Chapter 27 NURSING MANAGEMENT: lower respiratory tract problems
1. Describe the pathophysiology, types, clinical manifestations and multidisciplinary care of pneumonia.
2. Explain the nursing management of the patient with pneumonia.
3. Outline the pathogenesis, classification, clinical manifestations, complications, diagnostic abnormalities and nursing and collaborative management of tuberculosis.
4. Identify the causes, clinical manifestations and management of pulmonary fungal infections.
5. Explain the pathophysiology, clinical manifestations and nursing and collaborative management of bronchiectasis and lung abscess.
6. Outline the causative factors, clinical features and management of environmental lung diseases.
7. Outline the causes, risk factors, pathogenesis, clinical manifestations and nursing and collaborative management of lung cancer.
8. Identify the mechanisms involved and the clinical manifestations of pneumothorax, fractured ribs and flail chest.
9. Describe the purpose, methods and nursing responsibilities related to chest tubes.
10. Explain the types of chest surgery and appropriate preoperative and postoperative care.
11. Compare and contrast extrapulmonary and intrapulmonary restrictive lung disorders in terms of causes, clinical manifestations and collaborative management.
12. Describe the pathophysiology, clinical manifestations and management of pulmonary hypertension and cor pulmonale.
13. Discuss the use of lung transplantation as a treatment for pulmonary disorders.
A wide variety of problems affects the lower respiratory system. Lung diseases that are characterised primarily by an obstructive disorder, such as asthma, chronic obstructive pulmonary disease (COPD) and cystic fibrosis, are discussed in Chapter 28. All other lower respiratory problems are discussed in this chapter.
LOWER RESPIRATORY TRACT INFECTIONS
Respiratory tract infections are common. Lower respiratory tract infections are among the top 10 causes of death in the world.1 In Australia and New Zealand, chronic lower respiratory tract disease and pneumonia account for significant numbers of deaths each year despite the availability of effective treatments.2,3 Tuberculosis (TB), although potentially curable and preventable, remains a worldwide public health threat of epidemic proportions, with one-third of the world’s population currently infected with the TB bacillus.4
Acute bronchitis
Acute bronchitis is an inflammation of the bronchi in the lower respiratory tract, usually due to infection. It is one of the most common conditions seen in primary care. It usually occurs as a sequela to an upper respiratory tract infection. A type of acute bronchitis is acute exacerbation of chronic bronchitis. This represents acute infection superimposed on chronic bronchitis. It is a potentially serious condition that may lead to respiratory failure.
The cause of most cases of acute bronchitis is viral (rhinovirus, influenza). However, bacterial causes are also common both in smokers (e.g. Streptococcus pneumoniae, Haemophilus influenzae) and non-smokers (e.g. Mycoplasma pneumoniae, Chlamydia pneumoniae).
In acute bronchitis, persistent cough following an acute upper airway infection (e.g. rhinitis, pharyngitis) is the most common symptom. Cough is often accompanied by production of clear, mucoid sputum, although some patients produce purulent sputum. Associated symptoms include fever, headache, malaise and shortness of breath on exertion. Physical examination may reveal mildly elevated temperature, pulse and respiratory rate with either normal breath sounds or rhonchi and expiratory wheezing. Chest X-rays can differentiate acute bronchitis from pneumonia because there is no evidence of consolidation or infiltrates on X-ray with bronchitis.
Acute bronchitis is usually self-limiting and the treatment is generally supportive, including fluids, rest and anti-inflammatory agents. Cough suppressants or bronchodilators may be prescribed for symptomatic treatment of nocturnal cough or wheezing. Antibiotics are generally not prescribed unless the patient has a prolonged infection associated with systemic symptoms, is a smoker or has COPD. If the acute bronchitis is due to an influenza virus, treatment with antiviral drugs can be started, but it must be initiated within 48 hours of the onset of symptoms.5
Patients with an acute exacerbation of chronic bronchitis are usually treated empirically with broad-spectrum antibiotics. Often, patients with COPD are taught to recognise symptoms of acute bronchitis and to begin a 5–7 day course of antibiotics when symptoms occur. Many healthcare providers believe that a more severe infection often results if patients delay taking antibiotics until after the clinical examination. Early initiation of antibiotic treatment in COPD patients has resulted in a decrease in relapses and a decrease in hospital admissions.6
Pneumonia
Pneumonia is an acute inflammation of the lung parenchyma caused by a microbial agent. The discovery of sulfur drugs and penicillin was pivotal in the treatment of pneumonia and the last 50 years have seen remarkable progress in the development of antibiotics to treat pneumonia. However, despite the new antimicrobial agents, pneumonia is still common and is associated with significant morbidity and mortality rates. Pneumonia is the leading cause of death from infectious disease in Australasia.2,3
AETIOLOGY
Normal defence mechanisms
Normally, the airway distal to the larynx is sterile because of protective defence mechanisms. These mechanisms include the following: filtration of air; warming and humidification of inspired air; epiglottis closure over the trachea; cough reflex; mucociliary escalator mechanism; secretion of immunoglobulin A; and alveolar macrophages (see Ch 25).
Factors predisposing to pneumonia
Pneumonia is more likely to result when defence mechanisms become incompetent or are overwhelmed by the virulence or quantity of infectious agents. Decreased consciousness depresses the cough and epiglottal reflexes, which may allow aspiration of oropharyngeal contents into the lungs. Tracheal intubation interferes with the normal cough reflex and the mucociliary escalator mechanism. It also bypasses the upper airways in which filtration and humidification of air normally take place. The mucociliary escalator mechanism is impaired by air pollution, cigarette smoking, viral upper respiratory tract infections and normal changes of ageing. In cases of malnutrition the functions of lymphocytes and polymorph nuclear leucocytes are altered. Certain diseases, such as leukaemia, alcoholism and diabetes mellitus, are associated with an increased frequency of Gram-negative bacilli in the oropharynx. (Gram-negative bacilli are not normal flora in the respiratory tract.) Altered oropharyngeal flora can also occur secondary to antibiotic therapy given for an infection elsewhere in the body. The factors predisposing to pneumonia are listed in Box 27-1.
BOX 27-1 Factors predisposing to pneumonia
• Altered consciousness: alcoholism, head injury, seizures, anaesthesia, drug overdose, stroke
• Altered oropharyngeal flora secondary to antibiotics
• Bed rest and prolonged immobility
• Chronic diseases: chronic lung disease, diabetes mellitus, heart disease, cancer, end-stage renal disease
• Human immunodeficiency virus infection
• Immunosuppressive drugs (corticosteroids, cancer chemotherapy, immunosuppressive therapy after organ transplant)
• Inhalation or aspiration of noxious substances
• Intestinal and gastric feedings via nasogastric or nasointestinal tubes
• Tracheal intubation (endotracheal intubation, tracheostomy)
Acquisition of organisms
Organisms that cause pneumonia reach the lung by three methods:
1. Aspiration from the nasopharynx or oropharynx. Many of the organisms that cause pneumonia are normal inhabitants of the pharynx in healthy adults.
2. Inhalation of microbes present in the air. Examples include Mycoplasma pneumoniae and fungal pneumonias.
3. Haematogenous spread from a primary infection elsewhere in the body. An example is Staphylococcus aureus.
TYPES OF PNEUMONIA
Pneumonia can be caused by bacteria, viruses, Mycoplasma, fungi, parasites and chemicals. Although pneumonia can be classified according to the causative organism, a clinically effective way is to classify pneumonia as either community-acquired or hospital-acquired. Classifying pneumonia is important because of differences in the likely causative organisms and the selection of appropriate antibiotics (see Box 27-2).
BOX 27-2 Organisms associated with pneumonia
Community-acquired pneumonia
• Streptococcus pneumoniae*
*Most common cause of community-acquired pneumonia.
Community-acquired pneumonia
Community-acquired pneumonia (CAP) is defined as a lower respiratory tract infection of the lung parenchyma with onset in the community or during the first 2 days of hospitalisation. Estimates of the Australian incidence figures suggest that 2% of all overnight hospital admissions are for CAP.7 In New Zealand, CAP is the most common cause of hospital admission for adults, with an estimated rate of 859 per 100,000 population.8,9 The incidence of CAP is highest in the winter months. Smoking is an important risk factor. The causative organism is identified only 50% of the time. Organisms that are commonly implicated include S. pneumoniae and atypical organisms (e.g. Legionella, Mycoplasma, Chlamydia, viral) (see Box 27-2). The Royal Australian College of General Practitioners, the Australasian Society of Clinical and Experimental Pharmacologists and Toxicologists and the Pharmaceutical Society of Australia classify patients with CAP according to the severity of the illness, the presence of additional risk factors and other modifying factors, using the PORT Severity Index (PSI; see Table 27-1). However, a simpler scale, the CURB-65, is used in some healthcare centres in Australia (see Resources on p 672).
TABLE 27-1 PORT (Pneumonia Outcomes Research Team) Severity Index (PSI)
AHRQ Research in Action, Issue 7. Publication no. 02-0033. Rockville, MD:
Agency for Healthcare Research and Quality; 2002. Available at www.ahrq.gov/clinic/pneumonia/pneumonria.htm, accessed 2 April 2011.
BP, blood pressure; BUN, blood urea nitrogen.
*A risk score (total point score) for a given patient is obtained by summing the patient’s age in years (age − 10 for females) and the points for each applicable patient characteristic.
Source: Adapted and reprinted with permission. Stanton M. Improving treatment decisions for patients with community-acquired pneumonia.
Important risk factors include age greater than 65 years, alcoholism, multiple medical comorbidities and immunosuppressive disease. CAP has been classified to guide management as an outpatient or inpatient, with empirical treatment identified according to the isolated pathogen and other presenting features.10 Data have shown that early treatment reduces mortality.11 While the guidelines do not address length of time of antibiotic therapy, many experts suggest 10–14 days for the majority of patients and extended therapy for atypical CAP caused by atypical organisms.7
Hospital-acquired pneumonia
Hospital-acquired pneumonia (HAP) is pneumonia occurring 48 hours or longer after hospital admission and not incubating at the time of hospitalisation.12 One form of this, ventilator-associated pneumonia (VAP), refers to pneumonia that occurs more than 48–72 hours after endotracheal intubation. In general, the term hospital-acquired pneumonia is used to include any patient with a new-onset pneumonia who: (1) was hospitalised in an acute care hospital for 2 or more days within 90 days of the infection; (2) resided in a long-term care facility; (3) received intravenous antibiotic therapy, chemotherapy or wound care within the past 30 days of the current infection; or (4) attended a hospital or haemodialysis clinic. HAP is estimated to occur at a rate of 5–10 cases per 1000 hospital admissions and VAP has been found to be in the range of 6–33% of patients receiving mechanical ventilation, with greatest incidence in trauma patients.12 Pneumonia has the highest morbidity and mortality rates of any healthcare-associated infection and is second only to urinary tract infection as the most common healthcare-associated infection.13
The microorganisms responsible for HAP are different from those implicated in CAP (see Box 27-2). Bacteria are responsible for the majority of HAP infections, including Pseudomonas, Enterobacter, S. aureus and S. pneumoniae. Many of these organisms enter the lungs after aspiration of particles from the patient’s own pharynx. Immunosuppressive therapy, general debility and endotracheal intubation may be predisposing factors. Contaminated respiratory therapy equipment is another source of infection. Patients with HAP are classified into three groups based on the severity of the illness and which specific host or therapeutic factors predispose to specific pathogens.13 The three groups are:
Fungal pneumonia
Fungi may also be a cause of pneumonia (see the section on pulmonary fungal infections later in the chapter).
Aspiration pneumonia
Aspiration pneumonia refers to the sequelae resulting from abnormal entry of secretions or substances into the lower airway. It usually follows aspiration of material from the mouth or stomach into the trachea and subsequently the lungs. The patient with aspiration pneumonia usually has a history of loss of consciousness (e.g. due to seizure, anaesthesia, head injury, stroke, alcohol intake). With loss of consciousness the gag and cough reflexes are depressed and aspiration is more likely to occur. Another risk factor is tube feeding. The dependent portions of the lung are most often affected, primarily the superior segments of the lower lobes and the posterior segments of the upper lobes, which are dependent in the supine position.
The aspirated material—food, water, vomitus or toxic fluids—is the triggering mechanism for the pathology of this type of pneumonia. There are three distinct forms of aspiration pneumonia. If the aspirated material is an inert substance (e.g. barium), the initial manifestation is usually caused by mechanical obstruction of the airway. When the aspirated materials contain toxic fluids such as gastric juices, there is chemical injury to the lungs with infection as a secondary event, usually 48–72 hours later; this is identified as chemical (non-infectious) pneumonitis. The most important form of aspiration pneumonia is bacterial infection. The infecting organism is usually one of the normal oropharyngeal flora, and multiple organisms, including both aerobes and anaerobes, are isolated from the patient’s sputum with aspiration pneumonia. Antibiotic therapy is based on an assessment of the severity of illness, where the infection was acquired (community versus hospital) and the type of organisms present.
Opportunistic pneumonia
Certain patients with altered immune response are highly susceptible to respiratory infections. Individuals considered at risk include those who have severe protein–energy malnutrition, those who have immune deficiencies, those who have received transplants and been treated with immunosuppressive drugs, and those being treated with radiation therapy, chemotherapy drugs and corticosteroids (especially for a prolonged period). The individual has a variety of altered conditions, including altered B and T lymphocyte function, depressed bone marrow function and decreased levels or function of neutrophils and macrophages. In addition to the causative agents (especially Gram-negative bacteria), other agents that cause pneumonia in immunocompromised patients are Pneumocystis jirovecii (formerly Pneumocystis carinii), cytomegalovirus and fungi.
P. jirovecii is an opportunistic pathogen whose natural habitat is the lung. Although its classification has been historically considered to be protozoa, it is now considered a fungus. This organism rarely causes pneumonia in healthy individuals. P. jirovecii pneumonia affects 70% of human immunodeficiency virus (HIV)-infected individuals and is the most common opportunistic infection in patients with acquired immunodeficiency syndrome (AIDS). In this type of pneumonia, the chest X-ray usually shows a diffuse bilateral alveolar pattern of infiltration. In widespread disease the lungs are massively consolidated.
Clinical manifestations are insidious and include fever, tachypnoea, tachycardia, dyspnoea, non-productive cough and hypoxaemia. Pulmonary physical findings are minimal in proportion to the serious nature of the disease. Treatment consists of a course of trimethoprim-sulfamethoxazole as the primary agent. An alternative medication is dapsone.14 In patients at risk of developing P. jirovecii pneumonitis (e.g. patients with haematological malignancies or AIDS; see Ch 14), prophylaxis with trimethoprim-sulfamethoxazole may be advocated. An alternative is aerosolised pentamidine.
Cytomegalovirus (CMV) is a cause of viral pneumonia in immunocompromised patients, particularly transplant recipients. This virus is not highly contagious but it is a prevalent virus with 40–100% of the population generally exposed in childhood.15 CMV, a type of herpes virus, gives rise to latent infections and reactivation with shedding of infectious virus. This type of interstitial pneumonia can be a mild disease or it can be fulminant and produce pulmonary insufficiency and death. Often, CMV coexists with other opportunistic bacterial or fungal agents in causing pneumonia. Ganciclovir is recommended for treatment of CMV pneumonia.
PATHOPHYSIOLOGY
Pneumococcal pneumonia is the most common cause of bacterial pneumonia and the pathophysiology related to this type of pneumonia is similar to other types of pneumonia. The four characteristic stages are:
1. Congestion. After the pneumococcus organisms reach the alveoli via droplets or saliva, there is an outpouring of fluid into the alveoli. The organisms multiply in the serous fluid and the infection is spread. The pneumococci damage the host by their overwhelming growth and interference with lung function.
2. Red hepatisation. There is massive dilation of the capillaries and the alveoli are filled with organisms, neutrophils, red blood cells and fibrin (see Fig 27-1). The lung appears red and granular, similar to the liver, which is why the process is called hepatisation.
3. Grey hepatisation. Blood flow decreases and leucocytes and fibrin consolidate in the affected part of the lung.
4. Resolution. Complete resolution and healing occur if there are no complications.
The exudate becomes lysed and is processed by the macrophages. The normal lung tissue is restored and the individual’s gas-exchange ability returns to normal.
CLINICAL MANIFESTATIONS
Patients with pneumonia usually have a constellation of symptoms, including sudden onset of fever, chills, cough productive of purulent sputum and pleuritic chest pain (in some cases). In older or debilitated patients, confusion or stupor (possibly related to hypoxia) may be the predominant finding. On physical examination signs of pulmonary consolidation, such as dullness to percussion, increased fremitus, bronchial breath sounds and crackles may be found. The typical pneumonia syndrome is usually caused by the most common pathogen which is S. pneumoniae, but can also be due to other bacterial pathogens, such as H. influenzae.
Pneumonia may also manifest atypically with a more gradual onset, a dry cough and extra pulmonary manifestations, such as headache, myalgias, fatigue, sore throat, nausea, vomiting and diarrhoea. On physical examination crackles are often heard. This presentation of symptoms is classically produced by M. pneumoniae but can also be caused by Legionella and C. pneumoniae. Patients with haematogenous S. aureus pneumonia may have only dyspnoea and fever. This necrotising infection causes destruction of lung tissue and these patients are usually very sick.
Although the initial manifestations of viral pneumonia are highly variable, viruses also cause pneumonia that is usually characterised by an atypical presentation with chills, fever, dry non-productive cough and extra pulmonary symptoms. Primary viral pneumonia can be caused by influenza virus infection. However, viral pneumonia is also found in association with systemic viral diseases, such as measles, varicella zoster and herpes simplex.
COMPLICATIONS
Most cases of pneumonia generally run an uncomplicated course. However, complications can occur and they develop more frequently in individuals with underlying chronic diseases and other risk factors. The following complications may occur:
1. Pleurisy (inflammation of the pleura) is a relatively common accompanying problem of pneumonia.
2. Pleural effusion can occur and usually the effusion is sterile and is reabsorbed in 1–2 weeks. Occasionally, it requires aspiration by means of thoracentesis.
3. Atelectasis (collapsed, airless alveoli) of one or part of one lobe may occur. These areas usually clear with effective coughing and deep breathing.
4. Delayed resolution results from persistent infection and is seen on X-ray as residual consolidation. Usually, the physical findings return to normal within 2–4 weeks. Delayed resolution occurs most frequently in patients who are older, malnourished, alcoholic or have COPD.
5. Lung abscess is not a common complication of pneumonia. It is seen with pneumonia caused by S. aureus and Gram-negative pneumonias (see the section on lung abscess later in this chapter).
6. Empyema (accumulation of purulent exudate in the pleural cavity) is relatively infrequent but requires antibiotic therapy and drainage of the exudate by a chest tube or open surgical drainage.
7. Pericarditis results from spread of the infecting organism from infected pleura or via a haematogenous route to the pericardium (the fibroserous sac around the heart).
8. Arthritis results from systemic spread of the organism. The affected joints are swollen, red and painful and a purulent exudate can be aspirated.
9. Meningitis can be caused by S. pneumoniae. The patient with pneumonia who is disoriented, confused or somnolent should have a lumbar puncture to evaluate the possibility of meningitis.
10. Endocarditis can develop when the organisms attack the endocardium and the valves of the heart. The clinical manifestations are similar to those of acute bacterial endocarditis (see Ch 36).
DIAGNOSTIC STUDIES
The common diagnostic measures for pneumonia are presented in Box 27-3. A history, physical examination and chest X-ray often provide enough information to make management decisions without costly laboratory tests.
MULTIDISCIPLINARY CARE
Diagnostic studies
History and physical examination
Sputum culture and sensitivity test (if drug-resistant pathogen or organism not covered by empirical therapy)
Pulse oximetry or ABGs (if indicated)
Full blood count, differential and routine blood chemistries (if indicated)
Collaborative therapy
Appropriate antibiotic therapy (see Table 27-2)
Chest X-ray often shows a typical pattern characteristic of the infecting organism and is an invaluable adjunct in the diagnosis of pneumonia. Lobar or segmental consolidation suggests a bacterial cause, usually S. pneumoniae or Klebsiella. Diffuse pulmonary infiltrates are most commonly caused by infection with viruses, Legionella or pathogenic fungi. Cavitary shadows suggest the presence of a necrotising infection with destruction of lung tissue commonly caused by S. aureus, Gram-negative bacteria and Mycobacterium tuberculosis. Pleural effusions, which can occur in up to 30% of patients with CAP, can also be seen on X-ray.
Sputum cultures are recommended if a drug-resistant pathogen or an organism that is not covered by the usual empirical therapy is suspected. (Empirical therapy is based on observation and experience without always knowing the exact cause.) A Gram stain of the sputum provides information on the predominant causative organism. A sputum culture should be collected before initiating antibiotic therapy. Because of the poor sensitivity and specificity of sputum cultures, any sputum culture results should be correlated with the predominant organisms found on Gram stain results. If a delay in the time from collecting the sputum to incubation exceeds 2–5 hours, results are less reliable. Before treatment, two blood cultures may be done for patients who are seriously ill. Although microbial studies are expected before treatment, initiation of antibiotics should not be delayed.10
Arterial blood gases (ABGs), if obtained, usually reveal hypoxaemia. Leucocytosis is found in the majority of patients with bacterial pneumonia, usually with a white blood cell count greater than 15 × 109/L with the presence of bands (immature neutrophils).
MULTIDISCIPLINARY CARE
Prompt treatment with the appropriate antibiotic almost always cures bacterial and Mycoplasma pneumonia. In uncomplicated cases, the patient responds to drug therapy within 48–72 hours. Indications of improvement include decreased temperature, improved breathing and reduced chest pain. Abnormal physical findings can last for more than 7 days.
In addition to antibiotic therapy, supportive measures may be used, including oxygen therapy to treat hypoxaemia, analgesics to relieve the chest pain for patient comfort and antipyretics such as aspirin or paracetamol for significantly elevated temperature. During the acute febrile phase, the patient’s activity should be restricted and rest should be encouraged and planned.
Most individuals with mild-to-moderate illness who have no other underlying disease process can be treated on an outpatient basis. If there is a serious underlying disease or if the pneumonia is accompanied by severe dyspnoea, hypoxaemia or other complications, the patient should be hospitalised. Guidelines for hospitalisation for CAP are presented in Table 27-1.
Currently, there is no definitive treatment for viral pneumonia. The antiviral drug, amantadine, may be approved for oral use in the treatment of influenza A virus. The neuraminidase inhibitors, zanamivir and oseltamivir, may be active against both influenza A and B (see Ch 26). An influenza vaccine is available. It is modified annually to reflect the anticipated strains in the upcoming season. Influenza vaccine is considered a mainstay of prevention and is recommended annually for use in individuals considered to be at risk. Individuals at risk of influenza include older people, nursing home residents, patients with COPD or diabetes mellitus and healthcare workers. For older people with signs and symptoms of influenza, including those who have received the influenza vaccine, empirical treatment with amantadine or a neuraminidase inhibitor may be recommended. During epidemics of influenza A, especially in nursing homes, chemoprophylaxis with these agents is recommended for unvaccinated patients, immunodeficient patients or those who have received the vaccine within the past 2 weeks.16
Pneumococcal vaccine
Pneumococcal vaccine is indicated primarily for the individual considered at risk who: (1) has chronic illnesses, such as lung and heart disease and diabetes mellitus; (2) is recovering from a severe illness; (3) is 65 years of age or older; or (4) is in a long-term care facility. This is particularly important because the rate of drug-resistant S. pneumoniae infections is increasing. Pneumococcal vaccine can be given simultaneously with other vaccines, such as the flu vaccine, but each should be administered in a separate site.12 The vaccine is effective in preventing bacteraemic pneumococcal disease. Australia is one of only a few countries that has a national pneumococcal vaccination program for Indigenous adults to address the high incidence of the disease in that population.17
The current recommendation is that pneumococcal vaccine is good for a person’s lifetime. However, in immunosuppressed individuals at risk of developing fatal pneumococcal infection (e.g. asplenic patients; patients with nephrotic syndrome, renal failure or AIDS; or transplant recipients), revaccination is recommended every 5 years, although the efficacy of revaccination is unknown.18
Drug therapy
The main problems with using antibiotics in pneumonia are the development of resistant strains of organisms and the patient’s hypersensitivity or allergic reaction to certain antibiotics.
Most cases of CAP in otherwise healthy adults do not require hospitalisation. The oral antibiotic therapy administered is frequently empirical treatment with broad-spectrum antibiotics. Once the patient is categorised, empirical therapy can be based on the likely infecting organism. For example, in risk class I patients these organisms include S. pneumoniae, M. pneumoniae, respiratory viruses, C. pneumoniae and H. influenzae. Macrolides are the recommended therapy, including either azithromycin or roxithromycin, because erythromycin is not active against H. influenzae. Doxycycline is recommended for the patient who is allergic to macrolides but this antibiotic is not reliably active against pneumococcus (see Table 27-2).10 For HAP, it is recommended that empirical antibiotic therapy be based on the likely pathogens in the various patient groups (see Box 27-2).17 Even with extensive diagnostic testing, an aetiological organism is often not identified.
TABLE 27-2 Initial therapy for suspected bacterial community-acquired pneumonia in immunocompetent adults
Macrolides: erythromycin, azithromycin, clarithromycin
Respiratory fluoroquinolones: moxifloxacin, gatifloxacin, levofloxacin, gemifloxacin
Advanced macrolides: azithromycin, clarithromycin
β-lactams: high-dose amoxycillin, amoxycillin-clavulanate, cefpodoxime, cefprozil, cefuroxime
Antipseudomonal agents: piperacillin, imipenem/cilastatin, meropenem, cefepime, piperacillin-tazobactam
COPD, chronic obstructive pulmonary disease; Hf, heart failure.
Source: Adapted from the Infectious Disease society of America. Available at www.idsociety.org, accessed 2 April 2011.
When using empirical therapy, it is important to recognise the non-responding patient. Therapy may require modification based on the patient’s culture results or clinical response. Clinical response is evaluated by factors such as a change in fever, sputum purulence, leucocytosis, oxygenation or X-ray patterns. Improvement is often not apparent for the first 48–72 hours and empirical therapy need not be altered during this period unless deterioration is noted or culture results dictate that a different antibiotic be used.13 Patients with VAP may experience rapid deterioration. Patients who deteriorate or fail to respond to therapy require aggressive evaluation to assess non-infectious aetiologies, complications, other coexisting infectious processes or pneumonia caused by a resistant pathogen. It may be necessary to broaden antimicrobial coverage while awaiting results of cultures and other studies, such as computed tomography (CT), ultrasound or lung scans.
Nutritional therapy
Fluid intake of at least 3 L per day is generally recommended in the supportive treatment of pneumonia since this is thought to compensate for increased insensible loss arising from fever or rapid breathing. However, for some patients increased fluids can be harmful, such as if the patient has heart failure, and therefore fluid intake must be individualised.19 If oral intake cannot be maintained, IV administration of fluids and electrolytes may be necessary for the acutely ill patient. An intake of at least 6300 kJ per day should be maintained to provide energy for the increased metabolic processes in the patient. Small, frequent meals are better tolerated by the dyspnoeic patient.
NURSING MANAGEMENT: PNEUMONIA
Nursing assessment
Subjective and objective data that should be obtained from a patient with pneumonia are presented in Table 27-3.
Nursing diagnoses
Nursing diagnoses for the patient with pneumonia may include, but are not limited to, those presented in NCP 27-1.
Planning
The overall goals are that the patient with pneumonia will have: (1) clear breath sounds; (2) normal breathing patterns; (3) no signs of hypoxia; (4) normal chest X-ray; and (5) no complications related to pneumonia.
Nursing implementation
Health promotion
There are many nursing interventions to help prevent the occurrence of, as well as the morbidity associated with, pneumonia. Teaching the individual to practise good health habits, such as proper diet and hygiene, adequate rest and regular exercise, can maintain the natural resistance to infecting organisms. If possible, exposure to upper respiratory tract infections should be avoided. If an upper respiratory tract infection occurs, it should be treated promptly with supportive measures (e.g. rest, fluids). If symptoms persist for more than 7 days, the person should obtain medical care. Individuals at risk of pneumonia (e.g. the chronically ill, older adults) should be encouraged to obtain both influenza and pneumococcal vaccines.11
In the hospital, the nursing role involves identifying the patient at risk (see Box 27-1) and taking measures to prevent the development of pneumonia. The patient with altered consciousness should be placed in positions (e.g. side-lying, semi-recumbent) that prevent or minimise the risk of aspiration. The patient should be turned and repositioned at least every 2 hours to optimise gaseous exchange, facilitate lung expansion and discourage pooling of secretions. In VAP, a significant reduction in pneumonia incidence is found when patients are placed in a semi-recumbent position (ideally at 45°) and this is recommended in many guidelines, including those produced by the National Health and Medical Research Council (NHMRC) and the American Thoracic Society (ATS).20
The patient who has a feeding tube generally requires attention to measures to prevent aspiration (see Ch 39). Although the feeding tube is small, an interruption in the integrity of the lower oesophageal sphincter still exists, which can allow reflux of gastric and intestinal contents. Oral tubes rather than nasal tubes may be more effective at preventing healthcare-associated sinusitis.20 The patient who has difficulty swallowing (e.g. a stroke patient) needs assistance in eating, drinking and taking medications to prevent aspiration. The patient who has recently had surgery and those who are immobile need assistance with turning and deep-breathing measures at frequent intervals (see Ch 19). The nurse must be careful to avoid overmedication with opioids or sedatives, which can cause a depressed cough reflex and accumulation of fluid in the lungs. The gag reflex should be present in the individual who has had local anaesthesia to the throat before fluids or food are administered.
Adherence to infection control guidelines should be practised to reduce the incidence of healthcare-associated infections. Poor hand-washing practices allow the spread of pathogens via healthcare workers. Staff should wash their hands before and after they provide care to patients. Respiratory devices can harbour microorganisms and have been associated with outbreaks of pneumonia.
Acute intervention
Although many patients with pneumonia are treated on an outpatient basis, the nursing care plan for the patient with pneumonia (see NCP 27-1) is applicable to both outpatients and inpatients. It is important for the nurse to remember that pneumonia is an acute, infectious disease. Although most cases of pneumonia are potentially completely curable, complications can result. The nurse must be aware of these complications and their manifestations. The infection control nurse can be a valuable resource in assisting with the care of patients with pneumonia. Therapeutic positioning identifies the best position for the patient assuring stable oxygenation status. The ‘good lung down’ position is utilised for patients with unilateral lung disease where better oxygenation is achieved when the unaffected lung (the good lung) is placed in the down (lateral) position.21 For bilateral lung disease, research indicates the right lung down position has the best ventilation and perfusion.18 The idea of therapeutic positioning uses these concepts and identifies the best positioning for the patient based on lung disease and patient response to positioning. The use of bronchial hygiene techniques (postural drainage, percussion, vibration) is generally not warranted unless the patient is producing large volumes of sputum (>30 mL/day) or has X-ray evidence of mucous plugging and lobar collapse.13 Incentive spirometry, turning, coughing and deep breathing all increase lung volume, mobilise secretions and prevent atelectasis. Exercise and early ambulation augment bronchial hygiene and are encouraged as tolerated.
Ambulatory and community care
The patient needs to be reassured that complete recovery from pneumonia is possible. It is extremely important to emphasise the need to take the full course of the prescribed drug and to return for follow-up medical care and evaluation. The patient needs to be taught about drug–drug and food–drug interactions for the prescribed antibiotic. Adequate rest is needed to maintain progress towards recovery and to prevent a relapse. Patients should be told that it may be weeks before they feel their usual energy and sense of wellbeing. A prolonged period of convalescence may be necessary for older adults or chronically ill patients.
The patient considered to be at risk of pneumonia should be told about available vaccines and should discuss them with the healthcare provider. Deep-breathing exercises should be practised for 6–8 weeks after the patient is discharged from the hospital.
Tuberculosis
Tuberculosis (TB) is an infectious disease caused by Mycobacterium tuberculosis. It usually involves the lungs but it also occurs in the larynx, kidneys, bones, adrenal glands, lymph nodes and meninges and can be disseminated throughout the body. TB kills more people worldwide than any other infectious disease. It is estimated that between 19% and 43% of the world’s population is infected with M. tuberculosis. World Health Organization (WHO) statistics on the notification and detection of TB show that, in 2008, the Americas had 228,000 cases and an estimated 29,000 deaths; the Western Pacific Region (which includes Australia and New Zealand) had 1,946,000 cases and an estimated 261,000 deaths; and more than 1.8 million people worldwide are estimated to have died from TB.22 The highest incidence is seen in the developing countries of Africa and Asia, with a recent increase seen in the former Soviet Union.22
With the introduction of chemotherapeutic agents (streptomycin, isoniazid) in the late 1940s and early 1950s, there was a dramatic decrease in the prevalence of TB. The major factors that have contributed to the resurgence of TB in some countries include: (1) epidemic proportions of TB among patients with HIV infection; and (2) the emergence of multi-drug resistant (MDR) strains of M. tuberculosis. MDR strains of TB have developed because of poor compliance with drug therapy, leading to treatment failure and the development of resistant strains. Patients were lost to follow-up treatment or placed on drug regimens to which their infections were no longer susceptible. Today, case management and contact tracing are undertaken by public and community health nurses, with supervised therapy being normal practice.
TB is seen disproportionately in the poor, the underserved and minorities. Individuals at risk of TB include the homeless, residents of inner-city neighbourhoods, foreign-born persons, older adults, those in institutions (long-term care facilities, prisons), injecting drug users, the socioeconomically disadvantaged and the medically underserved of all ethnic groups. Immunosuppression from any aetiology (e.g. HIV infection, malignancy) increases the risk of TB infection. Healthcare workers with increased exposure to TB are also at high risk.
Although over past decades the incidence of TB in Australia and New Zealand has declined, it remains problematic among older people, Indigenous Australians, Māori and immigrants from endemic countries.2,3,23 As the majority of cases are found among the migrant population, current policies require that all immigrants be medically checked for TB prior to entry into Australia and New Zealand. In Australia, the notification rates for TB have remained stable since 1991 at 5–6 per 100,000 population.24 The majority of new cases are people born overseas; however, Indigenous Australians also have a high incidence, even though this rate is now reducing towards that of the rest of the popluation.23,24 TB incidence in New Zealand is mainly due to migration from high-incidence countries. Refugees and immigrants are not an important source of TB for most of the New Zealand-born population, but those caring for people from high-incidence countries should take the necessary precautions.25
AETIOLOGY AND PATHOPHYSIOLOGY
M. tuberculosis, a Gram-positive, acid-fast bacillus (AFB), is spread from person to person via airborne droplets, which are produced when the infected individual with pulmonary or laryngeal TB coughs, sneezes, speaks or sings. Once released into a room, the organisms are dispersed and can be inhaled. Brief exposure to a few tubercle bacilli rarely causes an infection. Rather, it is more commonly spread to the individual who has repeated close contact with an infected person. TB is not highly infectious and transmission usually requires close, frequent or prolonged exposure. Contrary to popular belief, the disease cannot be spread by hands, books, glasses, dishes or other fomites. There is a small risk of transmission during surgery or following trauma if the encapsulation is ruptured.
The very small droplet nuclei, 1–5 μm in size, contain M. tuberculosis. Because they are so small in size, the particles remain airborne for minutes to hours. When the bacilli are inhaled, they pass down the bronchial system and implant themselves on the respiratory bronchioles or alveoli. The lower parts of the lungs are usually the site of initial bacterial implantation. After implantation, the bacilli multiply with no initial resistance from the host. The organisms are engulfed by phagocytes (initially neutrophils and later macrophages) and may continue to multiply within the phagocytes.
While a cellular immune response is being activated, the bacilli can be spread through the lymphatic channels to regional lymph nodes and via the thoracic duct to the circulating blood. Thus organisms may be spread throughout the body before sufficient activation of the cell-mediated immune response is available to bring the infection under control. The organisms find favourable environments for growth primarily in the upper lobes of the lungs, kidneys, epiphyses of the bone, cerebral cortex and adrenal glands.
Eventually, cellular immunity limits further multiplication and spread of the infection. A characteristic tissue reaction called an epithelioid cell granuloma results after the cellular immune system is activated. This granuloma is a result of fusion of the infiltrating macrophages. The granuloma is surrounded by lymphocytes. This reaction usually takes 10–20 days. The central portion of the lesion (called a Ghon tubercle) undergoes necrosis characterised by a cheesy appearance and hence is named caseous necrosis. The lesion may also undergo liquefactive necrosis in which the liquid drains into connecting bronchi and produces a cavity. Tubercular material may enter the tracheobronchial system, allowing airborne transmission of infectious particles.
Healing of the primary lesion usually takes place by resolution, fibrosis and calcification. The granulation tissue surrounding the lesion may become more fibrous and form a collagenous scar around the tubercle. A Ghon complex is formed, consisting of the Ghon tubercle and regional lymph nodes. Calcified Ghon complexes may be seen on chest X-ray.
When a tuberculosis lesion regresses and heals, the infection enters a latent period in which it may persist without producing a clinical illness. The infection may develop into clinical disease if the persisting organisms begin to multiply rapidly or it may remain dormant.
TB disease is defined as active bacteria that multiply and cause tuberculosis disease. TB infection in a person who does not have active TB disease is not considered a case of TB and is often referred to as latent TB infection. Once infected with TB, 3–5% of individuals develop TB disease within 1 year and another 3–5% develop TB disease within their lifetime.26 People who are infected with M. tuberculosis but who do not have TB disease cannot spread the infection to other people.
Most people mount an effective immune response to encapsulate these organisms for the rest of their life, preventing primary infection from progressing to disease. If the initial immune response is not adequate, control of the organisms is not maintained and clinical disease results. Certain individuals are at a higher risk of clinical disease, including those who are immunosuppressed for any reason (e.g. patients with HIV infection, those receiving cancer chemotherapy or long-term corticosteroid therapy) or have diabetes mellitus.
Dormant but viable organisms persist for years. Reactivation of TB can occur if the host’s defence mechanisms become impaired. The reasons for reactivation are not well understood but they are related to decreased resistance found in older adults, individuals with concomitant diseases and those who receive immunosuppressive therapy.
CLASSIFICATION
An international diagnostic staging classification system for TB is useful for epidemiological and public health purposes (see Table 27-4).
TABLE 27-4 Classification of tuberculosis
| Class 0 | No TB exposure | No TB exposure, not infected (no history of exposure, negative tuberculin skin test) |
| Class 1 | TB exposure, no infection | TB exposure, no evidence of infection (history of exposure, negative tuberculin skin test) |
| Class 2 | Latent TB infection, no disease | TB infection without disease (significant reaction to tuberculin skin test, negative bacteriological studies, no x-ray findings compatible with TB, no clinical evidence of TB) |
| Class 3 | TB clinically active | TB infection with clinically active disease (positive bacteriological studies or both a significant reaction to tuberculin skin test and clinical or X-ray evidence of current disease) |
| Class 4 | TB, but not clinically active | No current disease (history of previous episode of TB or abnormal, stable X-ray findings in a person with a significant reaction to tuberculin skin test; negative bacteriological studies if done; no clinical or X-ray evidence of current disease) |
| Class 5 | TB suspect | TB suspect (diagnosis pending); person should not be in this classification for more than 3 months |
Source: American Thoracic society, 2000.
CLINICAL MANIFESTATIONS
In the early stages of TB the person is usually free of symptoms. Many cases are found incidentally when routine chest X-rays are taken, especially in older adults.
Systemic manifestations may initially consist of fatigue, malaise, anorexia, weight loss, low-grade fevers and night sweats. The weight loss may not be excessive until late in the disease and is often attributed to overwork or other factors.
A characteristic pulmonary manifestation is a cough that becomes frequent and may produce mucoid or mucopurulent sputum. Dyspnoea is unusual. Chest pain characterised as dull or tight may be present. Haemoptysis is not a common finding and is usually associated with more advanced cases. Sometimes TB has more acute, sudden manifestations; the patient has high fever, chills, generalised flu-like symptoms, pleuritic pain and a productive cough.
The HIV-infected patient with TB often has atypical physical examination and chest X-ray findings. Classic signs such as fever, cough and weight loss may be attributed to P. jirovecii pneumonia or other HIV-associated opportunistic diseases. Clinical manifestations of respiratory problems in patients with HIV must be carefully investigated to determine the cause.
COMPLICATIONS
Miliary TB
If a necrotic Ghon complex erodes through a blood vessel, large numbers of organisms invade the bloodstream and spread to all body organs. This is called miliary or haematogenous TB. It can occur as a result of primary disease or reactivation of latent infection.27 The patient may be either acutely ill with fever, dyspnoea and cyanosis, or chronically ill with systemic manifestations of weight loss, fever and gastrointestinal (GI) disturbance. Hepatomegaly, splenomegaly and generalised lymphadenopathy may be present.
Pleural effusion and empyema
A pleural effusion is caused by the release of caseous material into the pleural space. The bacteria-containing material triggers an inflammatory reaction and a pleural exudate of protein-rich fluid. A form of pleurisy called dry pleurisy may result from a superficial tuberculosis lesion involving the pleura. It appears as localised pleuritic pain on deep inspiration. Empyema is less common than effusion but may occur from large numbers of organisms spilling into the pleural space, usually from rupture of a cavity.
Tuberculosis pneumonia
Acute pneumonia may result when large amounts of tubercle bacilli are discharged from the liquefied necrotic lesion into the lungs or lymph nodes. The clinical manifestations are similar to those of bacterial pneumonia, including chills, fever, productive cough, pleuritic pain and leucocytosis.
Other organ involvement
Although the lungs are the primary site of TB, other body organs may be involved. The meninges may become infected. Bone and joint tissue may be involved in the infectious disease process. The kidneys, adrenal glands, lymph nodes and both female and male genital tracts may also be infected.
DIAGNOSTIC STUDIES
Tuberculin skin testing
The body’s immune response can be demonstrated by hypersensitivity to a tuberculin skin test. A positive reaction occurs 2–12 weeks after the initial infection, corresponding to the time needed to mount an immune response.
Purified protein derivative (PPD) of tuberculin is used in the Mantoux test primarily to detect the delayed hypersensitivity response. (The procedure for performing the Mantoux tuberculin skin test is described in Ch 25.) Once acquired, sensitivity to tuberculin tends to persist throughout life. A positive reaction indicates the presence of a TB infection but it does not show whether the infection is dormant or active, causing a clinical illness.
Because the response to TB skin testing may be decreased in the immunocompromised patient, induration reactions equal to or greater than 5 mm are considered positive. Two-step testing is recommended for initial testing for healthcare workers who get repeated testing and for those who have a decreased response to allergens. For these people a second PPD test later may cause an accelerated response (‘booster effect’) misinterpreted as a new PPD conversion.28 Table 25-11 provides guidelines for interpreting tuberculin skin tests. Recent developments of blood tests for diagnosis of infection offer an improvement on skin testing: since they appear to be more sensitive than skin tests, no return visit is needed and the results are available the next day.29
Chest X-ray
Although the findings on chest X-ray examination are important, it is not possible to make a diagnosis of TB solely on the basis of this examination. This is because other diseases can mimic the X-ray appearance of TB. The abnormality most commonly found in TB is multinodular lymph node involvement with cavitation in the upper lobes of the lungs. Calcification of the lung lesions generally occurs within several years of the infection.
Bacteriological studies
The demonstration of tubercle bacilli bacteriologically is essential for establishing a diagnosis. Microscopic examination of stained sputum smears for AFBs is usually the first bacteriological evidence of the presence of tubercle bacilli. This is a quick, easy examination that provides valuable information. Three consecutive sputum specimens collected on different days are obtained and sent for smear and culture. In addition to sputum, material for examination can be obtained from gastric washings, cerebrospinal fluid (CSF) or pus from an abscess.
The most accurate means of diagnosis is a culture technique. The major disadvantage of this method is that it may take 6–8 weeks for the mycobacterium to grow. The advantage is that it can detect small quantities (as few as 10 bacteria per millilitre of specimen).
A recent test for TB, nucleic acid amplification, is a rapid diagnostic test. Blood obtained from the patient is placed in chambers along with mycobacterial antigens. If the patient is infected with TB organisms, the lymphocytes in the blood will recognise these antigens and secrete gamma interferon, a cytokine produced by lymphocytes. Test results are available in a few hours. This does not replace routine sputum smears and cultures but it does offer healthcare providers increased confidence in the diagnosis.26,30
MULTIDISCIPLINARY CARE
Hospitalisation for initial treatment of TB is not necessary in most patients. Most patients are treated on an outpatient basis (see Box 27-4) and many can continue to work and maintain their lifestyles with few changes. Hospitalisation may be used for diagnostic evaluation, for the severely ill or debilitated and for those who experience adverse drug reactions or treatment failures.
BOX 27-4 Pulmonary tuberculosis
MULTIDISCIPLINARY CARE
The mainstay of TB treatment is drug therapy. Drug therapy is used to treat individuals with clinical disease and to prevent disease in infected people.
Drug therapy
Active disease
In view of the growing prevalence of MDR strains of TB, patients with active TB should be managed aggressively. MDR strains of TB occur when resistance develops to two or more anti-TB drugs. Standard therapy has been revised because of the increase in prevalence of drug-resistant TB. Treatment usually consists of a combination of at least four drugs. The reason for combination therapy is to increase the therapeutic effectiveness and to decrease the development of resistant strains of M. tuberculosis, because it has been shown that single-drug therapy can result in rapid development of resistant strains.
The primary drugs used are isoniazid, rifampicin, pyrazinamide and ethambutol (see Table 27-5). Fixed-dose combination antituberculous drugs may enhance adherence to treatment recommendations. Combinations of isoniazid and rifampicin and of isoniazid, rifampicin and pyrazinamide are available to simplify therapy but they are not widely used in Australasia. Patients on antiretroviral drugs for HIV cannot take rifampicin because it can impair the effectiveness of the antiretroviral drugs. Other drugs are primarily used for treatment of resistant strains or if the patient develops toxicity to the primary drugs. Many second-line drugs carry a greater risk of toxicity and require closer monitoring. Newer drugs for the treatment of TB that have not been placed in the categories of first- or second-line drugs include the quinolones, especially ciprofloxacin.
Source: American Thoracic society, CDC, and Infectious Diseases Society of America. Treatment of tuberculosis. MMWR 2003; 52(RR11):1–77. GI, gastrointestinal.
A problem with therapy for TB has been the length of time medication must be taken, but shorter courses of therapy (6–9 months) have now been shown to be effective. Various options for a treatment regimen are available (see Table 27-6). The 2-month rifampicin and pyrazinamide regimen was associated with severe liver disease and should be used with caution in patients with liver disease and alcoholism.31
TABLE 27-6 Regimen options for the initial treatment of tuberculosis
Source: American Thoracic society, CDC, and Infectious Diseases society of America. Treatment of tuberculosis. MMWR 2003; 52(RR11):1–77. DOT, directly observed therapy.
Treatment in geographical areas where drug resistance is known to be a problem may consist of initial addition of drugs not in the resistance pattern for that area. Drug regimens should be adapted to the resistance pattern evident from sputum culture. In follow-up care for patients on long-term therapy, it is important to monitor the effectiveness of drugs and the development of toxic side effects. Usually sputum specimens are obtained weekly at first and then monthly to assess the effectiveness of the medication. The regimen is considered to be effective if the patient converts to a negative TB sputum status.
Although TB tends to have a rapidly progressive course in patients co-infected with HIV, it responds well to standard medication. Co-infected patients should receive treatment for TB for at least 6 months beyond the conversion of sputum cultures to negative status.
An important reason for follow-up care in patients with TB is to ensure adherence to the treatment regimen. Non-compliance is a major factor in the emergence of MDR and treatment failures. Many individuals do not adhere to the treatment program in spite of understanding the disease process and the value of treatment. Directly observed therapy (DOT), or supervised therapy as it is sometimes known, is supported by WHO as being the best practice for patients known to be at risk of non-compliance with therapy.32 This approach involves observing the ingestion of every dose of medication for the patient’s entire course of treatment. Completing therapy is important because of the dangers of reactivation of TB and the emergence of MDR strains of TB seen in patients who do not complete the full course of therapy. The community health nurse often administers DOT at a clinic site, and in Queensland Aboriginal healthcare workers have been used to supervise this therapy in more remote areas.23 Patients need to have follow-up visits for 12 months after completion of therapy to check for the presence of MDR strains.
Teaching patients about the side effects of these drugs and when to seek prompt medical attention is critical. The TB medication may interact with other medications, such as oral contraceptives, and consequently patients need to understand the implications of the therapy. The major side effect of isoniazid, rifampicin and pyrazinamide is hepatitis. Liver function tests should be monitored.31 Baseline liver function tests are done at the start of treatment and routine monitoring of liver function tests is done if the baseline tests are abnormal.
Latent tuberculosis infection
Latent TB infection occurs when an individual becomes infected with M. tuberculosis but does not become acutely ill. Drug therapy can be used to prevent a TB infection from developing into clinical disease. The indications for treatment are presented in Box 27-5.
BOX 27-5 Indications for treatment of latent tuberculosis infection
• Newly infected patient at high risk
• Person with known or suspected human immunodeficiency virus infection and positive tuberculin skin test
• Exposure of household members and other close associates to newly diagnosed patient
• Significant tuberculin skin test reactors with abnormal chest X-ray
• Significant tuberculin skin test reactors in special clinical situations (immunosuppression therapy, use of corticosteroids, diabetes mellitus, silicosis, gastrectomy, end-stage renal disease, head and neck cancer)
• Other significant tuberculin skin test converters (10 mm increase within a 2-year period regardless of age)
• Other significant tuberculin skin test reactors (persons born in high-prevalence countries; medically underserved low-income populations, including high-risk racial or ethnic populations, residents in long-term care facilities, healthcare workers, mycobacteriology laboratory technicians)
Source: American Thoracic Society, 2000.
The drug generally used in the treatment of latent TB infection is isoniazid. It is effective and inexpensive and can be administered orally. Isoniazid is usually administered once daily for 6–9 months and can be given daily or twice weekly. The 9-month regimen is more effective but compliance issues may make the 6-month regimen preferable. For HIV patients and those with fibrotic lesions on chest X-ray, isoniazid is given for 9 months.
Vaccine
Immunisation with Bacille Calmette-Guérin (BCG) vaccine to prevent TB is currently in use in many parts of the world. Although millions of people have been vaccinated with BCG, the efficacy of the vaccine is not clear. BCG vaccination can result in a positive PPD reaction. The vaccine reaction will wane over time and the mean reaction size among those who receive BCG is less than 10 mm. In most cases, revaccination is not recommended practice.
NURSING MANAGEMENT: TUBERCULOSIS
Nursing assessment
It is important to determine whether the patient was ever exposed to a person with TB. The patient should be assessed for productive cough, night sweats, afternoon temperature elevation, weight loss, pleuritic chest pain and crackles over the apices of the lungs. If the patient has a productive cough, an early-morning sputum specimen will be required for an AFB smear to detect the presence of mycobacteria.
Nursing diagnoses
Nursing diagnoses for the patient with TB may include, but are not limited to, the following:
• ineffective breathing pattern related to decreased lung capacity
• imbalanced nutrition: less than body requirements related to chronic poor appetite, fatigue and productive cough
• non-compliance related to lack of knowledge of the disease process, lack of motivation and the long-term nature of treatment
• ineffective health maintenance related to lack of knowledge about the disease process and therapeutic regimen
• activity intolerance related to fatigue, decreased nutritional status and chronic febrile episodes.
Planning
The overall goals are that the patient with TB will: (1) comply with the therapeutic regimen; (2) have no recurrence of disease; (3) have normal pulmonary function; and (4) take appropriate measures to prevent the spread of the disease.
Nursing implementation
Health promotion
The ultimate goal related to TB in Australasia is eradication. Selective screening programs in known risk groups are of value in detecting individuals with TB. The person with a positive tuberculin skin test should have a chest X-ray to assess for the presence of TB. Another important measure is to identify the contacts of the individual who has TB. These contacts should be assessed for the possibility of infection and the need for chemoprophylactic treatment.
When an individual has respiratory symptoms, such as cough, dyspnoea or sputum production, especially if accompanied by a history of night sweats or unexplained weight loss, the nurse should assess for exposure to persons with TB. Even if the suspected respiratory problem is something else, such as emphysema, pneumonia or lung cancer, it is possible that the patient may also have TB.
Acute intervention
Acute in-hospital care is seldom required for patients with TB. If hospitalisation is needed, it is usually for a brief period. Patients strongly suspected of having TB should: (1) be placed in respiratory isolation; (2) receive four-drug therapy; and (3) receive urgent medical investigations, including chest X-ray, sputum smear and culture. Respiratory isolation is indicated for the patient with pulmonary or laryngeal TB until the patient is considered to be non-infectious (effective drug therapy, improving clinically, three negative AFB smears).32 A negative pressure isolation room that offers six or more exchanges per hour may be used. Ultraviolet radiation of the air in the upper part of the room is another approach to reduce airborne TB organisms. Ultraviolet lights are commonly seen in clinics and homeless shelters. Masks are needed to filter out droplet nuclei. High-efficiency particulate air (HEPA) masks are indicated because they can remove almost 100% of particles greater than 3 mm in diameter.33 The mask must fit tightly around the nose and mouth.
Patients should be taught to cover their nose and mouth with paper tissue every time they cough, sneeze or produce sputum. The tissues should be dropped into a paper bag and disposed of with the household rubbish, burned or flushed down the toilet. Patients should also be taught careful hand-washing techniques after handling sputum and soiled tissues. Special precautions should be taken during high-risk procedures, such as sputum induction, aerosolised pentamidine treatments, intubation, bronchoscopy or endoscopy.
Ambulatory and community care
Patients who have responded clinically are discharged home despite positive smears if their household contacts have already been exposed and the patient is not posing a risk to susceptible persons. Determination of absolute non-infectiousness requires negative cultures. Most treatment failures occur because the patient neglects to take the drug, discontinues it prematurely or takes it irregularly. On discharge, the doctor may order mixed-dose combination drugs to increase compliance and ensure that all drugs are being taken, reducing the risk of drug resistance.
It is important for the nurse to develop a therapeutic, consistent relationship with each patient. The nurse must understand each patient’s lifestyle and provide flexibility in planning a program that facilitates the patient’s participation in and completion of therapy. The nurse should teach the patient so that the need for dedication to the prescribed regimen is fully understood by the patient. Ongoing reassurance helps the patient understand that adherence can mean cure. If the patient cannot or will not adhere to a self-administered medication regimen, medication may have to be given by a responsible person on a daily or intermittent basis. The public health department must be notified if drug compliance is questionable so that follow-up of close contacts can be accomplished. In some cases the community health nurse will be responsible for DOT. In other situations, a spouse, grown child, other relative living with the patient or work colleague may be asked to supervise drug taking.
Some patients may feel that there is a social stigma attached to TB. These feelings should be discussed and the patient should be reassured that an individual with TB can be cured if the prescribed regimen is followed. Many people still remember when TB patients were sent away to TB sanatoriums and isolated from society. The Australian Lung Foundation provides excellent literature about the disease, as well as emotional support to the patient and family (see Resources on p 672).
When the chemotherapy regimen has been completed and there is evidence of negative cultures, the patient is improving clinically and there is radiological evidence of improvement, most individuals can be considered adequately treated. Follow-up care may be indicated during the subsequent 12 months, including bacteriological studies and chest X-ray. Because approximately 5% of individuals experience relapses, the patient should be taught to recognise the symptoms that indicate recurrence of TB. If these symptoms occur, immediate medical attention should be sought.
The patient needs to be instructed about certain factors that could reactivate TB, such as immunosuppressive therapy, malignancy and prolonged debilitating illness. If the patient experiences any of these events, the healthcare provider must be told so that reactivation of TB can be closely monitored. In some situations it may be necessary to put the patient on anti-TB therapy.
Atypical mycobacteria
Pulmonary disease that closely resembles TB may be caused by atypical acid-fast mycobacteria. This type of pulmonary disease is indistinguishable from TB clinically and radiologically but can be differentiated by bacteriological culture. These organisms are not believed to be airborne and thus are not transmitted by droplet nuclei.
Atypical mycobacteria that affect the lungs include M. kansasii, M. scrofulaceum, M. avium-intracellulare (MAI), M. avium complex (MAC) and M. xenopi. These bacteria (especially MAI and M. scrofulaceum) may also invade the cervical lymph nodes, causing lymphadenitis. MAC, an opportunistic mycobacteria found in water, causes pulmonary infection due to exposure to aerosols generated from baths, hot spas and swimming pools. This is one of the most common of the atypical mycobacteria presently encountered. This type of pulmonary disease typically occurs in light-skinned people with a history of COPD, cystic fibrosis or silicosis.34 MAI is a common cause of opportunistic infections in patients with HIV infection (see Ch 14).
Treatment depends on identification of the causative agent and determination of drug sensitivity. Many of the drugs used in treating TB are used in combating infections from atypical mycobacteria.
Pulmonary fungal infections
Pulmonary fungal infections are increasing in incidence. They are found most frequently in seriously ill patients being treated with corticosteroids, antineoplastic and immunosuppressive drugs or multiple antibiotics. They are also found in patients with AIDS and cystic fibrosis. Community-acquired pulmonary lung infections include aspergillosis, cryptococcosis and candidiasis.35 Types of fungal infections are presented in Table 27-7. These infections are not transmitted from person to person and the patient does not have to be placed in isolation. The clinical manifestations are similar to those of bacterial pneumonia. Skin and serology tests are available to assist in identifying the infecting organism. However, identification of the organism in a sputum specimen or in other body fluids is the best diagnostic indicator.
TABLE 27-7 Fungal infections of the lung
AIDS, acquired immunodeficiency syndrome; GI, gastrointestinal; TB, tuberculosis.
MULTIDISCIPLINARY CARE
Amphotericin B is the drug most widely used in treating serious systemic fungal infections. It must be given intravenously to achieve adequate blood and tissue levels because it is poorly absorbed from the GI tract. Amphotericin B is considered a toxic drug with many possible side effects, including hypersensitivity reactions, fever, chills, malaise, nausea and vomiting, thrombophlebitis at the injection site and abnormal renal function. Many of the side effects during infusion can be avoided by premedicating with aspirin, antihistamines and antiemetics before the infusion. Including a small amount of hydrocortisone in the infusion helps decrease the irritation of the veins. Monitoring of renal function and ensuring adequate hydration are essential while the patient is receiving this drug. Renal changes are at least partially reversible. Amphotericin B infusions are incompatible with most other drugs. Amphotericin B is frequently administered every other day after an initial period of several weeks of daily therapy. Total treatment with the drug may range from 4 to 12 weeks.
Oral imidazole and triazole compounds with antifungal activity, such as ketoconazole and fluconazole, have been successful in the treatment of fungal infections. Their effectiveness in treatment allows an alternative to the use of amphotericin B in many cases. Effectiveness of therapy can be monitored with fungal serology titres.
Flucytosine has also been used in selected types of pulmonary fungal infections. It is given by IV infusion. Common adverse reactions include nausea, vomiting, diarrhoea and abdominal discomfort. Antiemetics may be helpful. Hepatotoxicity and bone marrow suppression may occur. Frequent blood monitoring, including full blood count (FBC), potassium levels, and renal and hepatic function, is done.
Bronchiectasis
AETIOLOGY AND PATHOPHYSIOLOGY
Bronchiectasis is characterised by permanent, abnormal dilation of one or more large bronchi. The pathophysiological change that results in dilation is destruction of the elastic and muscular structures of the bronchial wall. There are two pathological types of bronchiectasis: saccular and cylindrical. Saccular bronchiectasis occurs mainly in large bronchi and is characterised by cavity-like dilations. The affected bronchi end in large sacs. Cylindrical bronchiectasis involves medium-sized bronchi that are mildly to moderately dilated.
Almost all forms of bronchiectasis are associated with bacterial infections. A wide variety of infectious agents can initiate bronchiectasis, including adenovirus, influenza virus, S. aureus, Klebsiella and anaerobes. Infections cause the bronchial walls to weaken and pockets of infection begin to form. When the walls of the bronchial system are injured, the mucociliary mechanism is damaged, allowing bacteria and mucus to accumulate within the pockets. The infection becomes worse and results in bronchiectasis.
The incidence of bronchiectasis has shown a decline in recent years. The emergence of atypical mycobacteria, especially MAI, presents a new threat as MAI can progress to bronchiectasis. MAI is an opportunistic infection found in patients with HIV.
CLINICAL MANIFESTATIONS
The hallmark of bronchiectasis is persistent or recurrent cough with production of greater than 20 mL of purulent sputum per day. The cough is paroxysmal and is often stimulated with position changes. Other manifestations include exertional dyspnoea, fatigue, weight loss, anorexia and fetid breath. On auscultation of the lungs, any combination of crackles, rhonchi and wheezing may be heard. Sinusitis frequently accompanies diffuse bronchiectasis. The manifestations of advanced, widespread bronchiectasis are generalised wheezing, digital clubbing and cor pulmonale.
DIAGNOSTIC STUDIES
An individual with a chronic productive cough with copious purulent sputum (which may be blood-streaked) should be suspected of having bronchiectasis. Chest X-rays are usually done and may show streaky infiltrates or may be normal. With the availability of CT scanning, detection of bronchiectasis has improved. High-resolution CT scan of the chest has excellent sensitivity for detecting bronchiectasis. Bronchoscopy can also be useful in identifying the source of secretions or the sites of haemoptysis or for collecting microbiological samples.
Sputum may provide additional information regarding the severity of impairment and the presence of active infection. Pulmonary function studies may be abnormal in advanced bronchiectasis, showing a decrease in vital capacity, expiratory flow and maximum voluntary ventilation. FBC may be normal or show evidence of leucocytosis or anaemia from chronic infection.
MULTIDISCIPLINARY CARE
Bronchiectasis is difficult to treat. Therapy is aimed at treating acute flare-ups and preventing decline in lung function. Antibiotics are the mainstay of treatment and are given on the basis of sputum culture results. Long-term suppressive therapy with antibiotics is occasionally used but is fraught with risks of antibiotic resistance. A form of treatment gaining popularity is the use of nebulised antibiotics. Studies indicate that it is safe and may reduce the number of flare-ups and hospitalisations in bronchiectatic patients.36 Antipseudomonal antibiotics, such as tobramycin, are commonly used. Concurrent bronchodilator therapy is given to prevent bronchospasm. Other forms of drug therapy may include mucolytic agents and expectorants. Maintaining good hydration is important to liquefy secretions. Chest physiotherapy and other airway clearance techniques such as humidification are important to facilitate expectoration of sputum. (These techniques are discussed in Ch 28.) The individual should reduce exposure to excessive air pollutants and irritants, avoid cigarette smoking and obtain pneumococcal and influenza vaccinations.
Surgical resection of parts of the lungs, although not used as often as previously, may be done if more conservative treatment is not effective. Surgical resection of an affected lobe or segment may be indicated for the patient with repeated bouts of pneumonia, haemoptysis and disabling complications. Surgery is not advisable when there is diffuse or widespread involvement. For selected patients who are disabled in spite of maximal therapy, lung transplantation may be an option. (Lung transplantation is discussed on p 669.)
NURSING MANAGEMENT: BRONCHIECTASIS
The early detection and treatment of lower respiratory tract infections will help prevent complications such as bronchiectasis. Any obstructing lesion or foreign body should be removed promptly. Other measures to decrease the occurrence or progression of bronchiectasis include avoiding cigarette smoking and decreasing exposure to pollution and irritants.
An important nursing goal is to promote drainage and removal of bronchial mucus. Various airway clearance techniques can be used effectively to facilitate secretion removal. The patient should be taught effective deep-breathing exercises and effective ways to cough (see Box 28-10). Chest physiotherapy with postural drainage should be done on affected parts of the lung (see Fig 28-16). Some individuals require elevation of the foot of the bed by 10–15 cm to facilitate drainage. Pillows may be used in the hospital and at home to help the patient to assume postural drainage positions. A Flutter mucus clearance device is a hand-held device that provides airway vibration during the expiratory phase of breathing (see Fig 28-18). Two to four 15-minute sessions daily by a patient who has been properly trained can provide satisfactory mucus clearance. Positive expiratory pressure (PEP) therapy is a breathing manoeuvre against an expiratory resistance often used in conjunction with nebulised medications. (Respiratory therapy procedures are explained in Ch 28.)
Administration of the prescribed antibiotics, bronchodilators or expectorants is important. The patient needs to understand the importance of taking the prescribed regimen of drugs to obtain maximum effectiveness. The patient should be aware of possible side effects or adverse effects that must be reported to the doctor.
Rest is important to prevent overexertion. Bed rest may be indicated during the acute phase of the illness. Becoming cold and excess fatigue should be avoided.
Nutrition is important and it may be difficult to maintain healthy levels because the patient is often anorexic. Oral hygiene to cleanse the mouth and remove dried sputum crusts may improve the patient’s appetite. Offering foods that are appealing may also increase the desire to eat. Adequate hydration to help liquefy secretions and thus make it easier to remove them is extremely important. Unless there are contraindications, such as concomitant congestive heart failure (CHF) or renal disease, the patient should be instructed to drink at least 3 L of fluid daily. To accomplish this, the patient should be advised to increase fluid consumption from the baseline by increasing intake by one glass per day until the goal is reached. Generally the patient should be counselled to use low-sodium fluids to avoid systemic fluid retention.
Direct hydration of the respiratory system may also prove beneficial in the expectoration of secretions. This is best achieved via a humidifier with or without oxygen.37 At home a steamy shower can prove effective; expensive equipment that requires frequent cleaning is usually unnecessary. It is important that the patient use an inhaled bronchodilator for 10–15 minutes before using a bland aerosol to prevent bronchoconstriction.
The patient and family should be taught to recognise significant clinical manifestations to be reported to the healthcare provider. These manifestations include increased sputum production, grossly bloody sputum, increasing dyspnoea, fever, chills and chest pain.
Lung abscess
AETIOLOGY AND PATHOPHYSIOLOGY
Lung abscess is a pus-containing lesion of the lung parenchyma that gives rise to a cavity. The cavity is formed by necrosis of the lung tissue. In many cases the causes and pathogenesis of lung abscess are similar to those of pneumonia. Most lung abscesses are caused by aspiration of material from the oral cavity (the gingival crevices) into the lungs. Risk factors for aspiration include alcoholism, seizure disorders, neuromuscular diseases, drug overdose, general anaesthesia and stroke. Infectious agents generally cause lung abscesses. The organisms involved cause infection and necrosis of the lung tissue. Examples include enteric Gram-negative organisms (e.g. Klebsiella), S. aureus and anaerobic bacilli (e.g. Bacteroides). Lung abscesses can also result from a lung infarct secondary to pulmonary embolus, malignant growth, TB and various parasitic and fungal diseases of the lung.
The areas of the lung most commonly affected are the superior segments of the lower lobes and the posterior segments of the upper lobes. Fibrous tissue usually forms around the abscess in an attempt to wall it off. The abscess may erode into the bronchial system, causing the production of foul-smelling sputum. It may grow towards the pleura and cause pleuritic pain. Multiple small abscesses can occur within the lung.
CLINICAL MANIFESTATIONS AND COMPLICATIONS
The onset of a lung abscess is usually insidious, especially if anaerobic organisms are the primary cause. A more acute onset occurs with aerobic organisms. The most common manifestation is cough producing purulent sputum (often dark brown) that is foul smelling and foul tasting. Haemoptysis is common, especially at the time that an abscess ruptures into a bronchus. Other common manifestations are fever, chills, prostration, pleuritic pain, dyspnoea, cough and weight loss.
Physical examination of the lungs indicates dullness to percussion and decreased breath sounds on auscultation over the segment of lung involved. There may be transmission of bronchial breath sounds to the periphery if the communicating bronchus becomes patent and drainage of the segment begins. Crackles may also be present in the later stages as the abscess drains. Oral examination often reveals dental cavities, gingivitis and periodontal infection.
Complications that can occur include chronic pulmonary abscess, bronchiectasis and brain abscess as a result of the haematogenous spread of infection, bronchopleural fistula and empyema from abscess perforation into the pleural cavity.
DIAGNOSTIC STUDIES
A chest X-ray will reveal a solitary cavitary lesion with fluid. CT scanning is used if it is suspected that cavitation is not clearly seen. Lung abscess, in contrast to other types of abscesses, does not require assisted drainage, as long as there is drainage via the bronchus. Routine sputum cultures can be collected but contaminants can confuse the results and it is difficult to isolate anaerobic bacteria. Pleural fluid and blood cultures may be obtained. Bronchoscopy may be used in cases of abscess in which drainage is delayed or in which there are factors that suggest an underlying malignancy.
NURSING AND COLLABORATIVE MANAGEMENT: LUNG ABSCESS
Antibiotics given for a prolonged period (up to 2–4 months) are usually the primary method of treatment. Penicillin has historically been the drug of choice because of the frequent presence of anaerobic organisms. However, studies suggest that β-lactamase production by the anaerobic bacteria is involved in abscesses of the lung and they are resistant to penicillin. Clindamycin has been shown to be superior to penicillin and is the standard treatment for an anaerobic lung infection. Patients with putrid lung abscesses usually show clinical improvement with decreased fever within 3–4 days of beginning antibiotics.
Because of the need for prolonged antibiotic therapy, the patient must be aware of the importance of continuing the medication for the prescribed period. The patient also needs to know about untoward side effects to be reported to the healthcare provider. Sometimes the patient is asked to return periodically during the course of antibiotic therapy for repeat cultures and sensitivity tests to ensure that the infecting organism is not becoming resistant to the antibiotic. When antibiotic therapy is completed, the patient is re-evaluated.
The patient should be taught how to cough effectively (see Box 28-10). Chest physiotherapy and postural drainage are sometimes used to drain abscesses located in the lower or posterior portions of the lung. Postural drainage according to the lung area involved will aid the removal of secretions (see Fig 28-16). Frequent mouth care (every 2–3 hours) is needed to relieve the foul-smelling odour and taste from the sputum.
Rest, good nutrition and adequate fluid intake are all supportive measures to facilitate recovery. If dentition is poor and dental hygiene is not adequate, the patient should be encouraged to obtain dental care.
Surgery is rarely indicated but occasionally may be necessary when re-infection of a large cavitary lesion occurs or to establish a diagnosis when there is evidence of an underlying neoplasm or chronic associated disease. The usual procedure in such cases is a lobectomy or pneumonectomy. An alternative to surgery is percutaneous drainage, but this has a high risk of contamination of the pleural space.
Environmental lung diseases
Environmental or occupational lung diseases are caused or aggravated by workplace or environmental exposure and are preventable.38 Environmental or occupational lung diseases result from inhaled dust or chemicals. The duration of exposure and the amount of inhalant have a major influence on whether the exposed individual will have lung damage. Another factor is the susceptibility of the host.
Pneumoconiosis is a general term for lung diseases caused by inhalation and retention of dust particles. The literal meaning of pneumoconiosis is ‘dust in the lungs’. Examples of this condition are silicosis, asbestosis and berylliosis. The classic response to the inhaled substance is diffuse parenchymal infiltration with phagocytic cells. This eventually results in diffuse pulmonary fibrosis (excess connective tissue). Fibrosis is the result of tissue repair after inflammation. Pneumoconiosis and other environmental lung diseases are presented in Table 27-8.
TABLE 27-8 Environmental lung diseases
CDC, Centers for Disease Control and Prevention; ICU, intensive care unit.
Hantavirus (caused by the Sin Nombre virus), a potentially fatal disease with outbreaks reported in the US and Canada, is transmitted by inhalation of aerosolised rodent excreta.39 Chemical pneumonitis results from exposures to toxic chemical fumes. Acutely there is diffuse lung injury characterised as pulmonary oedema. Chronically the clinical picture is that of bronchiolitis obliterans, which is usually associated with a normal chest X-ray or one that shows hyperinflation. An example is silo filler’s disease. Hypersensitivity pneumonitis, or extrinsic allergic alveolitis, is the response seen when antigens are inhaled to which the individual is allergic. Examples include bird fancier’s lung and farmer’s lung.
Lung cancer, either squamous cell carcinoma or adenocarcinoma, is the most frequent cancer associated with asbestos exposure. People with more exposure are at a greater risk of disease. There is a minimum lapse of 15–19 years between first exposure and the development of lung cancer. Mesotheliomas, both pleural and peritoneal, are also associated with asbestos exposure.
Occupational asthma refers to the development of symptoms of shortness of breath, wheezing, cough and chest tightness as a result of exposure to fumes or dust that trigger an allergic response. The obstruction initially may be reversible or intermittent but continued exposure results in permanent obstructive changes. The most common triggers are wood dust, grain dust, animal dander, fungi and chemicals (especially diisocyanates).40
CLINICAL MANIFESTATIONS
Acute symptoms of pulmonary oedema may be seen following early exposure to chemical fumes. However, symptoms of many environmental lung diseases may not occur until at least 10–15 years after the initial exposure to the inhaled irritant. Dyspnoea and cough are often the earliest manifestations. Chest pain and cough with sputum production usually occur later. Complications that often result are pneumonia, chronic bronchitis, emphysema and lung cancer. Cor pulmonale is a late complication, especially in conditions characterised by diffuse pulmonary fibrosis. Manifestations of these complications can be the reason the patient seeks healthcare.
DIAGNOSTIC STUDIES
Pulmonary function studies often show reduced vital capacity. A chest X-ray may reveal lung involvement specific to the primary problem. CT scans have been shown to be useful in detecting early lung involvement.
MULTIDISCIPLINARY CARE
The best approach to management is to try to prevent or decrease environmental and occupational risks. Well-designed, effective ventilation systems can reduce exposure to irritants. Wearing masks is appropriate in some occupations. Periodic inspections and monitoring of workplaces by health and safety agencies reinforce the obligations of employers to provide a safe work environment.
Cigarette smoking adds increased insult to the lungs and those at risk of occupational lung disease should not smoke. Additionally, second-hand smoke is an important source of occupational exposure with increased risk of developing lung cancer. This has led to regulations requiring a smoke-free workspace for all employees.
Early diagnosis is essential if the disease process is to be halted. Some places of employment, where there is a known risk of lung disease, may require periodic chest X-rays and pulmonary function studies for exposed employees. These measures can detect pulmonary changes before symptoms develop.
There is no specific treatment for most environmental lung diseases. The best treatment is to decrease or stop exposure to the harmful agent. Strategies are directed towards providing symptomatic relief. If there are coexisting problems, such as pneumonia, chronic obstructive pulmonary disease or asthma, they are treated.
Lung cancer
Lung cancer is the most common fatal cancer in Australia, with predictions of a 43% rise in incidence among Australian women by 2011 and a 22% rise for men.41 In New Zealand, female lung cancer mortality rates have increased by 36% since 1986, from 14.3 deaths per 100,000 population to 19.4 deaths per 100,000 in 1995. The 5-year survival rate for lung cancer in New Zealand is only 5% (compared with 11% in Australia).42 Although males are still more likely to die from lung cancer than females, the gap between the sexes has narrowed over the last decade. The US Surgeon General’s report, Women and smoking: a report of the Surgeon General, 2001, identified a 600% increase in women’s death rates from lung cancer and attributed this to smoking.43
Lung cancer most commonly occurs in individuals more than 50 years of age who have a long history of cigarette smoking. The disease is found most frequently in persons 40–75 years of age, with a peak incidence between 55 and 65 years of age.
The Australian Lung Foundation and the Cancer Society of New Zealand have published useful information sheets for health professionals and members of the public on lung cancer (see Resources on p 672).
AETIOLOGY
Cigarette smoking is the most important risk factor in the development of lung cancer, but this should change if smoking rates decrease following the current anti-smoking campaigns. Smoking is responsible for approximately 80–90% of all lung cancers. Tobacco smoke contains 60 carcinogens in addition to substances (carbon monoxide, nicotine) that interfere with normal cell development. Cigarette smoking, a lower airway irritant, causes a change in the bronchial epithelium, which usually returns to normal when smoking is discontinued. The risk of lung cancer is gradually lowered when smoking ceases and continues to decline with time; for example, 10 years after the cessation of smoking, lung cancer mortality risk is reduced 30–50%.44 The Memorial Sloan-Kettering Cancer Center has developed a tool that calculates the risk of developing lung cancer for older smokers and ex-smokers (see Resources on p 672).
The risk of developing lung cancer is directly related to total exposure to cigarette smoke measured by the number of cigarettes smoked in a lifetime, earlier age of smoking onset, depth of inhalation, tar and nicotine content and the use of unfiltered cigarettes. Side-stream smoke contains the same carcinogens found in mainstream smoke. This environmental tobacco smoke, when inhaled, poses a 35% increased risk of the development of lung cancer in non-smokers.45 Such exposure can occur early in life for children of smokers. Children are more vulnerable to environmental tobacco smoke than adults because their respiratory and immune systems are not fully developed. Recent data suggest that childhood exposure to this form of tobacco smoke is associated with an increased prevalence of asthma when adults and that such children are also more likely to become smokers.46
Those who smoke pipes and cigars have also been shown to have an increased risk of developing lung cancer, which is slightly higher than that of non-smokers. Cigar smokers have a higher rate for lung cancer than pipe smokers. However, heavy smoking of cigars and inhalation of smoke from small cigars have been shown to correlate with the rates of lung cancer observed in cigarette smokers.
Another major risk factor for lung cancer is inhaled carcinogens. These include asbestos, radon, nickel, iron and iron oxides, uranium, polycyclic aromatic hydrocarbons, chromates, arsenic and air pollution. Exposure to these substances is common for employees of industries involved in mining, smelting or chemical or petroleum manufacturing. Cigarette smokers who are also exposed to one or more of these chemicals or to high amounts of air pollution are at significantly higher risk of lung cancer.
There are marked variations in a person’s propensity to develop lung cancer. To date no genetic abnormality has conclusively been defined for lung cancer. It is known that the carcinogens in cigarette smoke directly damage deoxyribonucleic acid (DNA). One theory is that people have different genetic carcinogen-metabolising pathways.
PATHOPHYSIOLOGY
The pathogenesis of primary lung cancer is not well understood. More than 90% of cancers originate from the epithelium of the bronchus (bronchogenic). They grow slowly and it takes 8–10 years for a tumour to reach 1 cm in size, which is the smallest detectable lesion on an X-ray. Lung cancers occur primarily in the segmental bronchi or beyond and have a preference for the upper lobes of the lungs (see Fig 27-2). Pathological changes in the bronchial system show non-specific inflammatory changes with hypersecretion of mucus, desquamation of cells, reactive hyperplasia of the basal cells and metaplasia of normal respiratory epithelium to stratified squamous cells. (A pathological type of lung cancer is presented in Fig 27-3.)
Figure 27-3 Lung cancer. Peripheral adenocarcinoma. The tumour shows prominent black pigmentation, suggestive of having evolved in an anthracotic scar.
Primary lung cancers are often categorised into two broad subtypes (see Table 27-9): non-small cell lung cancer (80%) and small cell lung cancer (20%). Lung cancers metastasise primarily by direct extension and via the blood circulation and the lymph system. The common sites for metastatic growth are the liver, brain, bones, scalene lymph nodes and adrenal glands.
Paraneoplastic syndrome
Certain lung cancers cause the paraneoplastic syndrome, which is characterised by various systemic manifestations caused by factors (e.g. hormones, enzymes, antigens) produced by the tumour cells. Small cell lung cancers are most commonly associated with the paraneoplastic syndrome. The systemic manifestations seen are hormonal, dermatological, neuromuscular, vascular, haematological and connective tissue syndromes. These syndromes can respond temporarily to symptomatic treatment but they are impossible to control without successful treatment of the underlying lung cancer.
CLINICAL MANIFESTATIONS
Lung cancer is clinically silent for most individuals for the majority of its course. Asymptomatic patients whose cancer is found on routine chest X-ray account for about 10% of new cases. The clinical manifestations of lung cancer are usually non-specific and appear late in the disease process. Manifestations depend on the type of primary lung cancer, its location and metastatic spread. Often there is extensive metastasis before symptoms become apparent. Persistent pneumonitis that is a result of obstructed bronchi may be one of the earliest manifestations, causing fever, chills and cough.
One of the most significant symptoms and often the one reported first is a persistent cough that may be productive of sputum. Blood-tinged sputum may be produced because of bleeding caused by malignancy but haemoptysis is not a common early symptom. Chest pain may be present and localised or unilateral, ranging from mild to severe. Dyspnoea and an auscultatory wheeze may be present if there is bronchial obstruction.
Later manifestations may include non-specific systemic symptoms such as anorexia, fatigue, weight loss, and nausea and vomiting. Hoarseness may be present as a result of involvement of the recurrent laryngeal nerve. Unilateral paralysis of the diaphragm, dysphagia and superior vena cava obstruction may occur because of intrathoracic spread of the malignancy. There may be palpable lymph nodes in the neck or axilla. Mediastinal involvement may lead to pericardial effusion, cardiac tamponade and arrhythmias.
DIAGNOSTIC STUDIES
Chest X-rays are widely used in the diagnosis of lung cancer. The findings may show the presence of the tumour or abnormalities related to the obstructive features of the tumour, such as atelectasis and pneumonitis. The X-ray can also show evidence of metastasis to the ribs or vertebrae and the presence of pleural effusion.
CT scanning is the single most effective non-invasive technique for evaluating lung cancer. CT scans of the brain and bone scans complete the evaluation for metastatic disease. With CT scans, the location and extent of masses in the chest can be identified, as well as any mediastinal involvement or lymph node enlargement. Magnetic resonance imaging (MRI) may be used in combination with or instead of CT scans. Positron emission tomography (PET) is a useful diagnostic tool in early clinical staging. PET allows measurement of differential metabolic activity in normal and diseased tissues. Most new PET scanners are integrated with CT scanning hardware.
A definitive diagnosis of lung cancer is made by identifying malignant cells. Sputum specimens are usually obtained for cytological studies. An early-morning specimen that has been obtained by having the patient cough deeply provides the most accurate results. However, malignant cells may not be obtained even in the presence of lung cancer.47
The use of the fibreoptic bronchoscope is important in the diagnosis of lung cancer, particularly when the lesions are endobronchial or are in close proximity to an airway. It provides direct visualisation and enables biopsy specimens to be obtained. A biopsy is usually the best method for establishing the presence of a malignant tumour.
Mediastinoscopy involves the insertion of a scope via a small anterior chest incision into the mediastinum. This is done to examine for metastasis in the anterior mediastinum or hilum or in the chest extrapleurally. It is also used to determine the stage of the lung cancer, which is important in determining the treatment plan. Video-assisted thoracoscopy (VATS), which involves insertion of a scope into a small thoracic incision, may be used to explore areas inaccessible by mediastinoscopy.
Pulmonary angiography and lung scans may be performed to assess overall pulmonary status. Fine-needle aspiration may be used to obtain a tissue sample to determine tumour histology. This technique is most useful in cases involving a peripheral lesion near the chest wall and it is usually attempted in an effort to avoid a thoracotomy. If a thoracentesis is performed to relieve a pleural effusion, the fluid should be analysed for malignant cells. (Box 27-6 summarises the diagnostic management of lung cancer.)
Staging
Staging of non-small cell lung cancer is performed according to the TNM staging system in a manner similar to that for other tumours (see Table 27-10). Assessment criteria are T, which denotes tumour size, location and degree of invasion; N, which indicates regional lymph node involvement; and M, which represents the presence or absence of distant metastases. Depending on the TNM designation, the tumour is then staged, which assists in estimating prognosis and determining the appropriate therapy.
TABLE 27-10 Staging of non-small cell lung cancer
| Stages | Characteristics |
|---|---|
| I | Tumour is small and localised to lung. No lymph node involvement |
| A | Tumour <3 cm |
| B | Tumour >3 cm and invading surrounding local areas |
| II | |
| A | Tumour <3 cm with invasion of lymph nodes on same side of chest |
| B | Tumour >3 cm involving the bronchus and lymph nodes on same side of chest and tissue of other local organs |
| III | |
| A | Tumour spread to the nearby structures (chest wall, pleura, pericardium) and regional lymph nodes |
| B | Extensive tumour involving heart, trachea, oesophagus, mediastinum, malignant pleural effusion, contralateral lymph nodes, scalene or supraclavicular lymph nodes |
| IV | Distant metastasis |
Staging of small cell lung cancer has not been useful because the cancer has usually metastasised by the time a diagnosis is made and is always considered systemic. Instead, this type of cancer is defined as being limited (confined to one haemothorax and to regional lymph nodes) or extensive (any disease exceeding those boundaries). Only 10% of patients who receive aggressive treatment for this type of cancer survive 2 years or longer after diagnosis. Extensive small cell lung cancer means that some of the cancer extends to the chest wall or to other parts of the body. On average, these patients survive only 7–10 months.47
Screening for lung cancer
In Australia, the Cancer Strategies Group was formed in 1998 to provide expert advice to the Commonwealth government on best-practice strategies and interventions for implementing priorities in cancer control.48 Reducing cancer is a priority objective in the New Zealand Health Strategy, and the Ministry of Health, working in partnership with the New Zealand Cancer Control Trust, has developed a national lung cancer control strategy, which was launched in 2003. A similar program is in place in Australia: the National Lung Cancer program.
Early screening for lung cancer is controversial. The American College of Chest Physicians does not recommend ongoing screening for asymptomatic, low-risk individuals. The Cancer Council of Australia also does not advocate for population-wide screening for lung cancer due to insufficient evidence, although screening does occur in other countries, using high-resolution CT and/or sputum cytology. For example, in Japan, the standard of care for lung cancer screening includes chest X-ray and sputum cytology, and an increase has been seen in 5-year survival rates. However, overall there is insufficient evidence to recommend for or against screening asymptomatic persons.49 The Canadian Task Force states there is insufficient evidence to recommend screening for lung cancer with chest X-ray or CT and that smoking cessation should be emphasised as the preferred modality for reducing lung cancer mortality. The Early Lung Cancer Action Project is being conducted to determine the usefulness of CT in early lung cancer detection, and the National Screening Trial is examining the effectiveness of single-view chest X-ray and CT to detect early stage lung cancer.49 A non-invasive blood test that could detect lung cancer in its earliest stages is being studied at Duke University Medical Center.50
MULTIDISCIPLINARY CARE
Surgical therapy
Surgical resection is the treatment of choice in non-small cell lung cancer stages I and II, because the disease is potentially curable with resection. The 5-year survival in stage I disease with complete resection is 60–80%; in patients with stage II disease it is 40–60%.49 For other non-small cell lung cancer stages, surgery may be indicated in conjunction with radiation therapy and/or chemotherapy. Resectability of the tumour is a major consideration in planning the surgical intervention. Small cell carcinomas usually have widespread metastasis at the time of diagnosis, so surgery is usually contraindicated. In contrast, squamous cell carcinomas are more likely to be treated with surgery because they remain localised or, if they metastasise, they primarily do so by local spread. In small cell lung cancer stage I disease (which is rare) surgical resection, chemotherapy and radiation therapy may be recommended. A tumour may be considered inoperable. If operable, the type of surgery performed is usually a lobectomy (removal of one or more lobes of the lung) and less often a pneumonectomy (removal of one entire lung), lung-conserving resection or segmental or wedge resection procedures. When the tumour is considered operable, the patient’s cardiopulmonary status must be evaluated to determine their ability to withstand surgery. This is done by clinical studies of pulmonary function, ABGs and other tests, as indicated by the individual’s status. Contraindications for thoracotomy include hypercapnia, pulmonary hypertension, cor pulmonale and markedly reduced lung function. Coexisting conditions such as cardiac, renal and liver disease may also be contraindications for surgery.
Radiotherapy
Radiotherapy is used as a curative approach in the individual who has a resectable tumour but who is considered a poor surgical risk. Recent guidelines indicate radiation therapy as part of treatment for locally advanced unresectable non-small cell lung cancer.51 There has been improved survival when radiation therapy is used in combination with surgery and chemotherapy.44,52 Adenocarcinomas are the most radioresistant type of cancer cell. Although small cell lung cancers are radiosensitive, radiation (even when used in combination with chemotherapy) does not significantly improve the mortality rate because of the early metastases of this type of cancer. Complications of radiation therapy include oesophagitis, skin irritation and radiation pneumonitis. Hyperfractionated radiation, given twice daily, has improved response and survival rates in some small cell lung cancers. However, there is increased toxicity, particularly oesophagitis.53
Radiotherapy is also performed as a palliative procedure to reduce distressing symptoms such as cough, haemoptysis, bronchial obstruction and superior vena cava syndrome. It can be used to treat pain that is caused by metastatic bone lesions or cerebral metastasis. Radiotherapy used as a preoperative or postoperative adjuvant measure has not been found to increase survival significantly in patients with lung cancer.
Chemotherapy
Chemotherapy may be used in the treatment of non-resectable tumours or as adjuvant therapy to surgery in non-small cell lung cancers with distant metastases. A variety of chemotherapy drugs and multi-drug regimens (i.e. protocols), including combination chemotherapy, have been used. These drugs include etoposide, carboplatin, cisplatin, paclitaxel, vinorelbine, cyclophosphamide, ifosfamide, docetaxel, gemcitabine, topotecan and irinotecan.44,47
Chemotherapy has improved survival in patients with advanced non-small cell lung cancer and is now considered standard treatment. Treatment of limited stage small cell lung cancer includes combination chemotherapy and radiation therapy.54 Chemotherapy in small cell lung cancer has a strong response rate but the majority of patients (80%) still die from the disease.
Biological therapy
Biological therapy as adjuvant therapy has been used in individuals with cancer, including malignant lung tumours. (Biological therapy is discussed in Ch 15.)
Other therapies
Prophylactic cranial radiation
Brain metastasis is a common complication of small cell lung cancer. Most chemotherapy drugs do not adequately penetrate the blood–brain barrier. Prophylactic cranial radiation may be used as a potential way to improve the prognosis of patients, especially those who have a complete response to chemotherapy, although it is not known if it increases survival.54 Toxicity of this therapy may include scalp erythema, fatigue and alopecia.
Bronchoscopic laser therapy
Bronchoscopic laser therapy makes it possible to remove obstructing bronchial lesions. The neodymium: yttrium-aluminium-garnet (Nd:YAG) laser is most commonly used for laser resection. The thermal energy of the laser is transmitted to the target tissue. It is a safe and effective treatment of endobronchial obstructions from tumours.52 The procedure is complicated and often requires general anaesthesia to control the patient’s cough reflex. Relief of the symptoms from airway obstruction as a result of thermal necrosis and shrinkage of the tumour can be dramatic. However, it is not a curative therapy for cancer.
Phototherapy
Photodynamic therapy is a safe, non-surgical therapy for lung cancer. The tumour is exposed to laser light, which produces a toxic form of oxygen that destroys tumour cells. Necrotic tissue is removed through the bronchoscope.
Airway stenting
Stents can be used alone or in combination with other techniques for palliation of dyspnoea, cough or respiratory insufficiency. The advantage of an airway stent is that it supports the airway wall against collapse or external compression and can impede extension of tumour into the airway lumen.
Cryotherapy
Cryotherapy is a technique in which tissue is destroyed as a result of freezing. Bronchoscopic cryotherapy is used to ablate (destroy) bronchogenic carcinomas, especially polypoid lesions. A repeat bronchoscope is performed 8–10 days after the first session. The second examination enables assessment of cryodestruction, removal of any slough and repeat cryotherapy if required for the treatment of large lesions. There is insufficient evidence to support its success in the treatment of early stage lung cancer.52
NURSING MANAGEMENT: LUNG CANCER
Nursing assessment
It is important to determine the patient’s and family’s understanding concerning the diagnostic tests (those completed as well as those planned), the diagnosis or potential diagnosis, the treatment options and the prognosis. At the same time, the nurse can assess the patient’s level of anxiety and the degree of support provided and needed by the patient’s significant others. Subjective and objective data that should be obtained from the patient with lung cancer are presented in Table 27-11.
Nursing diagnoses
Nursing diagnoses for the patient with lung cancer may include, but are not limited to, the following:
• ineffective airway clearance related to increased tracheobronchial secretions and the presence of a tumour
• anxiety related to lack of knowledge of the diagnosis or unknown prognosis and treatments
• acute pain related to pressure of the tumour on surrounding structures and the erosion of tissues
• imbalanced nutrition: less than body requirements related to increased metabolic demands, increased secretions, weakness and anorexia
• ineffective health maintenance related to lack of knowledge about the disease process and therapeutic regimen
• ineffective breathing pattern related to decreased lung capacity.
Planning
The overall goals are that the patient with lung cancer will have: (1) effective breathing patterns; (2) adequate airway clearance; (3) adequate oxygenation of tissues; (4) minimal to no pain; and (5) a realistic attitude towards treatment and prognosis.
Nursing implementation
Health promotion
The best way to halt the epidemic of lung cancer is for people to stop smoking. Important nursing activities to assist in the progress towards this goal include promoting smoking cessation programs and actively supporting education and policy changes related to smoking. Important changes that have occurred as a result of the recognition that second-hand or passive smoking is a health hazard are laws requiring the designation of non-smoking areas in most public places or prohibiting smoking in bars and restaurants and a ban on smoking during airline flights. Other actions aimed at controlling tobacco use include restrictions on tobacco advertising on television and warning label requirements for cigarette packaging.
Efforts should be made to assist smokers to stop smoking. The evidence-based guideline developed in the US, Treating tobacco use and dependence, describes a framework (the five As) for approaching patients who are willing to attempt to quit smoking.45 The five As stand for the five strategies: ask, advise, assess, assist and arrange (see Table 10-12). The four stages of change identified in smokers attempting to quit include precontemplation (‘I want’), contemplation (‘I might’), preparation (‘I will’) and action (‘I am’).55 (The stages of change in relationship to patient teaching are discussed in Table 4-2.) Each stage requires specific actions to progress to the next stage. Nurses working with patients at their individual stages of change will help them to progress to the next stage. For patients unwilling to quit, motivational interviewing is recommended (see Ch 10).
The evidence-based guideline also offers the five Rs strategy for motivating smokers to quit: relevance, risks, rewards, roadblocks and repetition (see Table 10-12). Because some patients relapse months or years after having stopped smoking, nurses need to provide interactions continually to prevent relapse. (Tobacco use and dependence and strategies to assist patients to stop smoking are discussed in Ch 10 and Tables 10-12 and 10-13.)
Nicotine’s addictive properties make quitting a difficult task that requires much support. Nicotine replacement significantly lessens the urge to smoke and increases the percentage of smokers who successfully quit smoking. There is no evidence that one product has better results than another, so the choice of agent is dependent on the healthcare provider and patient preferences.56 Stop-smoking aids are presented in Table 10-13.
Research into smoking behaviours and successful strategies to promote smoking cessation is ongoing. A combination of both behavioural change and nicotine replacement products is the most effective strategy to help smokers quit.49,57 Therefore, all patients should be offered some form of nicotine replacement.
The advice and motivation of healthcare professionals can be a powerful force in smoking cessation (see the Evidence-based practice box on smoking cessation in Ch 10). Nurses are in a unique position to promote smoking cessation because they see large numbers of smokers who may be reluctant to seek help. Support for the smoker includes education that smoking a few cigarettes during a cessation attempt (a slip) is much different from resuming the full smoking habit (a relapse). Despite the slip, smokers should be encouraged to continue the attempt at cessation without viewing the effort as a failure. Measures to assist the individual in quitting should be directed towards the meaning that smoking has to that individual. The nurse needs to be aware of resources in the community to assist the individual who is interested in quitting.
Acute intervention
Care of the patient with lung cancer initially involves support and reassurance during the diagnostic evaluation. (Specific nursing measures related to the diagnostic studies are outlined in Ch 25.) Another major nursing responsibility is to help the patient and family to deal with the diagnosis of lung cancer. The patient may feel guilty about cigarette smoking having caused the cancer and may need to discuss this feeling with someone who has a non-judgemental attitude. Questions regarding each patient’s condition should be answered honestly. Additional counselling from a social worker, psychologist or religious leader may be needed. Nursing research focused on the effects of spirituality on the sense of wellbeing of people with lung cancer has found that people with more meaning in their life have decreased symptom distress. Additionally, prayer is associated positively with psychological wellbeing.58 This validates the impact of spiritual care for these patients and helps guide nursing practice in spiritual needs. Research regarding the role of the family has found that family disagreements about treatment decisions for patients with advanced lung cancer are common.59 These findings suggest the need for nurses to be aware of differences of opinion in order to facilitate family communication and improve patient satisfaction with treatment decisions. Nurses need the knowledge and skills to effectively perform health education.60 Nurses can have a great impact on the care of patients with lung cancer not only by focusing on assessment but also by implementing the appropriate interventions more frequently.
Specific care of the patient will depend on the treatment plan. Postoperative care for the patient having surgery is discussed later in this chapter. Care of the patient undergoing radiation therapy and chemotherapy is discussed in Chapter 15. The nurse has a major role in providing patient comfort, teaching methods to reduce pain and assessing indications for hospitalisation.
Ambulatory and community care
The patient who has had a surgical resection with intent to cure should be followed up carefully due to the risk of developing metastases. The patient and family should be told to seek advice if symptoms such as haemoptysis, dysphagia, chest pain and hoarseness develop.
For many individuals who have lung cancer, little can be done to prolong their lives significantly. Radiotherapy and chemotherapy may be used to provide palliative relief from distressing symptoms. Constant pain may become a major problem. (Measures used to relieve pain and care of the patient with cancer are discussed in Ch 15.)