Pneumonia

PNEUMONIA

Pneumonia is an inflammation of the lung parenchyma that is caused by a microbial agent. “Pneumonitis” is a more general term that describes an inflammatory process in the lung tissue that may predispose a patient to or place a patient at risk for microbial in-vasion. Pneumonia is the most common cause of death from in-fectious diseases in the United States. It is the seventh leading cause of death in the United States for all ages and both genders, result-ing in almost 70,000 deaths per year. In persons 65 years of age and older, it is the fifth leading cause of death (National Center for Health Statistics, 2000; Minino & Smith, 2001). It is treated extensively on both an inpatient and outpatient basis.

Bacteria commonly enter the lower airway but do not cause pneumonia in the presence of an intact host defense mechanism. When pneumonia does occur, it is caused by various microorgan-isms, including bacteria, mycobacteria, chlamydiae, mycoplasma, fungi, parasites, and viruses. Several systems are used to classify pneumonias. Classically, pneumonia has been categorized into one of four categories: bacterial or typical, atypical, anaerobic/ cavitary, and opportunistic. However, there is overlap in the micro-organisms thought to be responsible for typical and atypical pneumonias. A more widely used classification scheme categorizes the major pneumonias as community-acquired pneumonia, hospital-acquired pneumonia, pneumonia in the immunocompromised host, and aspiration pneumonia (Table 23-1). There is overlap in how specific pneumonias are classified because they may occur in differing settings.

Community-acquired pneumonia (CAP) occurs either in the community setting or within the first 48 hours of hospitalization or institutionalization. The need for hospitalization for CAP de-pends on the severity of the pneumonia. The agents that most fre-quently cause CAP requiring hospitalization are S. pneumoniae,H. influenzae, Legionella, Pseudomonas aeruginosa, and other gram-negative rods. The specific etiologic agent of CAP is identified in about 50% of the cases. The absence of a responsible caregiver in the home may be another indication for hospitalization. More than 5.5 million people develop CAP and as many as 1.1 million require hospitalization each year (Centers for Disease Control and Prevention [CDC], 1997; Marston, Plouffe, File et al., 1997).

Pneumonia caused by S. pneumoniae (pneumococcus) is the most common CAP in people younger than 60 without comor-bidity and in those older than 60 with comorbidity. It is most prevalent during the winter and spring, when upper respiratory tract infections are most frequent. S. pneumoniae is a gram-positive, capsulated, nonmotile coccus that resides naturally in the upper respiratory tract. The organism colonizes the upper respiratory tract and can cause the following types of illnesses: disseminated invasive infections, pneumonia and other lower respiratory tract infections, and upper respiratory tract infections, including oti-tis media and sinusitis (CDC, 1998). It may occur as a lobar or bronchopneumonic form in patients of any age and may follow a recent respiratory illness.

Mycoplasma pneumonia, another type of CAP, occurs most often in older children and young adults and is spread by infected respiratory droplets through person-to-person contact. Patients can be tested for mycoplasma antibodies. The inflammatory in-filtrate is primarily interstitial rather than alveolar. It spreads throughout the entire respiratory tract, including the bronchioles, and has the characteristics of a bronchopneumonia. Earache and bullous myringitis are common. Impaired ventilation and diffu-sion may occur.

H. influenzae is another cause of CAP. It frequently affects el-derly people or those with comorbid illnesses (eg, chronic obstruc-tive pulmonary disease [COPD], alcoholism, diabetes mellitus). The presentation of this pneumonia is indistinguishable from that of other forms of bacterial CAP. The presentation may be subacute, with cough or low-grade fever for weeks before diagnosis. Chest x-rays may reveal multilobar, patchy bronchopneumonia or areas of consolidation (tissue that solidifies as a result of collapsed alve-oli or pneumonia).

Viruses are the most common cause of pneumonia in infants and children but are relatively uncommon causes of CAP in adults. The chief causes of viral pneumonia in the immuno-competent adult are influenza viruses types A and B, adenovirus, parainfluenza virus, coronavirus, and varicella-zoster virus. In immunocompromised adults, cytomegalovirus is the most com-mon viral pathogen, followed by herpes simplex virus, adeno-virus, and respiratory syncytial virus. The acute stage of a viral respiratory infection occurs within the ciliated cells of the airways. This is followed by infiltration of the tracheobronchial tree. With pneumonia, the inflammatory process extends into the alveolar area, resulting in edema and exudation. The clinical signs and symptoms of a viral pneumonia are often difficult to distinguish from those of a bacterial pneumonia.

Hospital-acquired pneumonia (HAP), also known as nosoco-mial pneumonia, is defined as the onset of pneumonia symptomsmore than 48 hours after admission to the hospital. HAP ac-counts for approximately 15% of hospital-acquired infections but is the most lethal nosocomial infection. It is estimated to occur in 0.5% to 1% of all hospitalized patients and in 15% to 20% of intensive care patients. Ventilator-associated pneumonia can be considered a type of nosocomial pneumonia that is associated with endotracheal intubation and mechanical ventilation.

The common organisms responsible for HAP include the pathogens Enterobacter species, Escherichia coli, Klebsiella species, Proteus, Serratia marcescens, P. aeruginosa, and methicillin-sensitiveor methicillin-resistant Staphylococcus aureus. These respiratory infections occur when at least one of three conditions exists: host defenses are impaired, an inoculum of organisms reaches the pa-tient’s lower respiratory tract and overwhelms the host’s defenses, or a highly virulentorganism is present. Certain illnesses may pre-dispose a patient to HAP because of impaired host defenses. Examples include severe acute or chronic illness, a variety of co-morbid conditions, coma, malnutrition, prolonged hospitalization, hypotension, and metabolic disorders. The hospitalized patient is also exposed to potential bacteria from other sources (eg, respiratory therapy devices and equipment, transmission of pathogens by the hands of health care personnel). Numerous intervention-related factors also may play a role in the development of HAP (eg, therapeutic agents leading to central nervous system depres-sion with decreased ventilation, impaired removal of secretions, or potential aspiration; prolonged or complicated thoraco-abdominal procedures, which may impair mucociliary function and cellular host defenses; endotracheal intubation; prolonged or inappropriate use of antibiotics; use of nasogastric tubes). In addi-tion, immunocompromised patients are at particular risk. HAP is associated with a high mortality rate, in part because of the vir-ulence of the organisms, their resistance to antibiotics, and the patient’s underlying disorder.

Dominant pathogens for HAP are gram-negative bacilli (P. aeruginosa and Enterobacteriaceae/Klebsiella species, Enter-obacter, Proteus, Serratia) and S. aureus. Pseudomonal pneumo-nia occurs in patients who are debilitated, those with altered mental status, and those with prolonged intubation or with tra-cheostomies. Staphylococcal pneumonia can occur through in-halation of the organism or spread through the hematogenous route. It is often accompanied by bacteremia and positive blood cultures. Although responsible for less than 10% of cases of CAP, staphylococcal pneumonia may be responsible for more than 30% of cases of HAP. Its mortality rate is high. Specific strains of staphylococci are resistant to all available antimicrobials except vancomycin. These strains of S. aureus are referred to as methicillin-resistant S. aureus (MRSA). Overuse and misuse of antimicrobial agents are major risk factors for the emergence of these resistant pathogens. Because MRSA is highly virulent, steps must be taken to prevent the spread of this organism. The patient with MRSA should be isolated in a private room, and contact precautions (gown, mask, glove, and antibacterial soap) are used. The num-ber of people in contact with the patient should be minimized, and appropriate precautions must be taken when transporting the patient within or between facilities.

The usual presentation of an HAP is a new pulmonary infil-trate on chest x-ray combined with evidence of infection such as fever, respiratory symptoms, purulent sputum, and/or leuko-cytosis. Pneumonias from Klebsiella or other gram-negative organ-isms (E. coli, Proteus, Serratia) are characterized by destruction of lung structure and alveolar walls, consolidation, and bacteremia. Elderly patients and those with alcoholism, chronic lung disease, or diabetes are at particular risk. A sudden onset of cough is a common presentation, and blood-tinged sputum may be present. In the debilitated or dehydrated patient, sputum production may be minimal or absent. Pleural effusions, high fevers, and tachy-cardia are often observed. Even with treatment, the mortality rate remains high.

Pneumonia in the immunocompromised host is seen with greater frequency because immunocompromised hosts represent a growing portion of the patient population. Examples of pneu-monia in the immunocompromised host are Pneumocystis carinii pneumonia (PCP), fungal pneumonias, and mycobacterium tuberculosis. These types of pneumonia may also occur in the immunocompetent person and in different settings, but these are less common. Immunocompromised states occur with the use of corticosteroids or other immunosuppressive agents, chemother-apy, nutritional depletion, use of broad-spectrum antimicrobial agents, AIDS, genetic immune disorders, and long-term advanced life-support technology (mechanical ventilation). Patients with compromised immune systems commonly acquire pneumonia from organisms of low virulence. In addition, increasing numbers of patients with impaired defenses develop HAP from gram-negative bacilli (Klebsiella, Pseudomonas, E. coli, Enterobacteri-aceae, Proteus, Serratia).

Pneumonia in the compromised host may be caused by the or-ganisms also observed in CAP or HAP (S. pneumoniae, S. aureus,

         influenzae, P. aeruginosa, M. tuberculosis). PCP is rarely ob-served in the immunocompetent host and is often an initial AIDS-defining complication. Whether the patient is immuno-compromised or immunocompetent, the clinical presentation of pneumonia is similar. PCP has a subtle onset with progressive dyspnea, fever, and a nonproductive cough.

Aspiration pneumonia refers to the pulmonary consequences resulting from the entry of endogenous or exogenous substances into the lower airway. The most common form of aspiration pneumonia is bacterial infection from aspiration of bacteria that normally reside in the upper airways. Aspiration pneumonia may occur in the community or hospital setting; common pathogens are S. pneumoniae, H. influenzae, and S. aureus. Other substances may be aspirated into the lung, such as gastric contents, exogenous chemical contents, or irritating gases. This type of aspiration or ingestion may impair the lung defenses, cause inflammatory changes, and lead to bacterial growth and a resulting pneumonia.

Pathophysiology

Upper airway characteristics normally prevent potentially infec-tious particles from reaching the normally sterile lower respira-tory tract. Thus, patients with pneumonia caused by infectious agents often have an acute or chronic underlying disease that im-pairs host defenses. Pneumonia arises from normally present flora in a patient whose resistance has been altered, or it results from aspiration of flora present in the oropharynx. It may also result from bloodborne organisms that enter the pulmonary circulation and are trapped in the pulmonary capillary bed, becoming a po-tential source of pneumonia.

Pneumonia often affects both ventilation and diffusion. An inflammatory reaction can occur in the alveoli, producing an ex-udate that interferes with the diffusion of oxygen and carbon dioxide. White blood cells, mostly neutrophils, also migrate into the alveoli and fill the normally air-containing spaces. Areas of the lung are not adequately ventilated because of secretions and mucosal edema that cause partial occlusion of the bronchi or alveoli, with a resultant decrease in alveolar oxygen tension. Bron-chospasm may also occur in patients with reactive airway disease. Because of hypoventilation, a ventilation–perfusion mismatch occurs in the affected area of the lung. Venous blood entering the pulmonary circulation passes through the underventilated area and exits to the left side of the heart poorly oxygenated. The mix-ing of oxygenated and unoxygenated or poorly oxygenated blood eventually results in arterial hypoxemia.

If a substantial portion of one or more lobes is involved, the disease is referred to as “lobar pneumonia.” The term “bron-chopneumonia” is used to describe pneumonia that is distributed in a patchy fashion, having originated in one or more localized areas within the bronchi and extending to the adjacent sur-rounding lung parenchyma. Bronchopneumonia is more com-mon than lobar pneumonia (Fig. 23-2).

Risk Factors

Being knowledgeable about the factors and circumstances that commonly predispose a person to pneumonia will aid in identi-fying patients at high risk for this disorder (Chart 23-2).

Increasing numbers of patients who have compromised de-fenses against infections are susceptible to pneumonia. Some types of pneumonia, such as those caused by viral infections, occur in previously healthy people and often follow a viral illness.

Pneumonia is common with certain underlying disorders such as heart failure, diabetes, alcoholism, COPD, and AIDS. Certain diseases also have been associated with specific pathogens. For ex-ample, staphylococcal pneumonia has been noted after epidemics of influenza, and patients with COPD are at increased risk for de-veloping pneumonia caused by pneumococci or H. influenzae. In addition, cystic fibrosis is associated with respiratory infection caused by pseudomonal and staphylococcal organisms, and PCP has been associated with AIDS. Pneumonias occurring in hospitalized pa-tients often involve organisms not usually found in CAP, including enteric gram-negative bacilli and S. aureus.

The CDC has identified three specific strategies for preventing HAP: (1) staff education and infection surveillance, (2) interrup-tion of transmission of microorganisms through person-to-person transmission and equipment transmission, and (3) modification of host risk of infection (CDC, 1997). Providing anticipatory and preventive care is an important nursing measure.

To reduce or prevent serious complications of CAP in high-risk groups, vaccination against pneumococcal infection is ad-vised for the following:

·      People 65 years of age or older

·        Immunocompetent people who are at increased risk for ill-ness and death associated with pneumococcal disease because of chronic illness (eg, cardiovascular, pulmonary, diabetes mellitus, chronic liver disease)

·      People with functional or anatomic asplenia

·      People living in environments or social settings in which the risk of disease is high

·      Immunocompromised people at high risk for infection (CDC, 1998)

The vaccine provides specific prevention against pneumo-coccal pneumonia and other infections caused by this organism (otitis media, other upper respiratory tract infections). Vaccines should be avoided in the first trimester of pregnancy.

Clinical Manifestations

Pneumonia varies in its signs and symptoms depending on the organism and the patient’s underlying disease. However, regard-less of the type of pneumonia (CAP, HAP, immunocompro-mised host, aspiration), a specific type of pneumonia cannot be diagnosed by clinical manifestations alone. For example, the pa-tient with streptococcal (pneumococcal) pneumonia usually has a sudden onset of shaking chills, rapidly rising fever (38.5° to 40.5°C [101° to 105°F]), and pleuritic chest pain that is aggra-vated by deep breathing and coughing. The patient is severely ill, with marked tachypnea (25 to 45 breaths/min), accompanied by other signs of respiratory distress (eg, shortness of breath, use of accessory muscles in respiration). The pulse is rapid and bound-ing, and it usually increases about 10 beats/min for every degree of temperature (Celsius) elevation. A relative bradycardia for the amount of fever may suggest viral infection, mycoplasma infec-tion, or infection with a Legionella organism.

Some patients exhibit an upper respiratory tract infection (nasal congestion, sore throat), and the onset of symptoms of pneumonia is gradual and nonspecific. The predominant symp-toms may be headache, low-grade fever, pleuritic pain, myalgia, rash, and pharyngitis. After a few days, mucoid or mucopurulent sputum is expectorated. In severe pneumonia, the cheeks are flushed and the lips and nailbeds demonstrate central cyanosis (a late sign of poor oxygenation [hypoxemia]).

Typically, the patient has orthopnea (shortness of breath when reclining); he or she prefers to be propped up in bed lean-ing forward (orthopneic position), trying to achieve adequate gas exchange without coughing or breathing deeply. Appetite is poor, and the patient is diaphoretic and tires easily. Sputum is often pu-rulent; this is not a reliable indicator of the etiologic agent. Rusty, blood-tinged sputum may be expectorated with streptococcal (pneumococcal), staphylococcal, and Klebsiella pneumonia.

Signs and symptoms of pneumonia may also depend on under-lying conditions. Differing signs occur in patients with other con-ditions, such as cancer, or in those who are undergoing treatment with immunosuppressants, which lower the resistance to infection. Such patients have fever, crackles, and physical findings that indi-cate consolidation of lung tissue, including increased tactile fremi-tus (vocal vibration detected on palpation), percussion dullness, bronchial breath sounds, egophony (when auscultated, the spoken “E” becomes a loud, nasal-sounding “A”), and whispered pectoril-oquy (whispered sounds are easily auscultated through the chest wall). These changes occur because sound is transmitted better through solid or dense tissue (consolidation) than through normal air-filled tissue;.

Purulent sputum or slight changes in respiratory symptoms may be the only sign of pneumonia in patients with COPD. It may be difficult to determine whether an increase in symptoms is an exacerbation of the underlying disease process or an addi-tional infectious process.

Assessment and Diagnostic Findings

The diagnosis of pneumonia is made by history (particularly of a recent respiratory tract infection), physical examination, chest x-ray studies, blood culture (bloodstream invasion, called bac-teremia, occurs frequently), and sputum examination. The sputum sample is obtained by having the patient: (1) rinse the mouth with water to minimize contamination by normal oral flora, (2) breathe deeply several times, (3) cough deeply, and (4) expectorate the raised sputum into a sterile container.

More invasive procedures may be used to collect specimens. Sputum may be obtained by nasotracheal or orotracheal suctioning with a sputum trap or by fiberoptic bronchoscopy. Bronchoscopy is often used in patients with acute severe infec-tion, patients with chronic or refractory infection, or immuno-compromised patients when a diagnosis cannot be made from an expectorated or induced specimen.

Medical Management

The treatment of pneumonia includes administration of the ap-propriate antibiotic as determined by the results of the Gram stain. However, an etiologic agent is not identified in 50% of CAP cases and empiric therapy must be initiated. Therapy for CAP is continuing to evolve. Guidelines exist to guide antibiotic choice; however, the resistance patterns, prevalence of etiologic agents, patient risk factors, and costs and availability of newer antibiotic agents must all be taken into consideration.

Several organizations have published guidelines for the medical management of CAP (Bartlett et al., 2000; American Thoracic Society, 2001). Recommendations are classified by existing risk factors, setting (inpatient vs. outpatient treatment), or specific pathogens. Examples of risk factors that may increase the risk of infection with certain types of pathogens appear in Chart 23-3.

Recommendations for treatment of outpatients with CAP who have no cardiopulmonary disease or other modifying factors include a macrolide (erythromycin, azithromycin [Zithromax], or clarithromycin [Biaxin]), doxycycline (Vibramycin), or a flu-oroquinolone (eg, gatifloxacin [Tequin], levofloxacin [Levaquin]) with enhanced activity against S. pneumoniae (Bartlett et al., 2000; American Thoracic Society, 2001). Erythromycin should be avoided in areas where H. influenzae and S. aureus are more preva-lent (Kenreigh & Wagner, 2000; Lynch, 2000). For those out-patients who have cardiopulmonary disease or other modifying factors, treatment should include a beta-lactam (oral cefpodoxime [Vantin], cefuroxime [Zinacef, Ceftin], high-dose amoxicillin or amoxicillin/clavulanate [Augmentin, Clavulin]) plus a macrolide or doxycycline. Also, a beta-lactam plus an antipneumococcal fluoro-quinolone can be used (American Thoracic Society, 2001). These are guidelines; treatment for individual patients may be modified.

For patients with CAP who are hospitalized and do not have cardiopulmonary disease or modifying factors, management con-sists of intravenous azithromycin (Zithromax) or monotherapy with an antipneumococcal fluoroquinolone. For inpatients with cardiopulmonary disease or modifying factors, the treatment in-volves an intravenous beta-lactam plus an intravenous or oral macrolide or doxycycline. An intravenous antipneumococcal flu-oroquinolone may also be used alone (American Thoracic Soci-ety, 2001). For acutely ill patients admitted to the intensive care unit, management includes an intravenous beta-lactam plus either an intravenous macrolide or fluoroquinolone. For patients at high risk for P. aeruginosa, more select antipseudomonal anti-biotics are administered intravenously.

If specific pathogens have been identified for the CAP, more specific agents may be utilized. Mycoplasma pneumonia is treated with doxycycline or a macrolide. PCP responds best to pentamidine and trimethoprim–sulfamethoxazole (TMP-SMZ). Amantadine and rimantadine are effective with influenza A and have been shown to reduce the duration of fever and other systemic com-plications when administered within 24 to 48 hours of the onset of an uncomplicated influenza infection. These medications also reduce the duration and quantity of virus shedding in the res-piratory secretions. They are most effective when used in com-bination with influenza vaccine. Ganciclovir is used to treat cytomegalovirus in the non-AIDS patient; cytomegalovirus immunoglobulin may also be used.

HAP has a different etiology from CAP. In suspected HAP or nosocomial pneumonia, empirical treatment is usually ini-tiated with a broad-spectrum intravenous antibiotic and may be monotherapy or combination therapy. In patients who are mildly to moderately ill with a low risk of Pseudomonas, the following antibiotics may be used: second-generation cephalosporins (eg, cefuroxime [Ceftin, Zinacef] or cefamandole [Mandol]), non-pseudomonal third-generation cephalosporins (ceftriaxone [Ro-cephin], cefotaxime [Claforan], ampicillin-sulbactam [Unasyn]), or fluoroquinolones (eg, ciprofloxacin [Cipro], levofloxacin [Lev-aquin]). For combination therapy, any of the above may be used with an aminoglycoside.

For patients at high risk for Pseudomonas infection, an anti-pseudomonal penicillin plus an aminoglycoside (amikacin [Amikin], gentamicin) or beta-lactamase inhibitor (ampicillin/ sulbactam [Unasyn], ticarcillin/clavulanate [Timentin]) may be used. Other types of combination therapy may also be used de-pending upon the individual characteristics of the patient.

Of concern is the rampant rise in respiratory pathogens that are resistant to available antibiotics. Examples include vancomycin-resistant enterococcus (VRE) and drug-resistant S. pneumoniae (McGeer & Low, 2000). There is a tendency for clinicians to ag-gressively use antibiotics inappropriately or to use broad-spectrum agents when narrow-spectrum agents are more appropriate. Mechanisms to monitor and minimize the inappropriate use of antibiotics are in place. Education of clinicians to use evidence-based guidelines in the treatment of respiratory infection is im-portant. Monitoring and surveillance of susceptibility patterns for pathogens are also important.

Therapy with parenteral agents usually is changed to oral anti-microbial agents when there is evidence of a clinical response and the patient is able to tolerate oral medications. The recommended duration of treatment for pneumococcal pneumonia is 72 hours after the patient becomes afebrile. Most other forms of pneumo-nia caused by bacterial pathogens are treated for 1 to 2 weeks after the patient becomes afebrile. Atypical pneumonia is usually treated for 10 to 21 days (Bartlett, Dowell, Mandell et al., 2000).

Treatment of viral pneumonia is primarily supportive. Anti-biotics are ineffective in viral upper respiratory infections and pneumonia and may be associated with adverse effects. Treatment of viral infections with antibiotics is a major reason for the overuse of these medications in the United States. Antibiotics are indicated with a viral respiratory infection only when a secondary bacterial pneumonia, bronchitis, or sinusitis is present. Hydration is a nec-essary part of therapy because fever and tachypnea may result in insensible fluid losses. Antipyretics may be used to treat headache and fever; antitussive medications may be used for the associated cough. Warm, moist inhalations are helpful in relieving bronchial irritation. Antihistamines may provide benefit with reduced sneez-ing and rhinorrhea. Nasal decongestants may also be used to treat symptoms and improve sleep; however, excessive use may cause rebound nasal congestion. Treatment of viral pneumonia (with the exception of antimicrobial therapy) is the same as that for bac-terial pneumonia. The patient is placed on bed rest until the in-fection shows signs of clearing. If hospitalized, the patient is observed carefully until the clinical condition improves.

If hypoxemia develops, oxygen is administered. Pulse oximetry or arterial blood gas analysis is performed to determine the need for oxygen and to evaluate the effectiveness of the therapy. A high concentration of oxygen is contraindicated in patients with COPD because it may worsen alveolar ventilation by decreasing the patient’s ventilatory drive, leading to further respiratory de-compensation. Respiratory support measures include high oxygen concentrations (fraction of inspired oxygen [FiO₂]), endotracheal intubation, and mechanical ventilation.

Figure 23-3 provides an algorithm for patients with suspected CAP.

Gerontologic Considerations

Pneumonia in the elderly patient may occur as a primary prob-lem or as a complication of a chronic disease process. Pulmonary infections in the elderly frequently are difficult to treat and have a higher mortality rate than in younger patients. General deteri-oration, weakness, abdominal symptoms, anorexia, confusion, tachycardia, and tachypnea may signal the onset of pneumonia. The diagnosis of pneumonia may be missed because the classic symptoms of cough, chest pain, sputum production, and fever may be absent or masked in the elderly patient. Also, the presence of some signs may be misleading. Abnormal breath sounds, for example, may be due to microatelectasis that occurs in the aged as a result of decreased mobility, decreased lung volumes, and other respiratory function changes. Because chronic heart failure is often seen in the elderly, chest x-rays may be obtained to assist in differentiating it from pneumonia as the cause of clinical signs and symptoms.

Supportive treatment includes hydration (with caution and frequent assessment because of the risk of fluid overload in the elderly), supplemental oxygen therapy, assistance with deep breath-ing, coughing, frequent position changes, and early ambulation. All of these are particularly important in the care of the elderly patient with pneumonia. To reduce or prevent serious complica-tions of pneumonia in the elderly, vaccination against pneumo-coccal and influenza infections is recommended.

Complications

SHOCK AND RESPIRATORY FAILURE

Severe complications of pneumonia include hypotension and shock and respiratory failure (especially with gram-negative bacte-rial disease in elderly patients). These complications are encoun-tered chiefly in patients who have received no specific treatment or inadequate or delayed treatment. These complications are also en-countered when the infecting organism is resistant to therapy and when a comorbid disease complicates the pneumonia.

If the patient is seriously ill, aggressive therapy may include hemodynamic and ventilatory support to combat peripheral col-lapse, maintain arterial blood pressure, and provide adequate oxy-genation. A vasopressor agent may be administered intravenously by continuous infusion and at a rate adjusted in accordance with the pressure response. Corticosteroids may be administered par-enterally to combat shock and toxicity in patients who are ex-tremely ill with pneumonia and in apparent danger of dying of the infection. Patients may require endotracheal intubation and mechanical ventilation. Congestive heart failure, cardiac dys-rhythmias, pericarditis, and myocarditis also are complications of pneumonia that may lead to shock.

ATELECTASIS AND PLEURAL EFFUSION

Atelectasis (from obstruction of a bronchus by accumulated se-cretions) may occur at any stage of acute pneumonia. Parapneu-monic pleural effusions occur in at least 40% of bacterial pneumonias. A parapneumonic effusion is any pleural effusion associated with bacterial pneumonia, lung abscess, or bronchiec-tasis. After the pleural effusion is detected on a chest x-ray, a tho-racentesis may be performed to remove the fluid. The fluid is sent to the laboratory for analysis. There are three stages of para-pneumonic pleural effusions based on pathogenesis: uncompli-cated, complicated, and thoracic empyema. An empyema occurs when thick, purulent fluid accumulates within the pleural space, often with fibrin development and a loculated (walled-off) area where the infection is located. A chest tube may be inserted to treat pleural infection by establishing proper drainage of the empyema. Sterilization of the empyema cavity requires 4 to 6 weeks of antibiotics. Sometimes surgical manage-ment is required.

SUPERINFECTION

Superinfection may occur with the administration of very large doses of antibiotics, such as penicillin, or with combinations of antibiotics. Superinfection may also occur in the patient who has been receiving numerous courses and types of antibi-otics. In such cases, bacteria may become resistant to the antibiotic therapy. If the patient improves and the fever diminishes after initial antibiotic therapy, but subsequently there is a rise in temperature with increasing cough and evi-dence that the pneumonia has spread, a superinfection is likely. Antibiotics are changed appropriately or discontinued entirely in some cases.