (RBCs) also move into the alveoli and produce the blood-streaked or rusty appearance of the fluid (see Figure 15-1). 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 and rhonchi

• 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)

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 ↓

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 STAGES

Acute Alveolar Hyperventilation with Hypoxemia (Acute Respiratory Alkalosis)

pH	Paco₂		Pao₂
↑	↓	↓ (slightly)	↓

SEVERE STAGE

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

Abnormal sputum examination findings (see discussion of etiology in this chapter, Box 15-1)

RADIOLOGIC FINDINGS

Chest Radiograph

• Increased density (from consolidation and atelectasis)

• Air bronchograms

• Pleural effusions

The radiographic signs vary considerably depending on the causative agent. 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 (Figure 15-5). The process may appear patchy or uniform throughout the area. As the alveolar consolidation intensifies, alveolar density increases and air bronchograms may be seen (Figure 15-6). A pleural effusion may be identified on the chest radiograph (see Chapter 23).

FIGURE 15-5 Chest x-ray film of a 20-year-old woman with severe pneumonia of the left lung and patchy pneumonia in the right middle and lower lobes.

FIGURE 15-6 Air bronchogram. The branching linear lucencies within the consolidation in the right lower lobe are particularly well demonstrated in this example of staphylococcal pneumonia. (From Hansell DM, Armstrong P, Lynch DA, McAdams HP, eds: *Imaging of diseases of the chest,* ed 4, Philadelphia, 2005, Elsevier.)

Computed Tomography Scan

Alveolar consolidation and air bronchograms also can be seen on the computed tomography (CT) scan (Figure 15-7).

FIGURE 15-7 Air bronchograms shown by computed tomography in a patient with pneumonia. (From Hansell DM, Armstrong P, Lynch DA, McAdams HP, eds: *Imaging of diseases of the chest,* ed 4, Philadelphia, 2005, Elsevier.)

General Management of Pneumonia

The treatment of pneumonia is based on (1) the specific cause of the pneumonia, and (2) the severity of symptoms demonstrated by the patient. For bacterial pneumonia, the first line of defense is usually an antibiotic. Although there are a few viral pneumonias that may be treated with antiviral medications, the recommended treatment is usually the same as for the flu—bed rest and plenty of fluids. In addition, over-the-counter medications are often helpful to reduce fever, treat aches and pains, and depress the dry cough associated with pneumonia. In severe pneumonia, hospitalization may be required. The following is an overview of the treatments used for pneumonia.

Medications and Procedures Commonly Prescribed by the Physician

Antibiotics

Antibiotics are commonly administered to combat the infective agents that cause bacterial pneumonia. Table 15-1 provides an overview of the commonly encountered organisms responsible for pneumonia and the therapeutic agents currently used to treat them.

TABLE 15-1

Commonly Encountered Organisms Responsible for Pneumonia and the Therapeutic Agents Used to Treat Them

Organism Responsible for Pneumonia	Common Treatment Choices
Gram-Positive Organisms
Staphylococcus aureus	Methicillin-susceptible strains: nafcillin or oxacillin with or without rifampin Methicillin-resistant strains: vancomycin with or without rifampin Alternative choice: cephalosporins, clindamycin

Streptococcus

Penicillins: procaine penicillin G or aqueous penicillin G, amoxicillin

Alternative choice: macrolides, cephalosporins, doxycycline, quinolones

Cefotaxime or ceftriaxone; antipseudomonal fluoroquinolones (levofloxacin, gatifloxacin, moxifloxacin)

Gram-Negative Organisms Haemophilus influenzae Ampicillin, third- or fourth-generation cephalosporin, macrolides (azithromycin, clarithromycin), fluoroquinolones Klebsiella pneumoniae Third- and/or fourth-generation cephalosporins (cefotaxime, ceftriaxone) plus aminoglycoside, antipseudomonal penicillin, monobactam (aztreonam), or quinolone Pseudomonas aeruginosa Tobramycin (TOBI), aminoglycoside, and antipseudomonal agents (ticarcillin, piperacillin, mezlocillin, ceftazidime) Atypical Organisms Mycoplasma pneumoniae Doxycycline, macrolides or fluoroquinolones Legionella pneumophila Erythromycin ± rifampin (in severely compromised patient) or clarithromycin, or a macrolide (azithromycin), or a fluoroquinolone (ofloxacin, levofloxacin, sparfloxacin) Chlamydia pneumoniae Tetracycline, erythromycin, macrolide, quinolone

Anaerobic bacterial infections

Peptostreptococcus species

Bacteroides melaninogenica

Fusobacterium necrophorum

Bacteroides asaccharolyticus

Porphyromonas endodontalis

Porphyromonas gingivalis

Most of these organisms are oral contaminants. For anaerobic coverage use metronidazole (Flagyl) or clindamycin; or metronidazole + ceftriaxone; or penicillin + amoxicillin. Infections respond slowly; 4-6 weeks of therapy is generally recommended.

Most of the problem with aspiration pneumonia is secondary to the acid present in stomach contents, causing a chemical pneumonia. Quinolones, penicillins are also useful.

Aspiration fluid should be cultured immediately (even with bronchoscopy and special culture), then the patient started on coverage medication while culture results are awaited. If the culture is negative, stop the antibiotics, then reculture if chest x-ray findings or patient’s condition gets worse. Monitor closely for superinfections such as candida, other yeasts. May add vancomycin and Diflucan to cover nosocomial suprainfections.

Viral Causes Influenza virus

Type A: amantadine and rimantadine

Type A/B: zanamivir, oseltamivir phosphate

Respiratory syncytial virus Ribavirin (Virazole) Other Common Causes Pneumocystis jiroveci

Pentamidine (NebuPent)

Trimethoprim-sulfamethoxazole (TMP-SMZ), dapsone-trimethoprim, primaquine plus clindamycin

Fungal infections Amphotericin B, itraconazole, fluconazole, ketoconazole Tuberculosis (Mycobacterium tuberculosis) Isoniazid (INH), rifampin, pyrazinamide, ethambutol, streptomycin

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 at least partially refractory to oxygen therapy (see Oxygen Therapy Protocol, Protocol 9-1).

Bronchopulmonary Hygiene Therapy Protocol

Because of the airway secretions associated with the resolution stage of pneumonia, a number of bronchopulmonary hygiene treatment modalities may be used to enhance the mobilization of bronchial secretions. In addition, because of food particles in the aspirate, the bronchopulmonary hygiene protocol is useful in the treatment of aspiration pneumonia (see Bronchopulmonary Hygiene Therapy Protocol, Protocol 9-2).

Lung Expansion Therapy Protocol

Lung expansion therapy may be administered to attempt to offset the atelectasis associated with some pneumonias (see Lung Expansion Therapy Protocol, Protocol 9-3).

Thoracentesis

Therapeutically, thoracentesis may be used to treat pleural effusion (see Chapter 23). Fluid samples may be examined for the following:

• Lactic dehydrogenase (LDH)

• Amylase

• pH

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

• Aerobic, anaerobic, tuberculosis, and fungal cultures

• Cytology

A 47-year-old man was 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 room of the nearest hospital.

On physical examination, his vital signs were as follows: blood pressure 150/88, pulse 116/min, respiratory rate 28/min, and temperature (oral) 39.9° C. He was in moderate 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 values were pH 7.53, Paco₂ 27, 21, and Pao₂ 62. The respiratory therapist assigned to assess and treat the patient charted the following SOAP note.

Respiratory Assessment and Plan

S “I feel miserable.” Mild dyspnea.

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, and Pao₂ 62.

• 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%.)

The patient was started on oxygen (2 L/min) via a nasal cannula. The physician prescribed intravenous antibiotic therapy.

Over the next 72 hours, the patient steadily improved, although he felt nauseated and vomited three times. On the fourth hospital day, however, the patient complained of increased shortness of breath. He started to cough up large amounts (3 to 4 tablespoons every 2 hours) of foul-smelling, greenish-yellow sputum. He also complained of choking on his secretions (aspiration likely), a bitter taste in his mouth, belching, mild substernal discomfort, and chills.

On physical examination, the patient appeared anxious. His vital signs were blood pressure 120/82, pulse 140 bpm, respiratory rate 20/min, and oral temperature 40° C. His sputum was thick, yellow-green, and foul-smelling. His cough was strong. He had bronchial breath sounds, rhonchi, and nonclearing crackles in the right middle of the anterior chest and over both lower lobes posteriorly. There was mild cyanosis of the nail beds. The abdominal examination was unremarkable. There was no peripheral edema. A chest x-ray examination showed a new infiltrate in the right middle lung field and left lower lobe. The opaque infiltrate obstructed the view of the heart and was described by the radiologist as consolidation. On 2 L/min O₂ nasal cannula, his ABGs were as follows: pH 7.50, Paco₂ 29, 20, Pao₂ 36, and Sao₂ 69%. At this time the respiratory therapist charted the following SOAP progress note.

Respiratory Assessment and Plan

S Increased dyspnea. Symptoms of belching and substernal chest pain.

O Anxious appearance. BP 120/82, HR 140, RR 20, T 40° C. Cyanotic. Strong productive cough (sputum foul-smelling, yellow-green). Bronchial breath sounds, rhonchi, persistent crackles in right middle anterior chest and both bases. CXR: RML and LLL infiltrate and consolidation. ABG (on 2 L/min): pH 7.50, Paco₂ 29, 20, Pao₂ 36, and Sao₂ 69%.

• Aspiration complicating community-acquired pneumonia, involving RML and LLL (history, CXR)

• Alveolar consolidation (CXR)

• Excessive airway secretions (thick, yellow-green sputum)

• Good ability to mobilize secretions (strong cough)

• Acute alveolar hyperventilation with severe hypoxemia (ABG)

P Oxygen Therapy Protocol: Increase Fio₂ to 0.60 via HAFOE mask. Bronchopulmonary Hygiene Protocol: DB&C instruction, prn oropharyngeal suctioning. Trial P&D to lower lobes and RML q shift as tolerated). Aerosolized Medication Protocol: 2.0 mL 10% acetylcysteine with 0.5 mL albuterol q4h. ABG in 1 hour.

Discussion

A history of cold exposure in conjunction with the use of alcoholic beverages before the onset of pneumonia is not uncommon. The first part of this case begins with a classic presentation for community-acquired pneumonia with alveolar consolidation (see Alveolar Consolidation, Figure 9-9). For example, the fever and tachycardia represent a normal functioning immune response, and the tachycardia and tachypnea reflect the body’s response to shunt-induced hypoxemia. The auscultation of crackles and bronchial breath sounds also reflects the patient’s pulmonary consolidation. An attempt at improving his oxygenation, though not successful, was certainly in order. It was hoped that by providing an oxygen-enriched gas to both normal and partially consolidated alveoli, the effects of pulmonary shunting would be at least partially offset.

The second SOAP presents the complication of the patient’s community-acquired pneumonia with aspiration pneumonitis. Alcoholics frequently have gastritis or esophagitis, and the patient’s eructation (belching) and pyrosis (heartburn) were clues to the development of that complication. At this time there were new clinical manifestations associated with Excessive Bronchial Secretions (see Figure 9-12). For example, the patient demonstrated a cough, sputum, rhonchi, and crackles. The Bronchopulmonary Hygiene Therapy Protocol (e.g., mucolytic with a bronchodilator, DB&C, suctioning, and P&D) was appropriate. A trial of Lung Expansion Therapy (see Protocol 9-3) was not given in this case. However, Atelectasis (see Figure 9-8) often complicates aspiration pneumonia, and such a trial would not have been inappropriate.

In cases of pneumonia, the respiratory care practitioner is often tempted to do too much. Typically, volume expansion therapy, bronchodilator aerosol therapy, and bland aerosol therapy have all been ordered for affected patients, even in the acute, consolidative stage of their pneumonia. Often, however, all that is needed is the appropriate selection of antibiotics, rest, fluids, and supplementary oxygen. When the pneumonia “breaks up” (resolution stage) or is complicated by aspiration (as in this case), Excessive Bronchial Secretions (Figure 9-12) and even Bronchospasm (Figure 9-11) may appear. When this happens, use of other protocol modalities is necessary.