DIAGNOSIS.

Many lung cancers are detected on routine chest film in clients presenting for unrelated medical conditions without pulmonary symptoms, although 90% of the people with lung cancer are symptomatic at diagnosis. Unfortunately, chest radiograph is not sensitive enough to show tumors when they are small and operable and routine screening is not supported by the evidence.

A chest scan called low-dose spiral CT (LDCT) detects tumors too small to be seen on radiographs. There are some concerns with the LDCT (e.g., cost, false-positive findings, unnecessary biopsies of small benign tumors), although the availability of this type of diagnostic procedure may bring about annual screening for lung cancer for those at risk. However, mass screening for lung cancer with CT is not currently advocated because to date no randomized population trial has demonstrated a significant reduction in lung carcinoma mortality as a result of any screening intervention.^25,274

Lung imaging fluorescence endoscope (LIFE) can literally light up cancerous (and preinvasive cancerous) cells using intravenously administered radioactive tracer that attaches to these cells. When the person is imaged with a special camera, the cancer cells show up as bright spots. New endoscopy techniques that use white-light color images and tissue autofluorescence images have been used for early detection of lung lesions.⁴⁶⁴

Without the LDCT chest scan, diagnosis is usually established on sputum cytology for participants in a lung cancer detection program or on bronchoscopy in persons presenting with hemoptysis and a normal chest film. Localization of occult lung tumors is done by fiberoptic bronchoscopy that allows examination to the sixth or seventh branch of the bronchial tree. CT scans are routinely done to assess for metastasis to the mediastinum, liver, and adrenals. Other routine procedures include evaluation of serum chemistry values to look for electrolyte abnormalities (see Chapter 5), especially those associated with paraneoplastic syndrome (see Chapter 9), evaluation of renal and hepatic function, hematologic profiles, and ECG analysis.

At this point, there is no evidence to support sputum-based cellular diagnostics for cancer screening. New tests under development include the electronic nose that uses “smell prints” to identify individuals with cancer; blood tests for specific elevated proteins in serum; and testing for abnormal DNA in sputum.²²⁶

STAGING.

NSCLC of the lung is staged at the time of initial presentation and used to estimate the person’s prognosis and to determine intervention. The tumor, nodes, metastasis (TNM) staging system is used (see explanation in Chapter 9) and provides the basis for selecting cases for resection. Tumors confined to the lung without any metastases, regional or distant, are classified as stage I, and tumors associated with only hilar or peribronchial lymph node involvement (N1) are classified as stage II. Locally advanced tumors with mediastinal or cervical lymph node metastases and those with extension to the chest wall, mediastinum, diaphragm, or carina are classified as stage III tumors. Finally, tumors presenting with distant metastases (M1) are classified as stage IV.

SCLC is usually not considered a surgical disease requiring staging but rather is designated as limited or extensive disease. Limited disease is defined by involvement of one lung, the mediastinum, and either or both ipsilateral and contralateral supraclavicular lymph nodes (i.e., disease that can be encompassed in a single radiation therapy port). Spread beyond the lung, mediastinum, and supraclavicular lymph nodes is considered extensive disease.

TREATMENT.

Awareness of the influence of growth factors, oncogenes, and tumor suppressor genes, as well as signal transduction and angiogenesis pathways on the natural history of cancer cells, has led to attempts to develop new molecular-based strategies directed at interrupting tumor cell growth. Treatments using monoclonal antibodies, inhibitors, antiangiogenic substances, and gene transfer and alteration are still under investigation.⁶⁸

In the meantime, current treatment with new agents used in combination, as well as when combined with radiation and hormones, has led to an improved response rate in the treatment of some lung cancers.⁶⁷ Photodynamic therapy is used successfully with tumors in the airways. Photochemical sensitization of the tumor precedes laser therapy that causes necrosis of the cancer.³⁰⁵ Chemotherapy approaches are numerous and address different targets. Newer agents that inhibit epidermal growth factor receptors are showing promise alone and in combination with other drugs.⁴²⁰

PROGNOSIS.

The curability of lung cancer remains poor because by the time lung cancer is detected, invasion and metastasis have already occurred. The prognosis is influenced by the stage of the disease at presentation, the cell type, the treatment that can be given, and the status of the client at the time of diagnosis (e.g., people who are ambulatory respond to treatment better than those who are confined to bed more than 50% of the time).

Other factors associated with poor prognosis include weight loss of more than 10% of body weight in 6 months and generalized weakness. Overall 5-year survival rate among older blacks with NSCLC is significantly lower compared with whites, largely explained by lower rates of surgical treatment.²⁴ Although women appear to be more susceptible to lung cancer, they have higher survival rates.¹⁴²

Currently, with treatment, only 14% of people with lung cancer survive beyond 5 years after diagnosis, but if caught early, lung cancer can be cured up to 70% of the time. Survival without treatment is rarely possible, and most untreated persons die within 1 year of diagnosis, with a median survival of less than 6 months. Curative treatment requires effective control of the primary tumor before metastasis occurs. Chemotherapy is usually combined with surgery or irradiation for more advanced tumors.

Other factors thought to confer poor prognosis include male gender, age older than 70 years, prior chemotherapy, elevated serum lactic dehydrogenase levels, low serum sodium, and elevated alkaline phosphatase levels (see Tables 40-14 and 40-15).

Pulmonary Embolism and Infarction

DIAGNOSIS.

PE is difficult to diagnose because the signs and symptoms are nonspecific. PE may mimic (and even coexist with) pneumonia, congestive heart failure, pericarditis, myocardial infarction, pneumothorax, anxiety, and even rib fractures. The physician must also differentiate conditions that can mimic thromboembolism to the calf such as cellulitis, muscle strain or rupture, lymphangitis, and rupture of a Baker cyst. Circumstances such as the onset of chest pain or dyspnea in hospitalized, postsurgical, or trauma cases are highly suspicious of PE.

Clinical screen and need for further testing are conducted using Wells, Wicki, or Charlotte criteria and nonimaging laboratory tests (especially D-dimer, which is a by-product of fibrin crosslinks). Negative clinical assessment and D-dimer test may limit the need for further testing.²⁹³ ABGs are not helpful in the physician’s differential diagnosis.

Using combinations of additional tests to rule out or rule in PE to make the diagnosis is optimal. V/Q scans can rule out PE if it is normal in the presence of normal x-ray and with no other cardiopulmonary disease.²⁵⁴

Alveolar dead space evaluation in combination with D-dimer created a false negative response of less than 1%. Echocardiogram can detect PE in 80% of cases. Conventional angiogram has potential for serious side effects and has poor reliability. Spiral CT scan has become the initial diagnostic tool and is useful to exclude PE.²⁰¹ The major disadvantage of spiral CT is its inability to visualize beyond fourth-order branches of the pulmonary artery so that small distal emboli are not seen. Compression ultrasonography is used for the detection of DVT, but a negative result should not rule out DVT.

PREVENTION AND TREATMENT.

The management of DVT and PE has changed dramatically in the last few years. Given the mortality of PE and the difficulties involved in its clinical diagnosis, prevention of DVT and PE is crucial. Primary prevention of DVT through the prophylactic use of anticoagulants is important for persons undergoing total hip replacement, major knee surgery, abdominal or pelvic surgery, prostate surgery, and neurosurgery. In fact, anyone hospitalized should be evaluated for risk of PE and placed on prophylaxis as appropriate.

LMWH (anticoagulant now replacing unfractionated heparin) is the most common agent for prophylaxis because it prolongs the clotting time and allows the body time to resolve the existing clot, thereby preventing further development of the thrombus; it does not reduce the immediate embolic risk or enhance clot lysis. LMWHs have fewer major bleeding complications and do not require laboratory monitoring of coagulation tests to adjust medications. The U.S. FDA has approved outpatient treatment of DVT with the LMWH enoxaparin as a bridge to warfarin. Warfarin (Coumadin), an oral anticoagulant, is used simultaneously with heparin or during the transition from intravenous to oral anticoagulant with a targeted activated partial thromboplastin time of 1.5 to 2.5 times the baseline value and an international normalized ratio of 2 to 3 (see discussion in Chapter 40).

Prophylaxis and treatment with these medications for PE and DVT are different (see further discussion in the section on Thrombophlebitis in Chapter 12). Direct thrombin inhibitors, fondaparinux, idraparinux, and ximelagatran, have been shown to be at least as effective as LMWH and well tolerated.³¹³

Thrombolytic therapy (a controversial, expensive treatment used with massive embolism) to lyse pulmonary thromboemboli in situ is accomplished through the use of thrombolytic agents, such as streptokinase, urokinase, recombinant tissue plasminogen activator, and newer agents, such as reteplase, saruplase, and recombinant staphylokinase, that enhance fibrinolysis by activating plasminogen, generating plasmin.

Plasmin directly lyses thrombi both in the pulmonary artery and in the venous circulation and has a secondary anticoagulant effect. Successfully utilized, pulmonary embolism thrombolysis reverses right-sided heart failure rapidly and safely. There is limited evidence that thrombolytics are better than heparin for PE¹²² but moderate evidence that they effective in reducing postthrombotic syndrome and maintaining vessel patency.^443b

Surgical implantation of a filter in the vena cava may be used to prevent PE in anyone who cannot tolerate anticoagulation therapy by filtering the blood and preventing clots from moving past the screen. There is an increased risk of caval occlusion and dependent edema as a result of obstruction of the filter with this procedure. As temporary measures, the filters are helpful, but permanent filters have not improved survival rates.³¹³ Other procedures used in the case of massive DVT or hemodynamically unstable PE may include thrombectomy and embolectomy performed surgically in an angiography laboratory.

Mechanical compression reduces the risk of DVT by two-thirds alone and by 50% when used with anticoagulants. There was also a risk reduction for PE by two-fifths.³⁵⁹

PROGNOSIS.

PE is the primary cause of death for as many as 100,000 people each year (perhaps double that amount) and a contributory factor in another 100,000 deaths annually. About 10% of victims die within the first hour, but prognosis for survivors (depending on underlying disease and on proper diagnosis and treatment) is generally favorable. Clients with PE who have cancer, congestive heart failure, or chronic lung disease have a higher risk of dying within 1 year than do clients with isolated PE.

Small emboli resolve without serious morbidity, but large or multiple emboli (especially in the presence of severe underlying cardiac or pulmonary disease) have a poorer prognosis. PE may recur despite LMWH therapy, most commonly in people with massive PE or in whom anticoagulant therapy has been inadequate. PE is the leading cause of pregnancy-related mortality in the United States.

Pulmonary Hypertension

DIAGNOSIS.

PPH can be difficult to diagnose, and there is usually a delay of 1 to 2 years between onset of symptoms and diagnosis. Sometimes the first indication of pulmonary hypertension is seen incidentally on a chest radiograph or ECG. The x-ray study may show rib scalloping (erosion of the inferior aspect of the ribs) from dilation of the arteries supplying the ribs. Standard assessment should include a physical examination of heart and lung auscultation and observation and palpation for jugular vein distention, hepatomegaly, and peripheral edema. Chest x-ray, electrocardiogram, and Doppler echocardiogram are also part of the screening.

If PAH is suspected, then additional testing is done to determine severity and to choose appropriate treatment. Essential testing should include pulmonary function tests; oximetry; V/Q scan; blood tests, including complete blood count (CBC), HIV, and antinuclear antibody (ANA) tests; test for exercise capacity (usually 6-minute walk test); and right heart catheterization (with and without vasodilator).³¹ Additional tests, such as spiral CT or angiography, may be needed. Right heart catheterization is needed to confirm the diagnosis.

TREATMENT.

Synthetic prostacyclin and prostacyclin analogues (vasodilators) are effective in improving tolerance to exercise and hemodynamics. Intravenous administration of the synthetic prostacyclin, epoprostenol (Flolan), is the only treatment that has improved survival. Inhaled prostacyclins have shown some promise with short-term improvement and may be beneficial in early stages of PAH.¹⁰⁶

Endothelin-1 receptor antagonists work to counteract the vasoconstriction caused by overproduction of endothelin-1. Investigational oral drug therapy used to treat pulmonary hypertension (e.g., Sitaxsentan or Ambrisentan) has shown promise in improving exercise capacity and hemodynamics. The PDE5 inhibitor, Sildenafil, causes vasodilation and improvement of symptoms, although more research needs to be done with this medication.^149,234

Inhaled nitrous oxide (N₂O, not nitric oxide, which is NO), a vasodilator, has not been shown to be effective in treatment of PAH in children and has potential toxicity.⁴⁵ Calcium channel blockers have been effective in children in high doses. There are no controlled studies to support use of diuretics, digoxin, and oxygen in routine treatment of PAH. Anticoagulants are used with success in appropriate individuals, although guidelines need to be clarified.²⁶³ Balloon atrial septostomy and lung transplantation are used in end-stage PAH, and heart-lung transplants may be more beneficial because of cor pulmonale.

Other treatment approaches under investigation include gene therapy and focus on pathogenetic factors outside the pulmonary endothelium (e.g., potassium channel defect favoring vasoconstriction and cell proliferation, role of elastase, and circulating blood factors contributing to blood thrombosis). In secondary PH, it is essential to treat the underlying cause.

PROGNOSIS.

The progression of PPH varies for each affected individual, but prognosis is poor without heart-lung transplantation. Some individuals may live 5 to 6 years from the time of diagnosis, but most people have a downhill course over a shorter period of time (2 to 3 years) with a fatal outcome.

The cause of death is usually right ventricular failure or sudden death; sudden death occurs late in the disease process. Mortality in the United States has increased notably since 1979, although survival has improved in PPH with the advent of treatment with prostacyclin. Some portion of this reported increase may be related to improvements in diagnostic recognition, and some data suggest that the disease may be more common in the older population than has been previously recognized and reported.²⁶⁰

Secondary PH can be reversed if the underlying disorder is successfully treated. If the hypertension has persisted long enough for the medial smooth muscle layer to hypertrophy, secondary PH is no longer reversible.

Cor Pulmonale

DIAGNOSIS.

Diagnosis is made on the basis of physical examination, radiologic studies, and ECG or echocardiogram, sometimes both. Echocardiogram can be performed at bedside and can effectively and efficiently detect right ventricular enlargement, as well as excessive right ventricular afterload.²¹⁹ Pulmonary function tests usually confirm the underlying lung disease. Laboratory findings may include polycythemia present in cor pulmonale secondary to COPD. ECG and chest film may not be diagnostic in the early stages of cor pulmonale.

TREATMENT.

The primary goal of medical treatment is to reduce the workload of the right ventricle. This is accomplished by lowering pulmonary artery pressure, as in the treatment of pulmonary hypertension (see section in this chapter on Pulmonary Hypertension). Oxygen administration, salt and fluid restriction, and diuretics are essential, as well as treatment of the underlying chronic pulmonary disease, while at the same time relieving the hypoxemia, hypercapnia, or acidosis.

Surgical removal of embolic material is a controversial procedure performed only when a confirmed diagnosis of massive PE with accessible thrombus in the main pulmonary artery or its branches is available. There is no specific surgical treatment available for most causes of chronic cor pulmonale. Heart-lung transplantation for clients with PPH is valuable in late-stage disease.

PROGNOSIS.

Since cor pulmonale generally occurs late during the course of COPD and other irreversible disease, the prognosis is poor. Once congestive signs appear, the average life expectancy is 2 to 5 years, but survival is significantly longer when uncomplicated emphysema is the cause. Although cor pulmonale can be caused by obstructive and restrictive lung diseases, restrictive lung diseases have a lower life expectancy once they reach the stage of cor pulmonale.

Collagen Vascular Disease

Collagen vascular diseases, now more commonly referred to as diffuse connective tissue diseases (see Box 12-17), are often associated with pulmonary manifestations, including exudative pleural effusion, pulmonary nodules, rheumatoid nodules in association with coal workers’ pneumoconiosis (Caplan’s syndrome), interstitial fibrosis, and pulmonary vasculitis. All of these pulmonary conditions have been associated with rheumatoid arthritis; all except the nodules and pleural effusion have been seen with SLE; and pleuritis and pneumonitis have been observed in Sjögren’s syndrome, polymyositis, and dermatomyositis.

Pulmonary fibrosis or PH, or both, are commonly part of the clinical picture associated with scleroderma. Polymyalgia rheumatica and temporal arteritis may demonstrate granulomatous inflammation of the pulmonary parenchyma. Approximately one-half of clients with SLE develop lung disease, primarily pleuritis, pleural effusion, or acute pneumonitis. Pulmonary involvement may not be evident clinically, but pulmonary function tests reveal abnormalities in many persons with SLE.

Lupus pneumonitis causes recurrent episodes of fever, dyspnea, and cough. Interstitial pneumonitis leading to fibrosis occurs in a small proportion of people with SLE; the inflammatory phase may respond to treatment, whereas the fibrosis does not. Occasionally, PH develops. Rarely are ARDS and massive intraalveolar hemorrhage fatal pulmonary complications.

Interstitial lung disease can develop before joint involvement becomes evident in rheumatoid arthritis, particularly in men. People with rheumatoid arthritis who are receiving treatment with methotrexate or gold may develop interstitial lung disease that represents a drug hypersensitivity. Penicillamine therapy in clients with rheumatoid arthritis has been implicated in causing bronchiolitis obliterans.

Bilateral upper lobe fibrosis may develop late in ankylosing spondylitis. Lung involvement varies in systemic sclerosis, but there is radiographic evidence of pulmonary disease in a majority of clients. Cutaneous scleroderma can involve the anterior chest wall and abdomen, causing restrictive lung function.

General dryness and lack of airway secretions cause the major problems of hoarseness, cough, and bronchitis in Sjögren’s syndrome, and interstitial lung disease is possible. Only 5% to 10% of clients with polymyositis and dermatomyositis develop interstitial lung disease, but weakness of respiratory muscles contributing to aspiration pneumonitis is common.

Pneumothorax

DIAGNOSIS AND TREATMENT.

Diagnosis is made by chest film at inspiration. CT scan has been shown to be more sensitive in the person with chest trauma.³⁰¹ There are no specific laboratory tests, but blood gas measurements indicate the degree of respiratory impairment. The presence of dyspnea, tachycardia, decrease or loss of breath sounds, percussive hyperresonance, decreased fremitus, asymmetric chest wall movement, and subcutaneous emphysema (swelling and crepitus with palpation) will assist in the diagnosis.

Depending on the size of the pneumothorax, no specific treatment is required for PSP less than 20% beyond rest and the administration of oxygen to relieve dyspnea.⁴²⁸ However, recurrences are frequent and associated with increased mortality in SSP.

Thoracoscopic procedures of pleurodesis (pleural abrasion, talc poudrage, and pleurectomy) are recommended to prevent further recurrence in SSP and catamenial pneumothorax. Placement of a chest tube is standard procedure for traumatic pneumothoraces.³⁴ Surgical repair is sometimes warranted, particularly with major trauma. In catamenial pneumothorax, hormonal suppression of menses may be required.

Pneumothorax is an unwanted sequela to respiratory distress syndrome in premature infants. The use of prophylactic surfactant significantly reduces the incidence of pneumothorax in this population.³⁹⁶

It is not a good idea to travel by airplane (because of air pressure changes) or to have pulmonary function tests performed (e.g., CF) for at least 2 weeks after a pneumothorax has healed. Encouraging smoking cessation is essential.

PROGNOSIS.

There is a low mortality rate with idiopathic pneumothorax, but a corresponding 15% mortality rate for pneumothorax associated with underlying lung disease. From 30% to 50% of affected persons experience a recurrence, and after one recurrence, subsequent episodes are much more likely. The physiologic events associated with tension pneumothorax are life-threatening, requiring immediate treatment.

Pleurisy

Pleural Effusion

DIAGNOSIS.

Examination of the pleural fluid via transthoracic aspiration biopsy (surgical puncture and drainage of the thoracic cavity) includes analysis of pH; specific gravity; protein; stains and cultures for bacteria, TB, and fungi; eosinophilia count; and glucose concentration to aid in the differential diagnosis.³⁸⁰

Some markers, such as neutrophil-derived enzymes, may be indicators for necessity of chest tubes for drainage. Chest pain must be differentiated from pain of pericardial or musculoskeletal origin. Chest radiographs and physical examination with possible CT scan are necessary components of the diagnostic process.

TREATMENT.

Treatment may not be required when the individual is asymptomatic, or if the client is only mildly symptomatic, transthoracic aspiration may be all that is necessary. In the case of an underlying disease process (e.g., congestive heart failure or renal pathologic findings associated with transudates), treatment is aimed toward that condition.

Drainage of the fluid for exudate-caused effusion provides symptomatic improvement but does not significantly alter lung volumes or gas exchange. Removal of fluid associated with malignancy is considered only if the individual is symptomatic and could benefit from aspiration. Repeated aspiration is avoided since significant protein loss can occur and the fluid reaccumulates in 1 to 3 days.

Some (exudate) pleural effusions resolve with antibiotic therapy. Recurrent (exudate) pleural effusions may be treated by pleurectomy (surgically stripping the parietal pleura away from the visceral pleura) and pleurodesis (sclerosing substance introduced into the pleural space to create an inflammatory response that scleroses tissues together). Both of these procedures have negative effects that must be taken into consideration.

PROGNOSIS.

Prognosis depends on the underlying disease; in cancer, recurrent pleural effusion may be associated with the terminal stage of disease. Tumor-related effusion generally implies a poor prognosis.

Pleural Empyema

Pleural empyema (infected pleural effusion) is an accumulation of pus that occurs occasionally as a complication of pleurisy or some other respiratory disease, usually pneumonia. It is a normal response to infection but may also occur after external contamination (penetrating trauma, chest tube placement, or other surgical procedure) or esophageal perforation. Symptoms include dyspnea, coughing, ipsilateral pleural chest or shoulder pain, malaise, tachycardia, cough, and fever. In addition to chest films, transthoracic aspiration biopsy may be done to confirm the diagnosis and determine the specific causative organism.

The condition is treated with intercostal chest tube drainage, rest, and sedative cough mixtures. Long-term antibiotics are generally needed and attention must be paid to the person’s nutritional status.⁸⁴ Intrapleural fibrinolytic agents may have some use reducing need for surgery in patients with empyema.⁴²² See Special Implications for the Therapist: Pleural Effusion in this chapter.

Pleural Fibrosis

Pleural fibrosis may follow inflammation (especially from asbestos), hemorrhagic effusion, and infection of the pleurae. It can present as localized plaques or diffuse. There appears to be a complex interaction of inflammatory cells, coagulation, profibrotic mediators, and growth factors in this process.³¹⁶ Early use of corticosteroids may decrease the incidence but is not effective in reducing established fibrosis. Surgical decortication can be effective in resolving symptoms.²⁰⁷

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