Complications
Pneumonia is common in patients with lung cancer and is often caused by a large, central obstructing tumor. Patients may not present with classic symptoms of pneumonia such as fever, dyspnea, and productive cough. Chest x-ray findings can sometimes be difficult to interpret secondary to tumor-related changes (atelectasis).
Antibiotics should be initiated. Treatment to relieve the obstruction should be instituted relatively quickly for patients with severe pulmonary compromise.
Multiple modalities can be used, such as external beam radiation therapy, brachytherapy (temporary insertion of a radioactive source at the site of obstruction), stent placement, laser debulking of obstructing tumor, photodynamic therapy, and/or surgical resection. Photodynamic therapy is a minimally invasive modality that involves the interaction of light, a photosensitizing agent, and oxygen. Briefly, the photosensitizing agent is administered intravenously and is absorbed by cells throughout the body. Then a laser beam at a predetermined wavelength is focused via a flexible fiber bronchoscope on the endobronchial tumor. The photosensitizing agent absorbs photons of the appropriate wavelength, creating reactive oxygen species that are toxic to cancer cells.
Chemotherapy commonly causes hematologic toxicity (e.g., anemia, neutropenia, thrombocytopenia), which may lead to infection requiring antibiotics, bleeding, hospitalization, or the need for supportive care including blood transfusions.
While granulocyte colony stimulating factor (G-CSF) or granulocyte-macrophage colony stimulating factor (GM-CSF) is not recommended for use during concurrent chemotherapy and radiation for limited-stage SCLC, either G-CSF or trilaciclib may be used to minimize risk of chemotherapy-induced myelosuppression for extensive-stage SCLC.[5]
The most common cause of SVCS is lung cancer. Bulky mediastinal adenopathy or medial extension of a right upper lobe tumor can compress the superior vena cava (SVC), impeding the return of blood from the face and arms to the heart. Numerous collateral pathways develop when the SVC is compressed. The acuity and severity of symptoms depend on the speed of obstruction. The syndrome is characterized by facial and upper extremity edema, dyspnea, cough, and orthopnea. Physical exam demonstrates facial plethora and distended neck, chest wall, and occasionally abdominal wall veins.[80]
SVCS is rarely a medical emergency and every effort should be made to obtain a diagnosis before initiating therapy. Supplemental oxygen and head elevation are often helpful. Treatment depends on the clinical scenario and stage of disease. Patients with marked symptoms should have treatment initiated relatively quickly. Most patients will improve with radiation therapy and/or chemotherapy, but the response may take several days. Endovascular stents may be effective with more rapid symptomatic relief. Surgical intervention is rarely required.[80]
Treatment of the underlying tumor often alleviates symptoms from endocrine-mediated paraneoplastic syndromes (e.g., syndrome of inappropriate secretion of antidiuretic hormone, ectopic adrenocorticotropic hormone production). Neurologic paraneoplastic syndromes are more variable in responding to treatment of the underlying tumor. Other supportive measures depend on the underlying syndrome.
Esophagitis is a common adverse effect of radiation therapy. Symptoms typically develop 3 to 4 weeks after starting radiation therapy, peak toward the completion of treatment, and often persist for several weeks after radiation therapy. Pre-existing gastroesophageal reflux may exacerbate symptoms and should be treated. Severe acute esophagitis occurs in 15% to 25% of patients undergoing concurrent chemoradiation therapy. Rarely, patients may require hospitalization, endoscopy, or placement of a percutaneous endoscopic gastrostomy tube.
Late injury is less common, but may manifest itself between about 3 and 8 months after completion of radiation therapy as an esophageal stricture with dysphagia. Treatment may involve periodic dilation. Death related to tracheoesophageal fistula or esophageal perforation has been reported in up to 1% of patients.[81]
Immune checkpoint inhibitors can cause unique immune-mediated adverse events that are not seen with traditional cytotoxic chemotherapy, such as pneumonitis, colitis, dermatitis, myositis, and hypothyroidism, among others. In general, treatment includes corticosteroids and may require discontinuation of immunotherapy treatment in the case of high-grade toxicities or some neurologic, hematologic, and cardiac toxicities. Grade 3 or higher toxicities generally warrant high-dose corticosteroids tapered over 4 to 6 weeks, and additional immunosuppressive therapies (such as infliximab) may need to be used in some cases. For endocrinopathies controlled by hormone replacement, immune checkpoint inhibitor therapy may be continued even for high-grade toxicity. Consultation of guidelines for detailed organ-specific treatment recommendations is warranted.[59][60]
Radiation-induced lung injury is believed to result from inflammation and chronic oxidative stress, resulting in diffuse alveolar damage. The likelihood of injury depends on the dose and volume of irradiated lung.
Acute radiation pneumonitis may manifest 1 to 6 months after radiation therapy as shortness of breath, dry cough, and occasionally fever. Chest auscultation is typically unremarkable, although friction rub or rales are possible. Chest x-ray should be obtained but is often unrevealing. Radiation pneumonitis is a clinical diagnosis, made after excluding disorders that cause similar symptoms.
Primary treatment for symptomatic acute pneumonitis is oral corticosteroids. We recommend oral prednisone, 40 to 60 mg once daily for 1 to 2 weeks followed by a slow taper (reducing by about 10 mg every 1-2 weeks). The majority of patients with acute pneumonitis recover, and progressive symptoms requiring oxygen or hospitalization are uncommon.
Most patients who receive thoracic radiation therapy develop chronic opacities on imaging, often attributed to fibrosis. The majority of such patients are asymptomatic and do not require treatment. However, symptomatic pulmonary fibrosis can be chronic and debilitating, particularly in patients with poor baseline pulmonary reserve. Established radiation fibrosis is generally irreversible.[82]
Patients may present with acute or worsening hemoptysis in the setting of airway invasion or proximity of a tumor to an airway. Hemoptysis of more than 1 tablespoon should be a cause for urgent action, with further investigation of the source of bleeding (i.e., bronchoscopy) and consideration of palliative radiation if indicated. Prophylactic radiation is not specifically used for this purpose as it is hard to anticipate whether and/or when it may happen, even in the setting of endobronchial lesions.
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