Cancer of the Lung

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Cancer of the Lung

Anatomic Alterations of the Lungs

Cancer is a general term that refers to abnormal new tissue growth characterized by the progressive, uncontrolled multiplication of cells. This abnormal growth of new cells is called a neoplasm or tumor. A tumor may be localized or invasive, benign or malignant.

Benign tumors do not endanger life unless they interfere with the normal functions of other organs or affect a vital organ. They grow slowly and push aside normal tissue but do not invade it. They are usually encapsulated, well-demarcated growths. They are not invasive or metastatic; that is, tumor cells do not travel by way of the bloodstream or lymphatics and invade or form secondary tumors in other organs.

Malignant tumors are composed of embryonic, primitive, or poorly differentiated cells. They grow in a disorganized manner and so rapidly that nutrition of the cells becomes a problem. For this reason, necrosis, ulceration, and cavity formation are commonly associated with malignant tumors. They also invade surrounding tissues and may be metastatic. Although malignant changes may develop in any portion of the lung, they most commonly originate in the mucosa of the tracheobronchial tree.

Lung cancer arises from the epithelium of the tracheobronchial tree. Thus a tumor that originates in the bronchial mucosa is called bronchogenic carcinoma. The terms lung cancer and bronchogenic carcinoma are used interchangeably. As a tumor enlarges, the surrounding bronchial airways and alveoli become irritated, inflamed, and swollen. The adjacent alveoli may fill with fluid or become consolidated or collapse. In addition, as the tumor protrudes into the tracheobronchial tree, excessive mucous production and airway obstruction develop. As the surrounding blood vessels erode, blood enters the tracheobronchial tree. Peripheral tumors also may invade the pleural space and impinge on the mediastinum, chest wall, ribs, or diaphragm. A secondary pleural effusion is often seen in lung cancer. A pleural effusion further compresses the lung and causes atelectasis.

The major pathologic or structural changes associated with bronchogenic carcinoma are as follows:

Etiology and Epidemiology

Lung cancer is the leading cause of cancer deaths in the United States. According to the American Cancer Society 2008 surveillance report, it is estimated that more than 214,000 new cases of lung cancer are reported in the United States annually—about 114,000 in males and about 100,000 in females. Although lung cancer accounts for about 15% of all cancers in both men and women, it is responsible for about 31% of all cancer deaths in men and about 26% of all cancers in women. Among women, the lung cancer death rate is now higher than the death rate of any other cancer, including breast cancer (15% for breast cancer versus 26% for lung cancer). The higher incidence of lung cancer in women is primarily because of their increased rate of cigarette smoking. Death from lung cancer generally begins when patients are 35 to 44 years of age. A sharp increase in lung cancer deaths is seen among patients 45 to 55 years of age. The incidence of lung cancer death progressively increases to 74 years of age and then levels off and decreases in extremely old individuals.

Cigarette smoking is the most common cause of lung cancer. Although various studies and professional organizations report slightly different numbers, all the figures are grim. For example, according to the Centers for Disease Control and Prevention (CDC) and the Surgeon General’s report, male smokers are 22 times more likely to develop lung cancer than nonsmokers, whereas female smokers are 12 times more likely than female nonsmokers to develop lung cancer. Heavy smokers are 64 times more likely to develop lung cancer. It is estimated that cigarette smoke contains more than 4000 different chemicals, many of which have proved to be carcinogens. Passive, or second-hand, smoking is associated with as much as a 30% increase in the risk for lung cancer. A genetic predisposition toward developing lung cancer also plays a role in the incidence of lung cancer.

Environmental or occupational risk factors for lung cancer include the following:

Types of Cancers

There are four major types of bronchogenic tumors: (1) squamous (epidermoid) cell carcinoma, (2) adenocarcinoma (including bronchial alveolar cell carcinoma), (3) large cell carcinoma, and (4) small cell (oat cell) carcinoma (see Figure 26-1). For therapeutic reasons, these bronchogenic tumors are commonly divided into the following two groups:

Each group grows and spreads in different way. For example, SCLC spreads aggressively and responds best to chemotherapy and radiation therapy. It occurs almost exclusively in smokers and accounts for over 20% of all lung cancers in the United States. NSCLC is more common and accounts for about 80% of all lung cancers in America. When confined to a small area and identified early, this type of cancer often can be removed surgically. Table 26-1 provides general characteristics of these cancer cell types, including growth rates, metastasis, and means of diagnosis. A more in-depth description of each cancer cell type follows.

Table 26-1

Characteristics of Lung Cancers

Tumor Type Growth Rate Metastasis Means of Diagnosis
Squamous cell carcinoma Slow Late; mostly to hilar lymph nodes Biopsy, sputum analysis, bronchoscopy, electron microscopy, immunohistochemistry
Adenocarcinoma Moderate Early Radiography, fiberoptic bronchoscopy, electron microscopy
Large cell carcinoma Rapid Early and widespread Sputum analysis, bronchoscopy, electron microscopy (by exclusion of other cell types)
Small cell (oat cell) carcinoma Very rapid Very early; to mediastinum or distally in lung Radiography, sputum analysis, bronchoscopy, electron microscopy, immunohistochemistry, and clinical manifestations (cough, chest pain, dyspnea, hemoptysis, localized wheezing)

image

Modified from McCance KL, Huether SE: Pathophysiology: the biologic basis for disease in adults and children, ed 5, St Louis, 2006, Mosby.

Non–Small Cell Lung Carcinoma

Squamous cell carcinoma

Squamous cell carcinoma constitutes approximately 30% of the bronchogenic carcinomas. The incidence of this type of cancer has sharply declined over the past two decades. This type of tumor is commonly located near a central bronchus or hilus and projects into the large bronchi. Squamous cell tumors are often seen projecting into the bronchi during bronchoscopy. The tumor originates from the basal cells of the bronchial epithelium and grows through the epithelium before invading the surrounding tissues.

The tumor has a slow growth rate and a late metastatic tendency (mostly to hilar lymph nodes). These tumors generally remain fairly well localized and tend not to metastasize until late in the course of the lung cancer. Cavitation and necrosis within the center of the cancer is a common finding. Surgical resection is the preferred treatment if metastasis has not taken place. In about one third of the cases, squamous cell carcinoma originates in the periphery. Because of the location in the central bronchi, obstructive manifestations are generally nonspecific and include a nonproductive cough and hemoptysis. Pneumonia and atelectasis are often secondary complications of squamous cell carcinoma. Cavity formation with or without an air-fluid interface is seen in 10% to 20% of the cases (see Figure 26-1, A).

Adenocarcinoma

Adenocarcinoma arises from the mucous glands of the tracheobronchial tree. In fact, the glandular configuration and the mucous production caused by this type of cancer are the pathologic features that distinguish adenocarcinoma from the other types of bronchogenic carcinoma. It accounts for 35% to 40% of all bronchogenic carcinomas. Adenocarcinoma has the weakest association with smoking. However, among people who have never smoked, adenocarcinoma is the most common form of lung cancer. Adenocarcinoma tumors are usually smaller than 4 cm and are most commonly found in the peripheral regions of the lung parenchyma. The growth rate is moderate and the metastatic tendency is early. Secondary cavity formation and pleural effusion are common (see Figure 26-1, B). When the cancer is discovered early, surgical resection is possible in a high percentage of cases.

Bronchial alveolar cell carcinoma is included under the category of adenocarcinoma. These tumors typically arise from the terminal bronchioles and alveoli. They have a slow growth rate, and their metastasis pattern is unpredictable.

Small Cell Lung Carcinoma

Small cell carcinoma accounts for about 14% of all bronchogenic carcinomas. Most of these tumors arise centrally near the hilar region. They tend to arise in the larger airways (primary and secondary bronchi). Cell size ranges from 6 to 8 µm. The tumor grows very rapidly, becoming quite large, and metastasizes early. Because the tumor cells often are compressed into an oval shape, this form of cancer is commonly referred to as oat cell carcinoma. Staging for small cell carcinoma is divided into only two categories: limited disease (20% to 30%) or extensive disease (70% to 80%). Small cell carcinoma has the poorest prognosis. The average survival time for untreated small cell carcinoma is about 1 to 3 months. Small cell carcinoma has the strongest correlation with cigarette smoking and is associated with the worst prognosis (see Figure 26-1, A).

Screening and Diagnosis

A routine chest x-ray is the most common screening test used to identify an abnormal mass or nodule in a patient’s lung. Computed tomography (CT) and positron emission tomography (PET) scans are also frequently used to reveal extremely small lesions and determine whether the cancer has spread to other areas. A definitive diagnosis, however, can be made only by viewing a tissue sample (biopsy) under a microscope. Common procedures used to obtain a tissue biopsy include bronchoscopy, thoracoscopy, mediastinoscopy, transbronchial needle biopsy or open-lung biopsy, sputum cytology, thoracentesis, and videothoracoscopy (see Chapter 8).

Staging of Lung Cancer

Staging is the process of classifying information about cancer. The staging system describes the cancer cell type, the size of the tumor, the level of lymph node involvement, and the extent to which the cancer has spread. The patient’s prognosis and treatment depend, to a large extent, on the staging results. The system most often used for the staging of lung cancer is the TNM classification (Table 26-2). T represents the extent of the primary tumor, N denotes the lymph node involvement, and M indicates the extent of metastasis. On the basis of the TNM findings, roman numerals are used to identify stages I through IV, with 0 being the least advanced and IV the most advanced. Figure 26-2 provides five representative illustrations of the staging of lung cancer by the TNM classification system. A general overview and description of the staging process for non–small cell lung cancer and small cell lung cancer follows*:

Table 26-2

1997 Revised International System for Staging Lung Cancer

Symbol Definition
Primary Tumor (T)
T0 No evidence of tumor
Tx Tumor that cannot be assessed or is not apparently radiologically or bronchoscopically (malignant cells in bronchopulmonary secretions)
Tis Carcinoma in situ
T1 Tumor with the following characteristics:
 a  Size: ≤3 cm
 b  Airway location: in lobar bronchus or distal airways
 c  Local invasion: none, surrounded by lung or visceral pleura
T2 Tumor with any of the following characteristics:
 a  Size: >3 cm
 b  Airway location: tumor in the main bronchus (within 2 cm of the carina) or tumor with atelectasis involvement of the main bronchus (distance to the carina is 2 cm or more) or presence of atelectasis or obstructive pneumonitis that extends to hilar region but does not involve the entire lung
 c  Local invasion: involvement of the visceral pleura
T3 Tumor with the following location or invasion:
 a  Size: any
 b  Airway location: tumor in the main bronchus (within 2 cm of the carina) or tumor with atelectasis or obstructive pneumonitis of the entire lung
 c  Local invasion: invasion of chest wall (including superior sulcus tumors), diaphragm,mediastinal pleura, or parietal pericardium
T4 Tumor with the following location or invasion:
 a  Size: any
 b  Airway location: satellite tumor nodule(s) within the ipsilateral primary-tumor lobe of the lung
 c  Local invasion: invasion of the mediastinum, heart, great vessels, trachea, esophagus, vertebral body, or carina; or presence of malignant pleural/pericardial effusion
Lymph Nodes (N)
Nx Regional lymph nodes cannot be assessed
N0 Absence of regional lymph node involvement
N1 Presence of metastasis to ipsilateral peribronchial or ipsilateral hilar lymph nodes or both (including direct extension to intrapulmonary nodes)
N2 Presence of metastasis to ipsilateral mediastinal or subcarinal lymph nodes or both
N3 Presence of metastasis to any of the following lymph node groups: contralateral mediastinal, contralateral hilar, ipsilateral or contralateral scalene, or supraclavicular
Distant Metastasis (M)
Mx Metastasis cannot be assessed
M0 Absence of distant metastasis
M1 Presence of distant metastasis (separate metastatic tumor nodule[s] in the ipsilateral nonprimary-tumor lobe[s] of the lung also are grouped as M1)
Stage Grouping—TNM Subsets
Stage 0 TisN0M0
Stage IA T1N0M0
Stage IB T2N0M0
Stage IIA T1N1M0
Stage IIB T2N1N0; T3N0M0
Stage IIIA T3N1M0; T(1-3)N2M0
Stage IIIB T4, any N, M0; any T, N3M0
Stage IV Any T; any N; M1

image

From Mountain CF: Revisions in the international system for staging lung cancer. Chest 111(6):1710, 1997.

Non–Small Cell Lung Carcinoma

NSCLC is staged according to the size of the tumor, the level of lymph node involvement, and the extent to which the cancer has spread. The stages for non–small cell lung cancer include the following:

• Stage 0: The cancer is limited to the lining of the bronchial airways. There is no involvement of the lung tissue or distant metastasis. Stage 0 cancers usually are found during bronchoscopy. When found and treated early, cancers at this stage can often be cured. (TisN0M0)

• Stage I: The tumor is less than 3 cm and is located in lobar or distal airways. There is no lung tissue involvement or distant metastasis. (T1N0M0)

• Stage II: In this stage the cancer has invaded neighboring lymph nodes or spread to the chest wall. There is no distant metastasis. (T1N1M0)

• Stage IIIA: The tumor is any size. The tumor is in the main bronchus, or the tumor is accompanied by atelectasis or obstructive pneumonitis of the entire lung. Local invasion involves chest wall, diaphragm, mediastinal, pleural, or parietal pericardium. There is the presence of metastasis to ipsilateral peribronchial or ipsilateral hilar lymph nodes or both. There is no distant metastasis. (T3N1M0)

• Stage IIIB: The cancer has spread locally to areas such as the mediastinum, heart, great vessels, trachea, esophagus, vertebral body, or carina, or malignant pleural or pericardial effusion is present—all within the chest. There may be involvement of any of the lymph node groups. There is no distant metastasis. (T4, any N, M0)

• Stage IV: The cancer is of any size, involves any of the lymph node groups, and has spread to other parts of the body, such as the liver, bones, or brain. (any T; any N; M1)

Small Cell Lung Carcinoma

SCLC is staged differently than non–small cell cancer. Roman numerals are not used to identify the stages. Small cell lung cancer is usually classified as either limited or extensive:

image OVERVIEW of the Cardiopulmonary Clinical Manifestations Associated with Cancer of the Lung

The following clinical manifestations result from the pathologic mechanisms caused (or activated) by Atelectasis (see Figure 9-8), Alveolar Consolidation (see Figure 9-9), and Excessive Bronchial Secretions (see Figure 9-12)—the major anatomic alterations of the lungs associated with cancer of the lung (see Figure 26-1).

CLINICAL DATA OBTAINED FROM LABORATORY TESTS AND SPECIAL PROCEDURES

Pulmonary Function Test (PFT) Findings

Relative to where the malignancy originates, the PFT results may show either obstructive or restrictive values. For example, when the malignancy obstructs major airways, the PFT values may show obstructive pathology—especially when chronic obstructive pulmonary disease (COPD) is present. However, when large amounts of pulmonary tissue, chest wall, and/or diaphragm are involved (extensive bronchioalveolar carcinoma), then the pathology may show restrictive PFT values.

RADIOLOGIC FINDINGS

Chest Radiograph

A routine chest x-ray examination often provides the first indication or suspicion of lung cancer. Depending on how long the tumor has been growing, the chest x-ray film may show a small radiodense nodule (called a coin lesion) or a large irregular radiodense mass. Unfortunately, by the time a tumor is identified radiographically, regardless of its size, it is usually in the invasive stage and thus difficult to treat. Another common x-ray presentation of lung cancer is that of volume loss involving a single lobe or an individual segment within a lobe.

Because there are four major forms of lung cancer, chest x-ray findings are variable. In general, squamous cell and small cell carcinoma usually appear as a white mass near the hilar region; adenocarcinoma appears in the peripheral portions of the lung; and large cell carcinoma may appear in either the peripheral or the central portion of the lung. Figure 26-3 is a representative example of a large bronchogenic carcinoma in the right lung. Common secondary chest x-ray findings caused by bronchial obstruction include alveolar consolidation, atelectasis, pleural effusion, and mediastinal or diaphragmatic involvement. The x-ray appearance of cavity formation within a bronchogenic carcinoma is similar regardless of the type of cancer.

Clinically, a positron emission tomography (PET) scan is an excellent test to rule out a possible cancerous area identified on either a chest x-ray film or a computed tomography (CT) scan. For example, Figure 26-4 shows a chest radiograph that identifies two suspicious findings—one small nodule in the right upper lung lobe and a larger density in the left lower lung lobe, just behind the heart. Figure 26-5 shows two CT scans that also identify the two suspicious findings and their precise location. Figures 26-6, 26-7, and 26-8 show PET scans that all confirm a “hot spot” (likely cancer) in the lower left lobe. However, the PET scan shown in Figure 26-9 confirms that the nodule in the right upper lobe is benign (i.e., no hot spot is noted).

image
FIGURE 26-5 Same chest radiograph as shown in Figure 26-4. Note that the computed tomography (CT) scan also identifies the suspicious nodules and their precise location.

Finally, the PET/CT image provides an image of excellent quality and high sensitivity and specificity in detecting malignant lesions in the chest. Figure 26-10 shows a CT/PET scan alongside a CT scan and a PET scan; all the images show the same malignant nodule in the right upper lobe.

COMMON NONRESPIRATORY CLINICAL MANIFESTATIONS

When a bronchogenic tumor invades the mediastinum, it may involve the left recurrent laryngeal nerve, the esophagus, or the superior vena cava. When the tumor involves the left recurrent laryngeal nerve, the patient’s voice becomes hoarse. When the tumor compresses the esophagus, swallowing may become difficult. When a tumor invades the mediastinum and compresses the superior vena cava, blood return to the heart from the head and upper part of the body may be interrupted. When obstruction occurs, the symptoms include an increased ventilatory rate and cough, which is greatly aggravated by recumbency. Clinically, this condition is called superior vena cava syndrome.

GENERAL COMMENTS

The clinical manifestations associated with lung cancer may be caused by local effects, tumor extensions into the mediastinum, paraneoplastic endocrine syndromes, or tumor metastases. The most common local signs and symptoms are cough, chest pain, dyspnea, and hemoptysis. Less common signs and symptoms include superior vena cava syndrome, hoarseness resulting from vocal cord paralysis, wheezing, shoulder and upper back pain, and Horner’s syndrome (constriction of the pupil and enophthalmos) related to an apical (Pancoast) tumor. Symptoms of metastatic lung cancer include bone pain, weakness, weight loss, and central nervous system signs and symptoms such as headache, seizures, or symptoms mimicking those of a cerebrovascular accident (CVA). Asymptomatic axillary and supraclavicular lymph node metastasis also may be present. Deep venous thrombophlebitis is present at the time of diagnosis in 5% to 10% of patients with lung cancer.

General Management of Cancer of the Lung

The treatment of lung cancer depends on the patient’s overall health, the type of cancer, the size of the tumor, and the location. Common treatments include surgery, chemotherapy, and radiation therapy.

Surgery

Surgery is usually an option only for patients who have NSCLC that is limited to only one lung, up to stage IIIA. This is usually confirmed with a CT scan and PET scan. In addition, an adequate respiratory reserve must be present to allow good lung function after the lung tissue has been removed. Common surgical procedures include the following:

In the patient with adequate preoperative respiratory reserve (i.e., a predicted after-surgery forced expiratory volume in 1 second [FEV1] of 0.8 to 1 L), a lobectomy is the preferred option. A lobectomy reduces the chances of local recurrence. In the patient with an inadequate respiratory reserve, a wedge resection may be performed. The application of radioactive iodine brachytherapy at the margins of the wedge resection may minimize the need to perform a lobectomy.

Chemotherapy

Chemotherapy is the general term for any treatment involving the use of chemical agents or drugs that are selectively destructive to malignant cancer cells. Because chemotherapy can eliminate cancer cells at sites away from the original cancer, it is considered a systemic treatment. Unfortunately, because the drugs used in chemotherapy can damage healthy cells along with the cancer cells, serious side effects are common. Fast-growing cells are especially likely to be affected (e.g., cells in the digestive tract, bone marrow, and hair). In addition, the patient may experience nausea and vomiting, dizziness, fatigue, and increased risk of infection.

The primary treatment for SCLC is chemotherapy and radiation; surgery is usually not an option. Chemotherapy is also administered to patients with metastatic NSCLC. The type of chemotherapy is based on the tumor category. SCLC is commonly treated with cisplatin and etoposide. Combinations of carboplatin, gemcitabine, paclitaxel, vinorelbine, topotecan, and irinotecan are also commonly used. NSCLC is commonly treated with cisplatin or carboplatin, in combination with gemcitabine, docetaxel, etoposide, or vinorelbine.

Radiation Therapy

Radiation therapy (external radiation) is often given with chemotherapy. It may be used with curative intent in patients with NSCLC who are not eligible for surgery. This type of high-intensity radiation therapy is called radical radiotherapy. In the patient with potentially curable SCLC, radiation therapy and chemotherapy are commonly recommended. In both NSCLC and SCLC, a smaller dose of radiation therapy is often used for symptom control (called palliative radiotherapy). Brachytherapy (localized radiotherapy) may also be used when the tumor can be visualized with a bronchoscopy. Brachytherapy entails the use of small radioactive rods (called seeds) that are implanted near or directly into the tumor.

In the patient with limited-stage SCLC, prophylactic cranial irradiation (PCI) to the brain is often given. PCI is used to minimize the risk of cancer cell metastasis to the brain. Recent advances in targeting and imaging have led to the development of stereotactic radiation therapy (also called stereotactic external-beam radiation therapy and stereotaxic radiation therapy). This type of therapy uses special equipment to position the patient and precisely deliver radiation to a tumor. The total radiation dose is delivered in a small number of doses over several days. It is primarily used in patients who are not surgical candidates.

The goal of radiation therapy is to kill cancer cells without hurting normal tissue cells. Side effects of radiation therapy include redness, swelling, sloughing of skin at the point at which the radiation enters the patient’s body, an increased risk of infection, and radiation fibrosis of adjacent lung tissue. In addition, the patient may experience nausea, vomiting, change of taste, fatigue, and malaise.

Respiratory Care Treatment Protocols

Oxygen Therapy Protocol

Oxygen therapy is used to treat hypoxemia, decrease the work of breathing, and decrease myocardial work. Because hypoxemia is associated with lung cancer, supplemental oxygen may be required. However, capillary shunting is common because of the alveolar compression and consolidation often produced by lung cancer. Hypoxemia caused by capillary shunting often is refractory to oxygen therapy (see Oxygen Therapy Protocol, Protocol 9-1).

CASE STUDY

Cancer of the Lung

Admitting History

A 66-year-old retired man lives with his wife in a small, two-bedroom ranch house in Peoria, Illinois, during the summer months. During the rest of the year, they live in a 22-foot trailer in a retirement park just outside Las Vegas, Nevada. The trailer park is located conveniently on the casinos’ shuttle-bus route; a bus comes by at the top of every hour.

Both the man and his wife are described by their children as addicted gamblers. They gamble almost every day of the year. During the summer months, they play keno and blackjack on the Par-A-Dice Riverboat Casino, which is docked along the shores of the Illinois River in downtown East Peoria. While in Las Vegas, they play bingo, blackjack, and the slot machines at several different casinos. They dress in matching warm-up suits, ride the bus to one of the casinos, and gamble until 10 or 11 pm every day.

Their children, adults with their own families, homes, and jobs in the Peoria area, have been very concerned about their parents’ gambling. They have tried to no avail to get their parents to see a compulsive-gambling therapist, who actually is provided by the Par-A-Dice Riverboat Casino. Their children’s concern is justified. Their parents are always gambling on a shoestring budget. Although they still own their trailer and small home in Peoria, within the last 2 years they have gambled away most of their life savings, which included stocks, bonds, and mutual funds. Because they let their health insurance premium lapse, their policy recently was cancelled. They still receive a small monthly pension check, and some Social Security income.

Before he retired, the man worked for 17 years as a boiler tender for Methodist Hospital in Peoria. He also was a part-time firefighter. For more than 52 years, he smoked two and a half to three packs of unfiltered cigarettes daily. While in Las Vegas, the man began experiencing periods of dyspnea, coughing, and weakness. His cough was productive of small amounts of clear secretions. Also around this time, his wife first noticed that his voice sounded hoarse.

Although he missed several days of gambling and remained in bed because of weakness, he did not seek medical attention. He hated doctors and thought that he merely had a bad cold and the flu. When he returned to Peoria for the summer, however, the children became concerned and insisted that he see a doctor. Despite the man’s lack of health insurance, two medical students from the University of Illinois, who were working as a team, ordered a full diagnostic workup.

A pulmonary function test showed that the man had a restrictive and obstructive pulmonary disorder. CT scanning revealed several masses, ranging from 2 to 5 cm in diameter, in the right and left mediastinum in the hilar regions. The masses, especially on the right side, also could be seen clearly on the posteroanterior chest radiograph. Both the CT scan and the chest x-ray film showed an increased opacity consistent with atelectasis of the medial basal segments of the left lower lobe as well.

A bronchoscopic examination was conducted by the pulmonary physician, with the assistance of a respiratory care practitioner trained in special procedures. It showed several large, protruding bronchial masses in the second- and third-generation bronchi of the right lung; and in the second-, third-, and fourth-generation bronchi of the left lung. During the bronchoscopy, several mucous plugs were suctioned. Biopsy of three of the larger tumors was positive for squamous cell bronchogenic carcinoma, and the man was admitted to the hospital.

The physician told the patient that he had cancer and that his prognosis was poor. Treatment, at best, would be palliative. The patient asked what the odds were on his life expectancy. The physician stated that the patient had only about a 50% chance of living longer than 6 to 8 weeks. Surgery was out of the question. In the interim, however, the physician promised to do what was possible to make the man comfortable. The physician outlined a treatment plan of radiation therapy and chemotherapy and requested a respiratory care consultation.

Physical Examination

The respiratory care practitioner reviewed the admitting history information in the patient’s chart and found the man sitting up in bed in obvious respiratory distress. He appeared weak. His skin was cyanotic, and his face, arms, and chest were damp with perspiration. Wheezing was audible without the aid of a stethoscope. He stated in a hoarse voice that he had coughed up a cup of sputum since breakfast 2 hours earlier. He demonstrated a weak cough every few minutes or so. His cough was productive of large amounts of blood-streaked sputum. The viscosity of the sputum was thin. After each coughing episode, he stated that he wanted a cigarette and then laughed.

His vital signs were as follows: blood pressure 155/85, heart rate 90 bpm, respiratory rate 22/min, and temperature normal. Palpation was unremarkable. Percussion produced dull notes over the left lower lobe. On auscultation, rhonchi, wheezing, and crackles could be heard throughout both lung fields. His arterial blood gas values on a 2 L/min oxygen nasal cannula were as follows: pH 7.51, Paco2 29, image 24, and Pao2 66. His oxygen saturation measured by pulse oximetry (Spo2) was 94%. On the basis of these clinical data, the following SOAP was documented.

Respiratory Assessment and Plan

S “I’ve coughed up a cup of sputum since breakfast.”

O Vital signs: BP 155/85, HR 90, RR 22, T normal; perspiring and weak and cyanotic appearance; voice hoarse-sounding; weak cough; large amounts of blood-streaked sputum; dull percussion notes over left lower lobe; rhonchi, wheezing, and crackles throughout both lung fields; recent PFTs: restrictive and obstructive pulmonary disorder; CT scan and CXR: 2- to 5-cm masses in right and left mediastinum in hilar regions and atelectasis of left lower lobe. Bronchoscopy: protruding tumors in both left and right large airways, mucous plugging. Biopsy: squamous cell bronchogenic carcinoma. ABGs (2 L/min O2 by nasal cannula): pH 7.51, Paco2 29, image 24, Pao2 66; Spo2 94%.

A

P Initiate Oxygen Therapy Protocol (4 L nasal cannula and titration by oximetry). Also begin Aerosolized Medication Protocol (0.5 mL albuterol in 2 mL 10% acetylcysteine q6h), followed by Bronchopulmonary Hygiene Therapy Protocol (C&DB). Begin Lung Expansion Therapy Protocol (incentive spirometry q2h and prn). Closely monitor and reevaluate.

3 Days after Admission

A respiratory care practitioner evaluated the patient during morning rounds. After reviewing the patient’s chart, the practitioner went to the patient’s bedside and discovered that the man was not tolerating the chemotherapy well. He had been vomiting intermittently for the past 10 hours and was still in obvious respiratory distress. He appeared cyanotic and tired, and his hospital gown was wet from perspiration. His cough was still weak and productive of large amounts of moderately thick, clear, and white sputum. He stated in a hoarse voice that he still was not breathing very well.

His vital signs were as follows: blood pressure 166/90, heart rate 95 bpm, respiratory rate 28/min, and temperature normal. Dull percussion notes were elicited over both the right and left lower lobes. Rhonchi, wheezing, and crackles were auscultated throughout both lung fields. His ABG values were as follows: pH 7.55, Paco2 25, image 23, and Pao2 53. His Spo2 was 92%. On the basis of these clinical data, the following SOAP was documented.

Respiratory Assessment and Plan

S “I’m still not breathing very well.”

O Vital signs: BP 166/90, HR 95, RR 28, T normal; vomiting over past 10 hours; cyanosis, tiredness, and dampness from perspiration; cough: weak and productive of moderately thick, clear, and white sputum; dull percussion notes over both right and left lower lobes; rhonchi, wheezing, and crackles over both lung fields; ABGs: pH 7.55, Paco2 25, image 23, Pao2 53, Spo2 92%

A

P Up-regulate Oxygen Therapy Protocol (oxygen mask). Up-regulate Aerosolized Medication Protocol (increasing treatment frequency to q3h). Up-regulate Bronchopulmonary Hygiene Therapy Protocol (CPT and PD q3h). Up-regulate Lung Expansion Therapy Protocol (changing incentive spirometry to CPAP mask). Contact physician about possible ventilatory failure. Discuss therapeutic bronchoscopy. Closely monitor and reevaluate.

16 Days after Admission

Although the physician’s original intention and hope were to discharge the patient soon, stabilizing the man for any length of time proved difficult. Over the next 2 weeks, the patient had continued to be nauseated on a daily basis. He did, however, have occasional periods of relief during which he could breathe, but he generally was in respiratory distress. On day 16 the respiratory therapist observed and collected the following clinical data.

The patient was lying in bed in the supine position. His eyes were closed, and he was unresponsive to the therapist’s questions. The patient was in obvious respiratory distress. He appeared pale, cyanotic, and diaphoretic. No cough was observed at this time, but rhonchi easily could be heard from across the patient’s room. The nurse in the patient’s room stated that the doctor had called the rhonchi a “death rattle.” The patient’s vital signs were as follows: blood pressure 170/105, heart rate 110 bpm, respiratory rate 12/min and shallow, and rectal temperature normal. Percussion was not performed. Rhonchi, wheezing, and crackles were heard throughout both lung fields. His ABG values were as follows: pH 7.28, Paco2 63, image 28, and Pao2 66. His Spo2 was 89%. At that time, the following SOAP was recorded.

Respiratory Assessment and Plan

S N/A (patient comatose)

O Unresponsive; pale, cyanotic, and perspiring appearance; no cough noted; rhonchi heard without stethoscope; vital signs: BP 170/105, HR 110, RR 12 and shallow, T normal; rhonchi, wheezing, and crackles over both lung fields; ABGs: pH 7.28, Paco2 63, image 28, Pao2 66; Spo2 89%

A

P Contact physician about acute ventilatory failure, and discuss code status. Up-regulate Oxygen Therapy Protocol, Bronchopulmonary Hygiene Therapy Protocol, and Aerosolized Medication Therapy Protocol. Monitor and reevaluate.

Discussion

This case demonstrates the few specific treatments that a respiratory care practitioner can bring to the care of patients with lung cancer. Specifically, it illustrates that most of the patients have concomitant obstructive pulmonary disease with a need for good Bronchopulmonary Hygiene Therapy (see Protocol 9-2). The patient’s comfort must be kept in mind at all times.

The first assessment was performed soon after bronchoscopy and diagnosis. The patient’s blood-stained sputum could have reflected the primary tumor or, as likely, bleeding from the bronchoscopy sites. In such cases the practitioner must monitor this sputum as the days go along. No improvement in the patient’s wheezing can be expected if a bronchial tumor is the cause, but it may improve if bronchospasm (from cigarette smoking) is the causative factor.

The rhonchi, wheezing, and crackles indicated the need for vigorous bronchial hygiene therapy. The atelectasis in the left lower lobe suggested that a trial of careful Lung Expansion Therapy Protocol (Protocol 9-3) was in order (see Figure 9-8). The ABG values assessed with the patient on 2 L/min O2 showed acute alveolar hyperventilation with moderate hypoxemia. A trial of oxygen by Venturi mask (or nonrebreathing mask) would be helpful. Patient anxiety may be alleviated with appropriate treatment of the hypoxemia.

The second assessment revealed that the patient may have developed atelectasis in both the right and left lower lobes (where the tumor masses had been noted previously). This case may present a setting in which therapeutic bronchoscopy or laser-assisted endobronchial resection of the tumor masses may be helpful. The patient continued to be hypoxemic, despite alveolar hyperventilation. A higher Fio2 (for example, through a Venturi oxygen mask) was indicated. Vigorous suctioning was appropriate. Because of the impending ventilatory failure, ordering at least one cycle of ventilator support for such a patient would not be surprising, given that the patient had just recently received radiation and chemotherapy. The patient’s wishes in this respect should have been checked against his living will or durable power of attorney for health care, if such a document existed.

The last assessment indicates that the patient did not elect aggressive therapy and that he had slipped into acute ventilatory failure. All health-care personnel had agreed that the patient was close to death. The practitioner may be excused for not suggesting the use of chest physical therapy and postural drainage at this time, because of the patient’s wishes. Aerosolized morphine is now being used to relieve dyspnea in terminally ill cancer patients. If, however, aggressive therapy were still in order, formal evaluation and treatment of superimposed atelectasis or pneumonia, or both, would be in order.