Home CE Archive Published Ahead-of-Print Online Exclusives Collections Info & Services Journal Info
Skip Navigation LinksHome > February 2014 - Volume 44 - Issue 2 > Non-small cell lung cancer: Recent advances
Nursing:
doi: 10.1097/01.NURSE.0000441877.57254.95
Feature: CE Connection

Non-small cell lung cancer: Recent advances

Held-Warmkessel, Jeanne MSN, RN, ACNS-BC, AOCN; Schiech, Linda MSN, RN, AOCN

Free Access
Continued Education
Article Outline
Collapse Box

Author Information

Jeanne Held-Warmkessel and Linda Schiech are clinical nurse specialists at Fox Chase Cancer Center in Philadelphia, Pa.

The authors and planners have disclosed no potential conflicts of interest, financial or otherwise.

Figure
Image Tools

LUNG CANCER IS THE MOST common cause of cancer-related deaths in the United States, with most patients having distant metastases at the time of diagnosis.1 Black males have the highest incidence and death rates from lung cancer.1 The risk of dying from cigarette-induced lung cancer is almost the same for men and women.2

This article will discuss the risk factors, clinical manifestations, diagnosis, management, and nursing care of the patient diagnosed with the most common type of lung cancer, non-small cell lung cancer (NSCLC). NSCLC cell types include adenocarcinoma, adenocarcinoma in situ, squamous cell carcinoma, large-cell carcinoma, and mixed histology.3,4

Back to Top | Article Outline

Who's at risk?

The major cause of NSCLC is cigarette smoking, but studies indicate that nicotine isn't the culprit in the carcinogenesis process. Each inhalation of cigarette smoke introduces multiple carcinogens into the body, where a cancer-causing agent binds to cellular DNA. When it binds to an oncogene or tumor suppressor gene, the malignant process may be initiated.5 (See Malignant cells taking over.) Besides smoking, risk factors for NSCLC include exposure to radon, secondhand smoke, and air pollution; occupational exposure to silica and asbestos; and alcohol use and cured meat consumption.6,7 (See Prevention strategies.) As with many other cancers, lung cancer develops with age; most lung cancers are seen in patients over age 60.8,9

Other risk factors include a history of radiation therapy to the chest, pulmonary fibrosis, HIV infection, and a genetic/familial risk.10 A family history of cancer increases lung cancer risk.11,12 This is particularly important if the family member was diagnosed at a young age or if multiple family members have been diagnosed with cancer.11

A new category of lung cancer has recently been identified: nonsmoking-associated lung cancer.13 These patients tend to be women with adenocarcinoma of the lung. (Usually found in the outer parts of the lung, adenocarcinoma grows slower than other lung cancers and is more likely to be found before it's spread outside of the lung. About 40% of all lung cancers are adenocarcinomas.)4 These women may have been exposed to tobacco smoke in various settings or to chemicals in the workplace. Additional risk factors include a family history of cancer and a history of pulmonary disease. Estrogen and a diet high in meat also may play a role.13 The genetic mutations seen in smokers aren't seen as often in nonsmokers.14

Back to Top | Article Outline

Genetic changes under scrutiny

Research into nonsmoking-associated lung cancer has identified several genetic mutations associated with the adenocarcinoma histology. Mutations include those to EGFR-TK domain (the most common) and less commonly, KRAS, p53 tumor suppressor gene, and the EML4-ALK fusion gene.15,16 Mutations to KRAS and p53 often occur in smokers.15 Mutations in oncogenes, protooncogenes, tumor suppressor genes, and other regulators of cell function may result in a malignancy. Identification of these genetic changes has promoted development of new targeted therapeutic agents that act on the receptors or proteins involved in the cancer process.

Numerous gene rearrangements have been identified in patients with squamous cell lung cancer (cancer that starts in squamous cells and is often linked to smoking) and the carcinogenic pathway has been described.4,17 Along with other changes, this includes changes in chromosome 3, resulting in alteration of the lifecycle of the cell. Ongoing research is investigating potential cellular targets, but none has been as clearly explained as in the adenocarcinoma cell type.17

Back to Top | Article Outline

Assessing signs and symptoms

No screening tests are specific for lung cancer, and most lung cancers don't cause any symptoms until they've spread beyond the lung.4 (See Screening for lung cancer.) Once patients notice symptoms such as bone pain, neurologic changes (headache, weakness, paresthesias, balance problems, seizures, or dizziness), and jaundice, the cancer has spread to distant organs and may not be curable because it's so far advanced.4

Because many patients diagnosed with lung cancer are smokers or former smokers, they often have some symptoms associated with smoking, such as chronic cough, and may ignore advancing symptoms until they're severe. Common signs and symptoms of NSCLC include:

  • a cough that gets progressively worse
  • chest pain
  • hemoptysis
  • shortness of breath
  • multiple, repeated bronchial infections.18

Many of these patients aren't diagnosed until the disease has metastasized. Signs and symptoms of metastatic NSCLC include:

  • lymphadenopathy
  • neurologic changes such as headaches, dizziness, confusion, problems with balance, or seizures, which could be related to brain metastasis
  • abdominal pain and jaundice, which could be related to liver metastasis
  • unexplained fracture or bone pain in the back, arms, or pelvis, which could be related to bone metastasis.18
Back to Top | Article Outline

Serious syndromes

NSCLC can produce specific groups of signs and symptoms called syndromes before a patient has even been diagnosed with cancer.4 These syndromes can cause serious problems for patients and must be addressed immediately:

  • Horner syndrome, caused by Pancoast tumors, can damage the sympathetic nerve pathways (which consist of three nerves) that go from the upper chest up into the neck.19 Also called superior sulcus tumors or superior pulmonary sulcus tumors, these tumors are found at the apical pleuropulmonary groove, next to the subclavian vessels. This syndrome can cause shoulder pain, ptosis, miosis, and anhidrosis (decreased or lack of sweating), all on the affected side. These signs and symptoms are caused by nerve compression.18
  • Superior vena cava syndrome (SVCS) occurs when a tumor compresses the superior vena cava, resulting in increased central venous pressure and venous collateral formation. This causes edema above the level of the chest, including the face, neck, and periorbital region.20 Edema in the neck and head can produce a headache, shortness of breath, or dizziness. Most of the time signs and symptoms of SVCS progress slowly over many weeks and then improve due to the formation of venous collaterals or treatment.
  • Paraneoplastic syndromes occur when hormone-like substances produced by the tumor enter the bloodstream and affect tissues or organs, even though the cancer hasn't metastasized.4 Clinical manifestations of paraneoplastic syndromes include hypercalcemia, which can lead to nausea and vomiting, confusion and lethargy, or hypercoagulability that causes thrombus formation, either in superficial or deep veins, as well as other signs such as gynecomastia.4,18

These syndromes may help in the diagnosis of NSCLC in a patient without a history of cancer, or it may be evidence of cancer recurrence. Usually treating the underlying disease relieves the signs and symptoms of the syndromes.

Back to Top | Article Outline

Diagnostic studies

A chest X-ray is often the first imaging study done in patients with signs and symptoms of lung cancer. Chest computed tomography (CT) is the diagnostic imaging test of choice for evaluating patients with a potential lung cancer diagnosis.21 For many patients, a CT scan is performed to evaluate the size and location of the tumor and determine if it's surgically resectable. CT scans can also identify enlarged lymph nodes. Both positron emission tomography (PET) and CT are useful for evaluating the mediastinum for lymph node metastases and may be used together.21 A PET scan helps clinicians determine tumor cell metabolic activity by measuring glucose avidity. The most prevalent tumors will have a glucose avidity greater than 2.5 times the avidity of benign tissue.22

A biopsy is required to determine the lung cancer pathology. NSCLC has many cell types, and determining cell type is necessary to guide treatment.22 After the cell type is determined, the specimen is evaluated for molecular characteristics such as EGFR and ALK mutations.22

Biopsy specimens for lung cancer may be obtained in various ways. With squamous cell carcinoma, a bronchoscopy with bronchial washing, bronchial brushings, and/or biopsies often provides adequate tissue for diagnosis.23 Bronchoscopy can be associated with complications such as bleeding, aspiration, and anesthesia-related complications.6 A transesophageal approach with ultrasound may also be used to obtain a biopsy.6

Some central tumors (located near the mainstem bronchus) can be diagnosed by sputum cytology. Peripheral tumors (located farther into the lobe of the lung, away from the mainstem bronchus) are often biopsied percutaneously using CT guidance. After a fine-needle aspiration biopsy of the lung, a chest X-ray is obtained to assess for a pneumothorax. Patients with this complication require immediate medical intervention. If a patient has a pleural effusion, a thoracentesis may provide an adequate specimen for diagnosis via cytology as well as provide relief from shortness of breath.6

Back to Top | Article Outline

Staging lung cancer

Lung cancer is staged according to American Joint Committee on Cancer Staging guidelines, which are updated periodically based on research. The current edition was updated in 2009 by the International Staging Committee of the International Association for the Study of Lung Cancer. Stages are based on the size and location of the tumor, whether it's invaded lymph nodes and tissue, and whether it's metastasized.24 (See Setting the stage for lung cancer.)

Because lymph node numbers and locations are important in patients with tumors on the cusp of being determined operable or inoperable, a mediastinoscopy or an endobronchial ultrasound (EBUS) can be helpful. A mediastinoscopy before surgery is the gold standard of lymph node evaluation and testing for any patient with NSCLC.25,26 A mediastinoscopy is performed via a small transverse incision in the lower neck area, where the scope is placed to explore the area and to biopsy lymph nodes. EBUS uses a bronchoscope and ultrasound to locate and biopsy lymph nodes via a fine-needle aspiration.

Mediastinoscopy can be performed by the thoracic surgeon right before the surgery. Although it's a slightly less invasive procedure, EBUS is mostly performed by interventional pulmonologists separate from the surgery itself.27.26

Back to Top | Article Outline

Surgical approaches

Patients with early stage (Stage 0, I, or II) NSCLC are the best candidates for surgical resection.10 Options for surgery include lobectomy (removal of one lobe of the lung), segmentectomy (removal of part of one lobe) or wedge resection (removal of the tumor and an area of the lung around the tumor), or pneumonectomy (removal of the entire affected lung).24 Surgical approaches for these procedures include the following.

  • Open surgery can be performed in several different ways to access the chest cavity. The most common open procedure is the standard posterolateral thoracotomy. This procedure was frequently used until the mid-1990s and is still used if an open procedure is required.
Table
Table
Image Tools

This type of incision is large, from the patient's side just beneath the axilla, and extends posteriorly toward the patient's mid-upper back. This approach lets surgeons visualize the entire chest area including the mediastinum and all of the lymph nodes that could be involved. Surgeons remove the part of the lung that has cancer and the surrounding lymph nodes for pathologic review.28 The incision is closed with one to two chest tubes connected to closed drainage systems. The chest tubes allow for close monitoring of any drainage and lets the surgical opening heal internally while keeping the lungs inflated via the closed drainage system. The chest tubes are placed in the pleural space between the parietal and visceral pleurae and removed before the patient is discharged.

  • Video-assisted thoracic surgery (VATS) allows the clinician to pass a thoracoscope through small incisions in the patient's side and chest and into the chest cavity to perform biopsies and visual examinations. Tumors are removed in a wedge resection or segmentectomy.27,29,30
  • Robotic procedures are the newest surgical techniques in lung cancer surgery. One of the advantages of a robotic procedure over VATS is that the robotic scope can view in three dimensions, whereas VATS scopes can view in only two dimensions. One disadvantage to robotic procedures is that because the chest and all of the structures surrounding it are very inflexible, the rigid VATS instruments perform better around those structures. The other disadvantage to robotic procedures is that the robot doesn't perform well on vascular dissections in the chest. The staple gun attached to the VATS equipment works better in thoracic cases because it allows the surgeon to staple together or close certain areas in the chest cavity or to create and close internal incisions.

Similar to VATS, the incisions are small and hospitalizations generally shorter with a robotic procedure.31,32 Patients still have an incision or small incisions that must be monitored and chest tubes to allow drainage and restore negative pressure in the pleural space to reexpand the lungs.

Back to Top | Article Outline

Postsurgery care

Monitor patients for hemorrhage by observing the amount and quality of drainage from chest tubes and dressings. Drainage may look bloody immediately after surgery and then turn more serous. Generally, 250 mL/hour or less will drain from a chest tube within the first few hours. If the drainage is greater than 250 mL/hour, notify the surgeon immediately. Assess the color of chest tube drainage throughout the recovery period. A change in the color of drainage to a milky white could indicate a chyle leak (lymphatic fluid leaking from the thoracic ducts or lymphatic ducts).33

Frequently assess the chest tube to make sure it's securely sutured into the skin. The chest tube should also be securely connected to the closed drainage system tubing. The chest tube drainage must be free flowing with no twists or kinks in the tubing. Monitor for adequate suction and make sure the water seal chamber is filled to the correct mark. Inspect for drainage around the chest tube site; if a great deal of drainage is present, change the dressing and reassess the site frequently.

Assess at least once a shift for subcutaneous emphysema right at the chest tube exit site and then moving outward from the tube exit site (the tissue feels like crunchy rice cereal when pressed), which could indicate an air leak into the subcutaneous tissue from the pleural space.34,35 Also look for signs and symptoms of infection, such as fever, purulent sputum, leukocytosis, and a decline in oxygenation. Pneumonia is the most common post-op infection.

Monitor vital signs at least every 4 hours. To help prevent pneumonia and atelectasis, encourage the patient to perform incentive spirometry at least 10 times/hour. Patients should be out of bed and ambulated the first evening postop, if possible, or early the next day if their respiratory and cardiac status allows it to permit full inspiration and minimize hazards of immobility, such as venous thromboembolism.

Patients who've undergone a thoracotomy will usually experience pain caused by the spreading of the ribs during the procedure, the incision itself, and from the chest tubes, which are large and rigid. Administer pain medications via patient-controlled epidural analgesia (PCEA) or I.V. patient-controlled analgesia immediately after surgery. The PCEA or I.V. pain medication is continued until the chest tube is removed, and the pain medication is changed to an oral drug.

Assess surgical staple sites for signs and symptoms of infection, such as erythema, edema, or drainage. For patients who underwent minimally invasive procedures, monitor the small (2 cm) port-site incisions closed with skin closure strips.

Monitor patients for atrial fibrillation following a thoracotomy. Surgery-associated pericardial inflammation can cause acute atrial fibrillation. Between 12% and 44% of patients will develop this complication after pulmonary surgery.36 Age is a risk factor for developing atrial fibrillation following a thoracic procedure.37,38

Back to Top | Article Outline

Radiation therapy

Ranging in use from primary treatment with curative intent to palliative therapy for symptom management, radiation therapy (RT) is a major component of NCSLC treatment. Technical advances have allowed for enhanced tumor targeting and more precise delivery of radiation beams to the targeted area. Treatment planning includes the use of CT scans or CT/PET scans. Advances in lung cancer RT include intensity-modulated radiotherapy, image-guided radiotherapy, and respiratory-gated conformal radiotherapy (which limits the impact of respiratory movements during RT).39 New technology offers patients more precise RT delivery to enhance tumor cell destruction and reduce toxicity.

Because of smoking, advanced age, and other variables, some patients with NSCLC aren't eligible for surgery. Patients with nonoperable Stage I lung cancer may be treated with RT using stereotactic approaches, while those with Stage II cancer may receive conventional RT.40,41 With stereotactic RT, the patient receives one or a few high-dose treatments to a confined area using multiple radiation beams instead of small doses of radiation each day for several weeks.40

RT is also used to treat patients with Stage III NSCLC who aren't surgical candidates. It's often given in combination with chemotherapy to patients who can tolerate a more aggressive approach.42 RT may also be used preoperatively or postoperatively as adjuvant therapy for Stage III NSCLC in combination with chemotherapy.43 Palliative RT may be used to control pain or other distressing symptoms.

Potential adverse reactions from RT depend on the type of RT and the location of delivery. Common adverse reactions include pneumonitis, esophagitis, pharyngitis, and fatigue.44

When administered to centrally located tumors, stereotactic RT may cause musculoskeletal pain and radiation pneumonitis. Reduced pulmonary function, pleural effusion, skin reactions, pneumonia, and death are less common but serious adverse reactions.45

When stereotactic RT is used to treat peripheral lung tumors, adverse reactions include reduced pulmonary function, hypoxia, and pneumonitis.46 Other reported stereotactic RT adverse reactions include chest wall injury, neuropathy, brachial plexus injury, rib fractures, and esophagitis.41

Back to Top | Article Outline

Chemotherapy

Chemotherapy is a mainstay therapy in the management of NSCLC and is administered as a neoadjuvant treatment (given before surgery or other primary treatment) or as an adjuvant treatment for early stage disease (Stages II and IIIA) after surgery. It may be administered after surgery for patients with a Stage IB tumor larger than 4 cm; visceral pleural involvement; T3 tumors and resected metastases; and for metastatic disease with the potential for maintenance therapy (using a single agent) in patients who don't have disease progression using a single agent.7,47–50

The number of planned cycles of chemotherapy depends on the purpose of the therapy. A typical schedule for neoadjuvant and adjuvant therapy is four cycles; for patients with advanced disease or metastatic disease, four to six cycles of chemotherapy is administered.47

Cisplatin is considered the standard chemotherapy treatment for NSCLC. A cisplatin-based doublet therapy (consisting of two drugs) is the most common regimen, but carboplatin may be substituted in patients who can't tolerate cisplatin or who have concurrent diseases (such as renal disease) that contraindicate cisplatin administration.47 Many antineoplastics may be paired with cisplatin, including vinorelbine, etoposide, gemcitabine, or pemetrexed.47 Newer drug doublets that don't contain a platinum compound may also be used to treat advanced disease.51

Patients with nonsquamous-cell NSCLC may benefit from chemotherapy with cisplatin and pemetrexed.52 Some older patients may benefit from doublet chemotherapy (containing carboplatin as the platinum compound for better tolerability) compared with single-agent chemotherapy in terms of overall survival, time to progression, and overall response rate.53,54 Patients with a good functional status who respond to and tolerate first-line chemotherapy may be eligible for maintenance chemotherapy if the disease hasn't progressed.47 Chemotherapy-associated adverse reactions include acute kidney injury; nausea; vomiting; anorexia; diarrhea; hypersensitivity reactions; fatigue; myelosuppression with the potential for neutropenia, anemia, and thrombocytopenia; alopecia; and peripheral neuropathy.55

Back to Top | Article Outline

Combination therapy

Locally advanced Stage III NSCLC is a treatment challenge. This stage is characterized by heterogeneity in the tumor size, location, and extent of nodal involvement.56 With diagnostic imaging showing more advanced disease, patients are often upstaged to advanced NSCLC.57 In addition, Stage III patients may be older, have a poor functional status, comorbidities related to smoking, and poor lung function.57 As a result, many patients with Stage III NSCLC aren't surgical candidates and require alternative treatment, often with concurrent combination chemotherapy and RT. More effective than sequential therapy in terms of survival, this is considered the standard of care for these patients.57–59 RT is delivered weekdays daily for at least 6 weeks, with chemotherapy administered at various frequencies, from weekly to every 3 or 4 weeks, depending on the drugs and doses selected.59,60

Cisplatin-based chemotherapy regimens are the most commonly used and probably have better results than carboplatin.61 Cisplatin may be administered in low doses once a week or in higher doses every 3 or 4 weeks.59 Other patients who may benefit from concurrent chemoradiation are patients with inoperable Stage II cancer. Frail patients may benefit from sequential radiation and chemotherapy or RT alone.59

Back to Top | Article Outline

Targeted therapies

Research has identified certain driver mutations in NSCLC and led to new drugs that specifically target the mutations. Two common driver mutations in NSCLC are EGFR mutations and ALK mutations; for this reason, tumor specimens should be studied to assess for their presence.50 Patients who have these mutations will benefit from treatment with a tyrosine kinase inhibitor (TKI) directed toward the specific mutation present in the cells. Those without the mutation should receive chemotherapy.50

NSCLC cell types other than squamous cell carcinoma may respond to therapy with an antiangiogenesis agent such as bevacizumab with chemotherapy.62 These agents aren't indicated in patients with squamous cell NSCLC because they develop serious or fatal pulmonary bleeding.62 Adverse reactions from TKIs include nausea, vomiting, diarrhea or constipation, rash, and edema.63 A rare but serious adverse reaction to TKIs is interstitial lung disease.63

Back to Top | Article Outline

Posttherapy care

Patients with NSCLC benefit from nursing interventions and education directed at controlling and managing signs and symptoms and complications. Respiratory symptoms are common because of the nature of the disease, but TKIs may produce new or worsening respiratory symptoms. If so, the patient requires diagnostic testing to assess for interstitial lung disease, worsening lung cancer, or pneumonia.

Patients receiving RT may develop pneumonitis during therapy and for up to 6 months after therapy ends.6 Advise patients to report development of a cough or trouble breathing promptly; steroid therapy may be indicated.6

Advise patients to avoid sources of infection and protect themselves from injury to skin and mucous membranes. Educate patients about the signs and symptoms of infection such as fever, chills, rigors, pharyngitis, productive cough, or dyspnea and the need to immediately report any of these to the healthcare provider.

Fatigue is another common problem, so teach patients about alternating activities with planned rest periods, adequate sleep, well-balanced nutritious meals and snacks, and patient-appropriate individualized exercise. A physical therapy consult is useful in planning exercise.64

Anorexia, nausea, vomiting, or diarrhea may occur from targeted therapy or chemotherapy. Vomiting or diarrhea may lead to dehydration and electrolyte imbalances. Teach patients how to manage nausea, vomiting, and diarrhea with appropriate medications and dietary alterations. For example, nausea and vomiting may be managed with carbohydrates such as crackers and dry toast, bland cool foods, and a low-odor environment. Diarrhea is managed with increased fluid intake, dietary changes such as reduced fiber, antidiarrheal medications, and increased electrolyte consumption.

Esophagitis, a possible complication of RT, is best managed with pain medication and education on diet modifications. Encourage the patient to avoid irritating foods and beverages and increase fluid consumption.

Many patients develop skin problems related to RT or TKIs. RT may make the skin dry, irritated, or pruritic. Teach patients to wash the skin gently, rinse well, and pat dry, and to avoid applying any irritating or drying substances to the skin and to use recommended skin care products. TKIs dry the skin and may cause skin eruptions, so advise patients to use a thick emollient moisturizer on the skin and report any evidence of infection. Also advise them to avoid exposure to the sun because it worsens skin reactions and other adverse reactions to chemotherapy, RT, and TKIs.

An increasing number of chemotherapeutic drugs are taken orally by patients at home. It's critical that patients nderstand that these are potent medications that must be taken exactly as prescribed, without missing or skipping doses.

Back to Top | Article Outline

When cure isn't an option

Patients who have tumors considered inoperable and who've received chemotherapy and/or RT may benefit temporarily from ablative procedures. Radiofrequency ablation and cryoablation can obliterate or destroy the tumor itself, relieving some symptoms temporarily.65 Palliative procedures via bronchoscopy, such as endobronchial stenting or laser therapy, may help relieve malignant airway obstructions.

As the disease advances, patients commonly develop complications such as malignant pleural effusion (MPE). Some palliative procedures that can be performed to assist with the symptom management of a MPE include the following.

  • Thoracentesis to remove fluid from the pleural space can be done multiple times to drain an acute effusion.
  • Indwelling pleural catheter placement with intermittent drainage can be performed in the outpatient setting.
  • Chemical pleurodesis obliterates the pleural space by inducing pleural inflammation and fibrosis when a sclerosant (such as talc) is instilled into the pleural space via VATS or via a chest tube.

Patients with NSCLC can develop worsening shortness of breath and air hunger. Use of oxygen by whatever delivery method and at a level that the patient requires may ease this symptom. Research shows the use of opioids can also assist with the feeling of air hunger that patients experience at the end of life.66

Painful coughing is another symptom that can trouble patients as the disease progresses. It may disturb their sleep and exacerbate shortness of breath. Advise patients to seek medical attention if their cough worsens. For patients with diagnosed bacterial pneumonia, antibiotics should help relieve coughing. Antitussive (cough suppressant) agents such as dextromethorphan may be prescribed. Medications such as benzonatate, which help reduce the cough reflex, can also be useful. Opioids, such as codeine, have antitussive properties as well. If the cough is related to pulmonary edema, a diuretic may be prescribed.66

As a patient's clinical status worsens, hospice or palliative care should be considered. Research shows that patients may live longer and will die more peacefully if they're in a program early enough to take advantage of the supportive programs that are available to them.67

Patients may become agitated and delirious at the end of life. Medications such as anxiolytics can be helpful to decrease anxiety and agitation.

Back to Top | Article Outline

Advances in treatment

Over the past decade, progress has been made in the management of patients with NSCLC. Advances include new staging descriptions, new surgical procedures, new chemotherapeutic agents, and targeted therapeutics. Through clinical interventions and patient education, you play a central role in supporting the patient throughout the course of diagnosis and treatment.

Back to Top | Article Outline

Malignant cells taking over

Malignant cells proliferate in one or both lungs when previously normal cells change and multiply at an uncontrolled rate. The resulting lesions disrupt normal lung structure and function.

When malignant cells spread to neighboring tissues and lymph nodes, the patient's prognosis is poor.

Figure
Image Tools
Back to Top | Article Outline

Prevention strategies

Understanding the risk factors for developing NSCLC goes a long way in understanding how to prevent the cancer. The biggest risk factor for both males and females is cigarette smoking, so smoking cessation is the best strategy for preventing lung cancer. The chances of developing lung cancer decrease by approximately 50% within 15 years of quitting smoking.14 The risk of dying from lung cancer decreases 30% to 50% after 10 years of smoking cessation.71

Two well-documented categories of medications are available to help people quit smoking. Nicotine replacement therapy in the form of gum, inhalers, lozenges, and skin patches is available over the counter. Replacement therapy provides a low dose of nicotine, but not the multitude of other toxic substances found in cigarettes. The idea behind this type of therapy is to replace some of the nicotine the person was getting via cigarettes to reduce cravings and make quitting easier. The routes of administration work in different ways to release nicotine into the system. Nicotine has vasoconstrictive effects, so tell patients to discuss the use of these products with their healthcare provider and to follow the instructions on the package carefully.72

Various oral smoking cessation medications are available by prescription only and also help decrease cravings for tobacco and smoking. For example, bupropion is an antidepressant that decreases cravings for tobacco. Varenicline, a nicotinic receptor partial agonist, binds to neuronal nicotinic acetylcholine receptors to prevent nicotine from binding to these receptors.72

Tobacco control legislation is extremely important in the prevention of lung cancer. This type of legislation may include bans on smoking in workplaces, restaurants, and public spaces; requiring designated outside areas for smoking; and limiting the amount of employee exposure to smoke and carcinogens in the workplace.14,73

The most recent prevention workforce policy for hospitals and other places of business is testing for prospective employees' smoking history, or “tobacco-free hiring,” as well as employee health insurance incentives for not smoking.74 The rationale for this policy is for the employees' personal well-being and reducing healthcare costs.74

Awareness of radon and its potential to cause lung cancer has promoted the requirement that newer construction and older houses being sold are tested for radon. Radon tests are available for homes that haven't been on the market for testing and prevention.71

Human papillomavirus (HPV) has been linked to lung cancer. Much more research is needed on the subject, but if the link is confirmed, vaccinating both girls and boys against HPV between ages 11 and 26 has the potential to help prevent lung cancer.14

Back to Top | Article Outline

Screening for lung cancer

Traditionally, the most common method attempted for lung cancer screening has been the use of sputum specimens, which are easy to obtain, inexpensive, and noninvasive, even though they haven't proven accurate. Another method is the use of imaging studies, either with a two-view chest X-ray or a CT scan. Many studies have looked at the effectiveness of chest X-ray alone as a screening tool, and none have produced any difference in mortality.68,69

A large, multicenter randomized trial known as the National Lung Screening Trial (NLST) was started in 2002 with 53,454 former or present heavy smokers to compare low-dose helical chest CT to chest X-ray to detect lung cancer annually for 3 years. The trial was stopped in 2010, with the outcome highly in favor of the low-dose CT scan as a screening method. Cancers were discovered at an earlier stage when using the CT scan.68,69 High-risk patients to be screened under the NLST criteria are between ages 55 and 74; have a smoking history of at least 30 pack years; and are either current smokers or previous smokers who quit within the last 15 years.69

Radiation exposure using a low-dose CT scan is improving, allowing for shorter time in the scanner and enhanced image quality to improve cancer detection. During the NLST study, the average radiation dose was decreased to a more acceptable level than previous tests.68 Many comprehensive cancer centers now use a low-dose CT scan as their outreach screening method.

A new method being studied for lung cancer screening is to sample the breath for volatile organic compounds, which may be early indicators of lung cancer. The compounds isoprene, acetone, and methanol are detected in everyone's breath, but they exist in significantly lower measurable amounts in people who have a lung cancer diagnosis.70 Clinical trials are currently being done in the United States and Europe to see if this method is accurate and if it could be used to screen a large number of people at risk for lung cancer.

Back to Top | Article Outline

REFERENCES

1. Siegel R, Naishadham D, Jemal A. Cancer statistics, 2013. CA Cancer J Clin. 2013; 63:(1):11–30.

2. Thun MJ, Carter BD, Feskanich D, et al. 50-year trends in smoking-related mortality in the United States. N Engl J Med. 2013; 368:(4):351–364.

3. Larsen JE, Minna JD. Molecular biology of lung cancer: clinical implications. Clin Chest Med. 2011; 32:(4):703–740.

4. ACS. American Cancer Society. Lung cancer (non-small cell). 2013. http://www.cancer.org/acs/groups/cid/documents/webcontent/003115-pdf.pdf.

5. Hecht SS. Lung carcinogenesis by tobacco smoke. Int J Cancer. 2012; 131:(12):2724–2732.

6. Eaby-Sandy B. Lung cancer. In: Yarbro CH, Wujcik D, Gobel BH, eds. Cancer Nursing: Principles and Practice. 7th ed. Boston: Jones and Bartlett Publishers; 2010:1424–1457.

7. Molina JR, Yang P, Cassivi SD, Schild SE, Adjei AA. Non-small cell lung cancer: epidemiology, risk factors, treatment, and survivorship. Mayo Clin Proc. 2008; 83:(5):584–594.

8. Blanchard EM, Arnaoutakis K, Hesketh PJ. Lung cancer in octogenarians. J Thorac Oncol. 2010; 5:(6):909–916.

9. SEER Cancer Statistics Review 1975–2010. http://seer.cancer.gov/csr/1975_2010.

10. Midthun DE.. Overview of risk factors, pathology, and clinical manifestations of lung cancer. UpToDate. 2013. www.uptodate.com.

11. Matakidou A, Eisen T, Houlston RS. Systematic review of the relationship between family history and lung cancer risk. Br J Cancer. 2005; 93:(7):825–833.

12. Torok S, Hegedus B, Laszlo V, et al. Lung cancer in never smokers. Future Oncol. 2011; 7:(10):1195–1211.

13. Yano T, Haro A, Shikada Y, Maruyama R, Maehara Y. Non-small cell lung cancer in never smokers as a representative ‘non-smoking-associated lung cancer’: epidemiology and clinical features. Int J Clin Oncol. 2011; 16:(4):287–293.

14. de Groot P, Munden RF. Lung cancer epidemiology, risk factors, and prevention. Radiol Clin North Am. 2012; 50:(5):863–876.

15. Lee YJ, Kim JH, Kim SK, et al. Lung cancer in never smokers: change of a mindset in the molecular era. Lung Cancer. 2011; 72:(1):9–15.

16. Subramanian J, Govindan R. Lung cancer in ‘never-smokers’: a unique entity. Oncology (Williston Park). 2010; 24:(1):29–35.

17. Drilon A, Rekhtman N, Ladanyi M, Paik P. Squamous-cell carcinomas of the lung: emerging biology, controversies, and the promise of targeted therapy. Lancet Oncol. 2012; 13:(10):e418-e426.

18. American Cancer Society. How is non-small cell lung cancer diagnosed? 2013. http://www.cancer.org.

19. Arcasoy SM, Jett JR, Schild SD. Superior pulmonary sulcus (Pancoast) tumors. UpToDate. 2013. http://www.uptodate.com.

20. Drews RE, Rabkin DJ.. Malignancy-related superior vena cava syndrome. UpToDate. 2013. http://www.uptodate.com.

21. Christensen JD, Patz EF Jr.. Future trends in lung cancer diagnosis. Radiol Clin North Am. 2012; 50:(5):1001–1008.

22. Midthun DE. Overview of the initial evaluation, treatment and prognosis of lung cancer. UpToDate. 2013. http://www.uptodate.com.

23. Tyson LB. Patient assessment. In: Houlihan NG, ed. Lung Cancer. Pittsburgh, PA: Oncology Nursing Society; 2004:35–44.

24. West H. Patient information: non-small cell lung cancer treatment; stage I to II cancer. UpToDate. 2013. http://www.uptodate.com.

25. Rice DC.. Endobronchial ultrasound (EBUS) biopsy of mediastinal lymph nodes. 2013. http://www.ctsnet.org/sections/clinicalresources/thoracic/expert_tech-40.

26. Catarino PA, Goldstraw P. The future in diagnosis and staging of lung cancer: surgical techniques. Respiration. 2006; 73:(6):717–732.

27. Sherwood JT, Brock MV. Lung cancer: new surgical approaches. Respirology. 2007; 12:(3):326–332.

28. Shahani R.. Thoracic incisions. 2013. http://emedicine.medscape.com/article/1972596-overview.

29. Nikolouzos S, Lioulias A, Baltayiannis N, Charpidou A, Syrigos K. Minimally invasive surgical techniques in diagnosis and treatment of lung cancer. Hellenic J Surg. 2012; 84:113–119.

30. Hennon MW, Yendamuri S. Advances in lung cancer surgery. J Carcinog. 2012; 11:21.

31. Das-Neves JC, Riquet M, Le-Pimpec-Barthes F, Pego-Fernandes PM, Jatene FB.. Robotic surgery for lung cancer. 2010. http://www.intechopen.com/books/robot-surgery/robotic-surgery-for-lung-cancer.

32. Ng CS, Lau KK, Gonzalez-Rivas D, Rocco G. Evolution in surgical approach and techniques for lung cancer. Thorax. 2013; 68:(7):681.

33. Chen E, Itkin M. Thoracic duct embolization for chylous leaks. Semin Intervent Radiol. 2011; 28:(1):63–74.

34. Carroll P.. Chest tube and drainage management. 2013. http://www.rn.org/courses/coursematerial-98.pdf.

35. Bauman M, Handley C. Chest-tube care: the more you know, the easier it gets. American Nurse Today. 2011; 6:(9):27–32.

36. Fernando HC, Jaklitsch MT, Walsh GL, et al. The Society of Thoracic Surgeons practice guideline on the prophylaxis and management of atrial fibrillation associated with general thoracic surgery: executive summary. Ann Thorac Surg. 2011; 92:(3):1144–1152.

37. Fernando HC, Jaklitsch MT, Walsh GL, et al. The Society of Thoracic Surgeons practice guideline on the prophylaxis and management of atrial fibrillation associated with general thoracic surgery: executive summary. Ann Thorac Surg. 2011; 92:(3):1144–1152.

38. Park BJ, Zhang H, Rusch VW, Amar D. Video-assisted thoracic surgery does not reduce the incidence of postoperative atrial fibrillation after pulmonary lobectomy. J Thorac Cardiovasc Surg. 2007; 133:(3):775–779.

39. Haas ML. Advances in radiation therapy for lung cancer. Semin Oncol Nurs. 2008; 24:(1):34–40.

40. West HJ, Vallieres E, Schild SE.. Management of stage I and stage II non-small cell lung cancer. UpToDate. 2013. http://www.uptodate.com.

41. Stephans K. Stereotactic body radiotherapy for stage I non-small cell lung cancer. Cleve Clin J Med. 2012;79 Electronic suppl 1:eS26-eS31.

42. Schild SE, Ramalingam SS, Vallieres E.. Management of stage III non-small cell lung cancer. UpToDate. 2013. http://www.uptodate.com.

43. Gadgeel SM, Ramalingam SS, Kalemkerian GP. Treatment of lung cancer. Radiol Clin North Am. 2012; 50:(5):961–974.

44. Houlihan NG, Inzeo D, Joyce M, Tyson LB. Site Specific Cancer Series: Lung Cancer. Pittsburgh, PA: Oncology Nursing Society; 2004:103–124.

45. Timmerman R, McGarry R, Yiannoutsos C, et al. Excessive toxicity when treating central tumors in a phase II study of stereotactic body radiation therapy for medically inoperable early-stage lung cancer. J Clin Oncol. 2006; 24:(30):4833–4839.

46. Timmerman R, Paulus R, Galvin J, et al. Stereotactic body radiation therapy for inoperable early stage lung cancer. JAMA. 2010; 303:(11):1070–1076.

47. Ettinger DS, Akerley W, Bepler G, et al. Non-small cell lung cancer. J Natl Compr Canc Netw. 2010; 8:(7):740–801.

48. Heon S, Johnson BE. Adjuvant chemotherapy for surgically resected non-small cell lung cancer. J Thorac Cardiovasc Surg. 2012; 144:(3):S39-S42.

49. Sibille A, Wauters I, Vansteenkiste J. Maintenance therapy for advanced non-small-cell lung cancer: ready for clinical practice. Expert Rev Anticancer Ther. 2012; 12:(4):529–539.

50. Lilenbaum RC.. Overview of the treatment of advanced non-small cell lung cancer. UpToDate. 2013. http://www.uptodate.com.

51. Jiang J, Liang X, Zhou X, Huang R, Chu Z, Zhan Q. Non-platinum doublets were as effective as platinum-based doublets for chemotherapy-naïve advanced non-small-cell lung cancer in the era of third-generation agents. J Cancer Res Clin Oncol. 2013; 139:(1):25–38.

52. Syrigos KN, Vansteenkiste J, Parikh P, et al. Prognostic and predictive factors in a randomized phase III trial comparing cisplatin-pemetrexed versus cisplatin-gemcitabine in advanced non-small-cell lung cancer. Ann Oncol. 2010; 21:(3):556–561.

53. Aggarwal C, Langer CJ. Older age, poor performance status and major comorbidities: how to treat high-risk patients with advanced nonsmall cell lung cancer. Curr Opin Oncol. 2012; 24:(2):130–136.

54. Qi WX, Tang LN, He AN, Shen Z, Lin F, Yao Y. Doublet versus single cytotoxic agent as first-line treatment for elderly patients with advanced non-small-cell lung cancer: a systematic review and meta-analysis. Lung. , 2012; 190:(5):477–485.

55. Wilkes GM, Barton-Burke M. Oncology Nursing Drug Handbook. Burlington, MA: Jones & Bartlett Learning; 2013.

56. Edge SB, Byrd DR, Compton CC, Fritz AG, Trotti A. eds. AJCC Cancer Staging Handbook. 7th ed. New York: Springer; 297–330.

57. Videtic GM. Locally advanced non-small cell lung cancer: what is the optimal concurrent chemoradiation regimen. Cleve Clin J Med. 2012;79 Electronic suppl 1:eS32-eS37.

58. Curran WJ Jr, Paulus R, Langer CJ, et al. Sequential vs. concurrent chemoradiation for stage III non-small cell lung cancer: randomized phase III trial RTOG 9410. J Natl Cancer Inst. 2011; 103:(19):1452–1460.

59. Ettinger DS, Akerley W, Borghaei H, et al. Non-small cell lung cancer, version 2.2013. J Natl Compr Canc Netw. 2013; 11:(6):645–653.

60. Expert Panel on Radiation Oncology-Lung, Gewanter RM, Movsas B, et al. Nonsurgical treatment for non-small-cell lung cancer: good performance status/definitive intent. American College of Radiology ACR Appropriateness Criteria. 2010. http://www.acr.org/~/media/ACR/Documents/AppCriteria/Oncology/NonsurgicalTreatmentForNSCLCGoodPerformanceStatusDefinitiveIntent.pdf.

61. Salama JK, Vokes EE. New radiotherapy and chemoradiotherapy approaches for non-small-cell lung cancer. J Clin Oncol. 2013; 31:(8):1029–1038.

62. Sandler A, Gray R, Perry MC, et al. Paclitaxel-carboplatin alone or with bevacizumab for non-small-cell lung cancer. N Engl J Med. 2006; 335:(24):2542–2550.

63. Thomas A, Rajan A, Giaccone G. Tyrosine kinase inhibitors in lung cancer. Hematol Oncol Clin North Am. 2012; 26:(3):589–605.

64. Joyce M, Schwartz S, Huhmann M. Supportive care in lung cancer. Semin Oncol Nurs. 2008; 24:(1):57–67.

65. Sharma A, Abtin F, Shepard JA. Image-guided ablative therapies for lung cancer. Radiol Clin North Am. 2012; 50:(5):975–999.

66. National Cancer Institute. Last days of life. 2013. http://www.cancer.gov.

67. Meier DE, McCormick E.. Palliative care: benefits, services, and models of care. UpToDate. 2013. http://www.uptodate.com.

68. Deffebach ME, Humphrey L.. Screening for lung cancer. UpToDate. 2013. http://www.uptodate.com.

69. Schmidlin EJ, Sundaram B, Kazerooni EA. Computed tomography screening for lung cancer. Radiol Clin North Am. 2012; 50:(5):877–894.

70. Bajtarevic A, Ager C, Pienz M, et al. Noninvasive detection of lung cancer by analysis of exhaled breath. BMC Cancer. 2009; 9:348.

71. National Cancer Institute. Lung cancer prevention. 2013. http://www.cancer.gov/cancertopics/pdq/prevention/lung/HealthProfessional.

72. National Institutes of Health. How does smoking affect the heart and blood vessels? 2011. http://www.nhlbi.nih.gov/health/health-topics/topics/smo.

73. Salgia R, Skarin AT.. Chemoprevention of lung cancer. UpToDate. 2013. http://www.uptodate.com.

74. Sulzberger AG.. Hospitals shift smoking bans to smoker ban. The New York Times. 2011. http://www.nytimes.com.

75. American Joint Committee on Cancer. Lung cancer staging. 2013. http://www.cancer.net/cancer-types/lung-cancer/stages.

76. Rami-Porta R, Crowley JJ, Goldstraw P. The revised TNM staging system for lung cancer. Ann Thorac Cardiovasc Surg. 2009; 15:(1):4–9.

77. Rusch VW, Asamura H, Watanabe H, et al. The IASLC lung cancer staging project: a proposal for a new international lymph node map in the forthcoming seventh edition of the TNM classification for lung cancer. J Thorac Oncol. 2009; 4:(5):568–577.

Wolters Kluwer Health | Lippincott Williams & Wilkins

Login