25: Thoracic Flashcards
Which pulmonary nodes are not assessed by mediastinascopy
Aorto-pulmonary (AP) window nodes (left lung drainage)
[UpToDate: SCM can easily access pretracheal (1, 3), paratracheal (2R, 2L, 4R, 4L), anterior subcarinal (7) and occasionally hilar (10) nodes (figure 1). It is not able to sample subaortic (5) or para-aortic (6), inferior (8, 9), posterior subcarinal (7), or lobar/interlobar (11 to 14) stations. Use of the video mediastinoscope can extend access to the posterior subcarinal nodes (station 7). SCM is best used to sample lymph nodes in these selected stations, particularly when other staging modalities have failed or are not available.]
What is the difference between the granulomas seen in tuberculosis and sarcoidosis?
- TB = Caseating granulomas
- Sarcoidosis = Non-caseating granulomas
[Wikipedia: “caseation” (literally: turning to cheese) refers to a form of necrosis that, to the unaided eye (i.e., without a microscope), appears cheese-like (“caseous”), and is typically (but not uniquely) a feature of the granulomas of tuberculosis. The identification of necrosis in granulomas is important because granulomas with necrosis tend to have infectious causes.]
[UpToDate: Microscopy of tissue biopsy specimens in the setting of tuberculosis typically demonstrates granulomatous inflammation. Granulomas of tuberculosis characteristically contain epithelioid macrophages, Langhans giant cells, and lymphocytes. The centers of tuberculous granulomas often have characteristic caseation (“cheese-like”) necrosis; organisms may or may not be seen with acid-fast staining. The demonstration of characteristic caseating granulomas on a tissue section in the appropriate clinical and epidemiologic circumstances strongly supports a diagnosis of active tuberculosis, but it is not pathognomonic; culture is required to establish a laboratory diagnosis
The sarcoid granuloma is a focal, chronic inflammatory reaction formed by the accumulation of epithelial cells, monocytes, lymphocytes, macrophages, and fibroblasts. Multinucleated giant cells are frequently found among the epithelioid cells within the granuloma follicle and often have cytoplasmic inclusions, such as asteroid bodies, Schaumann bodies, and birefringent crystalline particles (calcium oxalate and other calcium salts). Most sarcoid granulomas gradually resolve and leave few or no residual manifestations of previous inflammation. Small amounts of central fibrinoid necrosis may be seen, but large amounts of necrosis suggest an alternate diagnosis or necrotizing sarcoid granulomatosis.]
What are the accessory breathing muscles?
- Sternocleidomastoid
- Pectoralis major and minor
- Serratus posterior
- Scalenes (anterior, medius, and posterior)
[Also the Inferior fibers of serratus anterior and latissimus dorsi]
What is the most common type of lung cancer?
Adenocarcinoma
[UpToDate: Adenocarcinoma is the most common type of lung cancer in contemporary series, accounting for approximately one-half of lung cancer cases. The increased incidence of adenocarcinoma is thought to be due to the introduction of low-tar filter cigarettes in the 1960s, although such causality is unproven. The World Health Organization (WHO) classification emphasizes that tissue specimens should be managed not only for pathologic diagnosis, but also to preserve tissue for molecular studies, which may have important treatment implications such as use of targeted therapies for certain subsets of patients. Patients with advanced lung adenocarcinoma and other non-small carcinomas not otherwise specified should have their tumors tested for the presence of a driver mutation (eg, mutated epidermal growth factor receptor, ALK translocation, and increasingly, other mutations).]
What percent of lung carcinoid tumors have metastases at the time of diagnosis?
5%
[Lung carcinoid tumors are uncommon and tend to grow slower than other types of lung cancers. They are made up of special kinds of cells called neuroendocrine cells.]
[UpToDate: Bronchial neuroendocrine (carcinoid) tumors (NETs) are an uncommon group of pulmonary neoplasms that are characterized by neuroendocrine differentiation and relatively indolent clinical behavior.
Like neuroendocrine tumors at other body sites, bronchial NETs are thought to derive from peptide- and amine-producing neuroendocrine cells. NETs can arise at a number of sites throughout the body, including the thymus, lung, gastrointestinal (GI) tract, and ovary. The GI tract is the most frequently involved site, while lung is the second most common.]
This is a neuroendocrine lung tumor that usually occurs centrally
Carcinoid tumor
[UpToDate: Bronchial neuroendocrine (carcinoid) tumors are a rare group of pulmonary neoplasms that are often characterized by indolent clinical behavior. Like other carcinoid tumors, bronchial carcinoids are thought to derive from peptide- and amine-producing neuroendocrine cells. Bronchial neuroendocrine tumors (NETs) can arise at a number of sites throughout the body, including the thymus, lung, gastrointestinal (GI) tract, and ovary. The GI tract is the most frequently involved site for NETs, while lung is the second most common.
Bronchial NETs are characterized by strikingly heterogeneous pathological features and clinical behavior. At one end of the spectrum are typical carcinoid tumors, which are well differentiated, low-grade slowly-growing neoplasms that seldom metastasize to extrathoracic structures. At the other end of the spectrum are the poorly-differentiated and high-grade neuroendocrine carcinomas, as typified by small-cell lung cancer (SCLC), which behaves aggressively, with rapid tumor growth and early distant dissemination. The biologic behavior of atypical carcinoid tumors, which are of intermediate grade and differentiation, is intermediate between typical carcinoid tumors and SCLC. The terms “typical” and “atypical” carcinoid of the lung correspond roughly to the terms “low-grade” and “intermediate-grade,” which are used more commonly in extrathoracic NETs.
Multifocal disease is not uncommon in patients with low-grade bronchial NETs. An extreme example is diffuse idiopathic pulmonary neuroendocrine cell hyperplasia (DIPNECH), a benign condition characterized by diffuse hyperplasia of pulmonary neuroendocrine cells and formation of multiple carcinoid tumorlets.]
What kind of pleural fluid collection has:
- >1,000 WBCs (>50,000 is highly specific)
- pH <7.30
- Pleural fluid protein to serum ratio >0.5
- Pleural fluid LDH to serum ration >0.6?
Empyema
[UpToDate: Pleural fluid LDH levels above 1000 IU/L (with upper limit of normal for serum of 200 IU/L) are characteristically found in empyema, rheumatoid pleurisy, and pleural paragonimiasis, and are sometimes observed with malignancy.
Increased acid production by pleural fluid cells and bacteria (empyema) cause pleural fluid acidosis (pH <7.30).
The total pleural fluid nucleated cell count is virtually never diagnostic. There are, however, some settings in which the count may be helpful. Counts above 50,000/microL are usually found only in complicated parapneumonic effusions, including empyema.]
What tumor invades the apex of the chest wall and results in patients having Horner’s syndrome?
Pancoast tumor
[Horner syndrome results from invasion of the sympathetic chain and is characterized by ptosis, miosis, and anhidrosis, and/or ulnar nerve symptoms.]
How is a diagnosis of a lung hamartoma made?
CT with a repeat CT in 6 months to confirm the diagnosis
[UpToDate: Hamartomas cause approximately 10% of benign nodules found in the lung. They typically present in middle age, grow slowly over years, and are histologically heterogeneous. Cartilage (with scattered calcification), fat, muscle, myxomatous tissue, and fibroblastic tissue may all exist. The characteristic appearance of a hamartoma on a chest radiograph is a SPN with “popcorn” calcification, although this pattern is observed in less than 10% of cases. High-resolution CT scanning of the lesion is particularly useful because it may demonstrate focal areas of fat, or calcification alternating with fat, which are virtually diagnostic of a hamartoma. Less common benign neoplasms such as fibromas, leiomyomas, hemangiomas, amyloidoma, and pneumocytoma do not have characteristic features on imaging.]
What is the treatment for a mediastinal teratoma?
- Resection
- Possible chemotherapy
[UpToDate: Treatment of mature mediastinal teratomas is surgical excision, and this is almost always curative. Resection generally is through a median sternotomy or posterolateral thoracotomy, depending upon the location of the tumor, although thoracoscopic resection is occasionally possible.
Subtotal resection with relief of compressive symptoms is performed if benign teratomas cannot be excised completely without endangering surrounding vital structures. If only subtotal resection is possible, it is not clear that additional treatment with chemotherapy or radiotherapy offers any benefit. Mature teratomas are relatively insensitive to both chemotherapy and radiation therapy (RT).]
Whiteout on chest xray with a midline shift away from the whiteout is most likely due to what?
Effusion (Place chest tube)
What is the most common anterior mediastinal mass in adults?
Thymoma
[UpToDate: The thymus arises from the third pharyngeal pouch at the sixth week of gestation. After the first year of life, the thymus decreases in size and mass until middle age. The relationship of the thymus to other mediastinal structures is shown in the figure. Thymic lesions account for approximately one-half of all anterior mediastinal masses, and can include a range of benign and malignant histologies.
Thymomas account for about 20% of mediastinal neoplasms. Most thymoma patients are between 40 and 60 years of age, and there is a similar incidence in men and women. There are no known risk factors, although there is a strong association with myasthenia gravis and other paraneoplastic syndromes.
Thymomas are associated with a variety of paraneoplastic syndromes. The most common is myasthenia gravis, which occurs in approximately 30% of patients with thymoma. Furthermore, some patients who are diagnosed with myasthenia gravis will be found to have a thymic mass on imaging. Evaluating patients with thymoma for the presence of myasthenia prior to pursuing treatment can be very important, because of the potential impact on a patient’s response to general anesthesia.
Patients with a thymic mass who have not been evaluated for myasthenia gravis should be tested for anti-acetylcholine receptor antibodies. Patients who test positive for these antibodies should be evaluated prior to undergoing anesthesia to determine if they have myasthenia gravis.]
What are the two preferred chemotherapy agents for stage II or higher non-small cell lung cancer?
Carboplatin and Taxol
[UpToDate: Patients with advanced NSCLC should have tumor assessed for the presence of a somatic driver mutation (eg, EGFR, ALK fusion oncogene). The choice of initial therapy (chemotherapy versus molecularly targeted agents) is guided by this information. This information is also useful in guiding subsequent therapy.
For patients whose tumor does not contain a driver mutation, we recommend combination therapy that incorporates a platinum (cisplatin, carboplatin) based doublet (Grade 1A). For patients with nonsquamous NSCLC, we suggest that initial treatment also include bevacizumab (Grade 2B). For patients in whom the increased toxicity or cost of bevacizumab is a significant issue, chemotherapy alone is a reasonable alternative.
- Combinations using cisplatin have a slightly higher response rate but inconsistent survival benefits compared with carboplatin-based regimens. For the majority of patients who will receive a chemotherapy doublet, we suggest using a carboplatin-based regimen (Grade 2B). However, a cisplatin-based regimen is a reasonable alternative in appropriate patients.
- We recommend that the duration of treatment with the initial doublet chemotherapy regimen be limited to four to six cycles (Grade 1A).
For patients with an objective response following the initial cycles of platinum based chemotherapy, we suggest that patients continue on maintenance therapy (Grade 2B). Options included single agent chemotherapy, bevacizumab, or targeted therapy with an epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor. An alternative approach might be close observation with initiation of second-line therapy at the earliest sign of progression for selected patients who are well informed about the risks and benefits of such approach.
For patients whose initial regimen included bevacizumab in addition to a chemotherapy doublet, the bevacizumab is generally continued in the absence of toxicity until there is evidence of progressive disease, without the addition of cytotoxic chemotherapy.
- For patients whose initial regimen did not include bevacizumab, and whose tumors do not contain a driver mutation, we suggest maintenance chemotherapy with single agent chemotherapy rather than an EGFR tyrosine kinase inhibitor (Grade 2C). For patients with non-squamous NSCLC who are treated with maintenance chemotherapy, we suggest pemetrexed (Grade 2C). Docetaxel and gemcitabine are appropriate alternatives, and the EGFR tyrosine kinase inhibitor erlotinib may also be an alternative in selected patients.
- For patients with squamous cell NSCLC who are treated with maintenance chemotherapy, we suggest either docetaxel or gemcitabine, rather than pemetrexed (Grade 2C).]
Arterio-venous malformations (AVMs) are connections between the pulmonary arteries and pulmonary veins and can be seen in association with which condition?
Osler-Weber-Rendu disease
[UpToDate: Hereditary hemorrhagic telangiectasia (HHT, Osler-Weber-Rendu syndrome), an autosomal dominant vascular disorder, has a variety of clinical manifestations. Among the most common are epistaxis, gastrointestinal bleeding, and iron deficiency anemia, along with characteristic mucocutaneous telangiectasia. In addition, arteriovenous malformations (AVMs) commonly occur in the pulmonary, hepatic, and cerebral circulations, demanding knowledge of the risks and benefits of screening and treatment of patients with these complications.]
When is surgery indicated for treatment of spontaneous pneumothorax?
- Recurrence
- If air leak lasts greater than 7 days
- Non-reexpansion of the lung
- High-risk profession (pilot, diver, mountain climber)
- Patient lives in a remote area
[UpToDate: We suggest a preventive intervention for patients experiencing their first PSP if they are undergoing VATS or tube thoracostomy as part of their initial management, or have a vocation in which recurrence of the pneumothorax is dangerous to the patient or others (eg, airplane pilot or deep sea diver). Otherwise, we prefer to forego preventive interventions until a patient experiences recurrent PSP.
Once it has been determined that a preventive procedure is required, we recommend VATS with pleurodesis, rather than tube thoracostomy with chemical pleurodesis (Grade 1B). This procedure reduces the recurrence rate to less than 5%.
For patients who are not operative candidates or who refuse VATS, we recommend tube thoracostomy with chemical pleurodesis, rather than tube thoracostomy drainage alone, once it has been determined that a preventive intervention is indicated (Grade 1A). This procedure reduces the recurrence rate to less than 25%.]
Which type(s) of bronchial adenoma is slow growing, can have 10-year survival with incomplete resection, and is treated with resection (XRT can provide good palliation if unresectable)?
Adenoid cystic adenoma
[UpToDate: Adenoid cystic carcinoma (ACC) was previously considered to be the most common form of malignant minor salivary gland tumor. Many of these cases subsequently have been reclassified as polymorphous low-grade adenocarcinoma (PLGA). ACC arises in both major and minor salivary glands. The tumor is locally aggressive, with recurrences often arising after many years.
Three basic growth patterns are commonly seen: tubular, cribriform, and solid. These patterns are often mixed. The biologic aggressiveness of ACC correlates with the amount of the solid component within the tumor. The solid areas generally contain cells with larger, more pleomorphic nuclei, increased mitotic activity, and often, foci of necrosis. A grading scheme attempts to integrate the varied histologic components: grade 1 tumors are composed entirely of tubules or cribriform areas, while the presence of a solid component defines higher-grade tumors. A 30% solid component serves as the breakpoint between grade 2 and 3 tumors.
In a study of 129 cases, clinical stage, solid growth pattern, and p53 expression were found by multivariate analysis to be the most important prognostic features in head and neck ACC. Increased proliferative activity has also been reported as an adverse prognostic factor. ACC frequently demonstrates bone and perineural invasion. As with other tumors that commonly invade perineural spaces, neural cell adhesion molecule (NCAM), nerve growth factor (NGF) and its receptor, and TrkA are commonly expressed in adenoid cystic carcinoma, and may provide the molecular basis underlying its behavior.
Surgical resection is the treatment of choice for malignant tracheal tumors whenever possible, given retrospective data suggesting improved disease outcomes and acceptable postoperative morbidity. Because of the lack of suitable replacement material, the suggested maximum resected length of trachea is 5 cm. Decisions on resectability are based on imaging studies and the expertise of the surgical team. Studies have suggested that between 50% and 70% of patients have resectable disease at diagnosis.
The superiority of surgery, with or without radiation, to radiation alone was suggested in a Netherlands database series in which 34 patients underwent surgical resection (24 of whom also received radiation) and 156 patients were treated with RT alone. The five-year survival among patients who underwent surgical resection was 53% versus 11% among those receiving RT alone. A retrospective analysis of adenoid cystic carcinoma (ACC) of the head and neck similarly noted that radiotherapy combined with surgery resulted in better local control and survival than treatment with radiation alone. A limitation in the interpretation of these retrospective studies is that the group of patients treated nonsurgically included those with unresectable disease and therefore a worse prognosis, which biases the results toward surgical treatment.]
Which test is needed for centrally located lung tumors?
Bronchoscopy
[to check for airway invasion]
[UpToDate: Bronchoscopy with endobronchial ultrasound (EBUS)-directed biopsy has emerged as the most common modality used for diagnosis and staging of suspected NSCLC due to its high diagnostic accuracy for accessing central primary tumors and most mediastinal lymph nodes. Furthermore, EBUS-directed biopsy in patients with mediastinal adenopathy on computed tomography (CT) scan may be performed quickly and reduce the time to establishing of treatment decisions. If initial tissue sampling provides inconclusive results or is insufficient for essential immunohistochemical or molecular characterization, a second biopsy procedure is required. The selection of a second biopsy procedure should favor modalities with a higher diagnostic yield (eg, surgical sampling). The selection of modality and procedures used for tissue biopsy of NSCLC are discussed separately. Although genetic and molecular microarray techniques of both tissue and peripheral blood have been studied as potential diagnostic tools designed to enhance the sensitivity of bronchoscopy for the diagnosis of lung cancer, further study is required before they can be recommended for routine use.]
Injury at what level of the thorax results in a right-sided chylothorax?
Below T5-T6
[UpToDate: Generally, the thoracic duct ascends from the cisterna chyli (sac at the lower end of the thoracic duct into which the intestinal and two lumbar lymphatic trunks drain), which lies just anterior to the first or second lumbar vertebra, and passes through the aortic hiatus of the diaphragm to enter the posterior mediastinum, although wide anatomic variation exists. The thoracic duct continues cephalad in a rightward position between the aorta and azygos vein until it reaches the approximate level of the fifth thoracic vertebra, where it crosses over the vertebral column behind the esophagus and continues in the left posterior mediastinum. The thoracic duct in this region is 2 to 3 mm in diameter and passes behind the aortic arch adjacent to the left side of the esophagus and behind the left subclavian artery. It then arches over the subclavian artery in the anterolateral superior mediastinum, descending to empty into the venous circulation in the region of the left jugular and subclavian veins.
In some patients, two thoracic ducts exist within the mediastinum, and occasionally a single thoracic duct may empty into right-sided venous structures.
The anatomy of the thoracic duct determines the location of the effusion seen with duct injury or obstruction. Because the thoracic duct crosses the mediastinum at the fifth thoracic vertebral body, lymphatic injury or obstruction below this level generally results in a right–sided pleural effusion. In contrast, disease above this level usually leads to a left-sided effusion.]
Lung adenocarcinoma usually occurs where?
Peripherally
[UpToDate: Adenocarcinoma is the most common type of lung cancer in contemporary series, accounting for approximately one-half of lung cancer cases. The increased incidence of adenocarcinoma is thought to be due to the introduction of low-tar filter cigarettes in the 1960s, although such causality is unproven. The World Health Organization (WHO) classification emphasizes that tissue specimens should be managed not only for pathologic diagnosis, but also to preserve tissue for molecular studies, which may have important treatment implications such as use of targeted therapies for certain subsets of patients. Patients with advanced lung adenocarcinoma and other non-small carcinomas not otherwise specified should have their tumors tested for the presence of a driver mutation (eg, mutated epidermal growth factor receptor, ALK translocation, and increasingly, other mutations).]
Do lung hamartomas require resection?
No
[UpToDate: Hamartomas cause approximately 10% of benign nodules found in the lung. They typically present in middle age, grow slowly over years, and are histologically heterogeneous. Cartilage (with scattered calcification), fat, muscle, myxomatous tissue, and fibroblastic tissue may all exist. The characteristic appearance of a hamartoma on a chest radiograph is a SPN with “popcorn” calcification, although this pattern is observed in less than 10% of cases. High-resolution CT scanning of the lesion is particularly useful because it may demonstrate focal areas of fat, or calcification alternating with fat, which are virtually diagnostic of a hamartoma. Less common benign neoplasms such as fibromas, leiomyomas, hemangiomas, amyloidoma, and pneumocytoma do not have characteristic features on imaging.]
Recurrent pleural effusions can be treated with what?
Mechanical pleurodesis (Talc pleurodesis for malignant pleural effusions)
[UpToDate: Patients who have symptoms due to recurrent or persistent pleural effusion despite therapy directed at the underlying cause are candidates for additional therapies. Asymptomatic patients do not require additional interventions.
Prior to proceeding with more invasive therapy, the underlying cause of the NMPE should be reconfirmed (with thoracoscopic pleural biopsy) to ensure that primary treatment has been appropriate; infectious causes, hepatic hydrothorax, and trapped lung should also be excluded.
We suggest talc pleurodesis or implanted pleural catheters and intermittent drainage for patients who have symptoms due to refractory nonmalignant pleural effusions (Grade 2C).
We suggest talc pleurodesis for patients who have symptoms due to refractory nonmalignant pleural effusions and in whom repeat therapeutic thoracenteses have become burdensome (Grade 2C). The greatest pleurodesis experience is with talc; however, this choice is controversial due to concerns about immediate and long-term side effects of talc. Pleurodesis, however, should only be performed in this setting after a multi-disciplinary discussion of the risks, benefits, and alternatives.]
What is the treatment for lung carcinoid tumors?
Resection
[Treat like cancer. Outcome closely linked to histology]
[UpToDate: For patients with either a typical or atypical resectable bronchial NET whose medical condition and pulmonary reserve will tolerate it, we recommend surgical resection and mediastinal lymph node sampling or dissection (Grade 1B). The presence of mediastinal lymph node metastases does not preclude cure.
For most patients, endobronchial resection is a suboptimal method of definitive treatment, and we suggest not pursuing this approach over definitive surgical resection (Grade 2C). Endobronchial laser resection is best reserved for palliative treatment of patients with central airway occlusion who are poor surgical candidates (eg, elderly, debilitated).
Although some disagree, we suggest not administering postoperative adjuvant therapy for most resected bronchial NETs even in the setting of positive lymph nodes (Grade 2C). Adjuvant platinum-based chemotherapy with or without radiation therapy (RT) is a reasonable option for patients with histologically aggressive-appearing stage III atypical bronchial NETs (ie, relatively high mitotic rate, extensive necrosis, etc.), although there is only limited evidence to support this.
RT is a reasonable option for atypical bronchial NETs if gross residual disease remains after surgery, although whether this improves outcomes is unproven.]
What is the most common early complication after tracheal surgery?
Laryngeal edema
[UpToDate: Evidence suggests that laryngeal inflammation and edema are detected after extubation in more than half of patients, although not every case is associated with significant symptomatology.
Following extubation, most patients complain of mild to moderate symptoms including sore throat, dysphonia, and dysphagia thought to be due to laryngeal inflammation from the ETT.
More severe symptoms include stridor (sometimes requiring reintubation), which may be due to coexistent impairment in vocal cord mobility. As an example, one prospective study, clinically significant laryngeal edema occurred in approximately 5-13% of patients and required reintubation in approximately 1%.
Laryngeal edema may be suspected prior to extubation or following extubation failure and may be supported by the presence of a negative cuff leak test.]
When is surgery indicated in a clotted hemothorax?
- Involvement of greater than 25% of lung
- Air-fluid levels are present
- Signs of infection
[surgery in 1st week to avoid peel]
[UpToDate: Hemothorax is treated with tube thoracostomy using a large (minimum 36 French) chest tube. Immediate bloody drainage of ≥20 mL/kg (approximately 1500 mL) is generally considered an indication for surgical thoracotomy. Shock and persistent, substantial bleeding (generally >3 mL/kg/hour) are additional indications. Vital signs, fluid resuscitation requirements, and concomitant injuries are considered when determining the need for thoracotomy.
In general, a pneumohemothorax is treated with drainage by tube thoracostomy. Small, clinically insignificant collections may be treated with needle aspiration or drainage, at the discretion of the trauma surgeon.]
Which pulmonary nodes are assessed by mediastinoscopy?
- Ipsilateral (N2)
- Contralateral (N3)
- Mediastinal nodes
[if mediastinal nodes are positive, the tumor is unresectable.]
[UpToDate: SCM can easily access pretracheal (1, 3), paratracheal (2R, 2L, 4R, 4L), anterior subcarinal (7) and occasionally hilar (10) nodes. It is not able to sample subaortic (5) or para-aortic (6), inferior (8, 9), posterior subcarinal (7), or lobar/interlobar (11 to 14) stations. Use of the video mediastinoscope can extend access to the posterior subcarinal nodes (station 7). SCM is best used to sample lymph nodes in these selected stations, particularly when other staging modalities have failed or are not available.]
What are the different TNM stages of lung cancer?
- Stage I: T1-2, N0, M0
- Stage IIa: T1, N1, M0
- Stage IIb: T2, N1, M0 or T3, N0, M0
- Stage IIIa: T1-3, N2, M0 or T3, N1, M0
- Stage IIIb: any T4 or N3 Stage IV: M1
Which stages of lung cancer are resectable?
Stage I, stage II, and possibly stage IIIa (T3,N1,M0)
[UpToDate: A patient with lung cancer may be “resectable” by virtue of having a surgically removable NSCLC, but may not be “operable” due to poor pulmonary function or comorbidities. Advances in surgical technique, the role of limited resection, and postoperative care may provide the opportunity for surgical resection in patients who previously might not have been considered candidates for aggressive treatment.
Patients with stage I or II NSCLC should be treated with complete surgical resection whenever possible. Postoperative adjuvant chemotherapy improves survival in patients with pathologic stage II disease and may have a role for patients with stage IB disease.
Patients with stage I or II disease who are not candidates for surgical resection or who refuse surgery may be candidates for nonsurgical local therapy. Radiation may be applied by stereotactic techniques or conventional methods. Radiofrequency ablation (RFA) and cryoablation are alternatives to radiation. Photodynamic therapy may also be useful as a primary treatment modality in carefully selected patients with superficial airway lesions.
For patients with pathologically proven stage III disease prior to definitive therapy, a combined modality approach using concurrent chemoradiotherapy is generally preferred. The role of surgery following chemoradiotherapy is an area of active investigation. Surgery may also retain a role for carefully selected patients with T3 or T4 lesions and negative mediastinal lymph nodes.]
How can one go about assessing enlarged Aorto-pulmonary (AP) window nodes?
Chamberlain procedure (anterior thoracotomy or parasternal mediastinotomy)
[Go through the left 2nd rib cartilage.]
[UpToDate: A left anterior mediastinotomy (Chamberlain procedure) is a surgical procedure that requires general anesthesia. The incision is made over the left second or third intercostal space to access lymph nodes in station 5. Due to lymphatic drainage patterns, cancers of the left upper lobe preferentially drain to this regions. However, this region are traditionally difficult to access and cannot be reached by minimally invasive techniques or by standard cervical mediastinoscopy.
A left anterior mediastinotomy is the traditional surgical procedure used to stage left-sided cancer when suspected nodes are located in station 5. It has the added advantage of accessing left upper lobe tumors for concurrent resection, if there is no evidence of nodal or distant disease.
Because it is often the only option when suspicious lymph nodes are identified in this region, there is a paucity of data regarding its diagnostic accuracy. Nonetheless, one meta-analysis of four small studies reported a sensitivity and negative predictive value of 71% and 91% respectively. No studies have directly compared its performance to ECM, VATS), or to endoscopic ultrasound-guided fine needle aspiration which can occasionally reach this region.]
What kind of pneumothorax occurs in temporal relation to menstruation and is caused by endometrial implants in the visceral lung pleura?
Catamenial pneumothorax
[UpToDate: Thoracic endometriosis should always be suspected in young women with catamenial or non-catamenial pneumothorax or hemothorax, who have a history of prior uterine surgical procedures or pelvic endometriosis (present in 65% to 84%). In such patients, the diagnostic and therapeutic approach is often performed simultaneously (eg, thorascopic biopsy, blebectomy, and pleurodesis).]
What is the treatment for the second phase of empyema (fibro-proliferative phase - 2nd week)?
- Chest tube
- Antibiotics
- Possible VATS deloculation
[UpToDate: In patients with a parapneumonic effusion or an empyema, an empiric, broad spectrum antibiotic that includes coverage for anaerobic organisms should be initiated promptly, because empyemas often harbor multiple species of bacteria, particularly anaerobes.
In patients with an uncomplicated parapneumonic effusion, one that is small to moderate in size, free flowing, and has a pH of 7.20 or greater, we recommend observation rather than placement of a chest tube for drainage (Grade 1B).
In patients with a large, loculated, or complicated parapneumonic effusion, we recommend prompt drainage of any remaining pleural fluid rather than observation (Grade 1B). For further drainage of the pleural space, we suggest tube thoracostomy rather than a more invasive procedure (eg, thoracoscopy, decortication) (Grade 2C). Computed tomography (CT) or ultrasound-guided placement of multiple tubes may be needed when pleural loculations prevent adequate drainage by a single tube. Video-assisted thoracoscopic surgery (VATS) with debridement may be preferred in patients with multiple loculations and a thick pleural peel.
When tube thoracostomy is used for initial drainage of an empyema, a chest CT scan should be obtained within 24 hours after chest tube placement to document appropriate placement of the tube and assess drainage. For patients with ongoing signs of infection (fever, leukocytosis, anorexia) or those who do not have good drainage of empyema fluid from a well-placed chest tube, we suggest intrapleural administration of a combination of tissue plasminogen activator (TPA) 10 mg and deoxyribonuclease (DNase) 5 mg, twice daily for three days rather than no intrapleural therapy or either agent alone (Grade 2B).
Continued signs of infection together with failure of adequate pleural drainage should prompt thoracoscopy or thoracotomy to lyse adhesions, fully drain the pleural space, and optimize chest tube placement. The choice between thoracoscopic debridement and decortication depends on several factors; those favoring decortication include more adhesions, greater visceral pleural thickness, and larger empyema cavity size.]
Do all thymomas require resection?
Yes
[UpToDate: Surgical management should include a complete resection of the thymus. The current standard of care is an open surgical approach via a median sternotomy. A minimally invasive (thoracoscopic or robotic) approach is not recommended except in the context of specialized centers with experience in these techniques.
The ability to completely resect a thymoma or thymic carcinoma is determined by the extent of tumor, including the degree of invasion and/or adhesion of the tumor to contiguous structures. The likelihood of long-term survival depends upon the completeness of surgical resection. Resection of the pericardium as well as accompanying lung parenchyma is sometimes required to achieve a complete resection with histologically negative margins.
An inflammatory fibrous reaction can mimic tumor invasion, and tumor may be adherent to adjacent structures without being invasive. In such cases, the surgeon should identify the site of adhesion on the resection specimen, so the pathologist can take careful sections from that area.
Extension of a tumor along one or both phrenic nerves can create a dilemma since division of the phrenic nerves may impair respiratory function. Preoperative pulmonary function studies should be obtained in all patients so that the extent of respiratory compromise following division of the phrenic nerve can be estimated.
Resection of one involved phrenic nerve, followed by dissection of the other nerve away from the surrounding tumor, is recommended if possible to reduce postoperative respiratory disability. However, if the patient has myasthenia gravis, resection of even one phrenic nerve may lead to significant respiratory problems.]
What is the treatment of post-intubation stenosis?
- Serial dilatation
- Bronchoscopic resection
- Laser ablation (if minor)
- Tracheal resection with end-to-end anastamosis if severe or if it keeps recurring
[UpToDate: Stenosis of the larynx and/or trachea is a late complication of ETT placement taking weeks to months to develop after the initial intubation. The risk of developing stenosis is increased in those with prolonged intubation >7 days, and is rare in those intubated for short periods (eg, <3 days). The incidence is unknown but reports range from 1-21%.
- Glottic (laryngeal) stenosis is thought to be due to pressure from the ETT itself, resulting in local tissue ischemia, inflammation, necrosis, and scarring. In support of this mechanism, inflammatory changes are seen in this region in as few as two to five days after intubation and most cases are located in the posterior glottis and interarytenoid regions, where the ETT rests.
- Tracheal stenosis is caused by high ETT cuff pressure. When the ETT cuff pressure exceeds the mean capillary pressure in the tracheal mucosa (approximately 20 cm H2O), obstruction of capillary blood flow causes ischemia, inflammation, and erosion of the mucosa. This leads to necrosis, destruction of the tracheal architecture, and scarring.
Patients who are extubated may develop subacute or progressive dyspnea and/or or stridor while those who remain intubated (usually tracheostomized may present with failure to wean from mechanical ventilation. Tracheal stenosis usually becomes symptomatic within five weeks after extubation, sometimes longer (eg, months), and symptoms may become progressive over time. Stenosis may remain occult in a sedentary or deconditioned individual who is physically inactive. Pulmonary function testing may demonstrate upper airway obstruction. If the patient remains intubated, a negative cuff leak test may support the diagnosis. Definitive diagnosis requires bronchoscopy or laryngoscopy, although emerging data suggests that spiral computed tomography (CT) with virtual bronchoscopy may be equally effective.
Tracheal stenosis may require endoscopic stenting, balloon dilations, laser resection, or an alternative endoscopic intervention. Rates of success with endoscopic procedures are variable. Mitomycin C, an antineoplastic agent has been used anecdotally to prevent tracheal restenosis, although randomized studies are lacking. Surgical resection is usually reserved for those with symptoms from extensive stenosis or those who fail endoscopic procedures. In contrast, stenotic lesions that involve the larynx are typically less amenable to endoscopic procedures and subspecialty consultation is advised.
More rarely, an obstructive fibrinous tracheal pseudomembrane may cause tracheal obstruction and be responsible for extubation failure. In such cases, fiberoptic bronchoscopy reveals a thick, circular, rubber-like membrane adhering to the tracheal wall at the site of the endotracheal tube cuff. Rigid bronchoscopy is usually required for the removal of the pseudomembrane.]
What is the single best test for M status of lung cancer?
PET scan
What is the treatment for a pericardial cyst?
Leave it alone (benign)
[UpToDate: Pericardial cysts occur with an incidence of 1 in 100,000 patients. Seventy percent arise in the right cardiophrenic angle. Symptoms can include shortness of breath, right heart failure secondary to compression, infection, and bleeding.
Asymptomatic pericardial cysts can be observed, but resection may be needed if the diagnosis is not completely established by imaging. Simple drainage is generally not recommended because these cysts typically recur without complete resection.]
Tracheo-innominate artery fistula can occur after what procedure?
Tracheostomy
[Can cause rapid exsanguination]
[UpToDate: Massive hemorrhage due to a tracheoarterial fistula is the most devastating complication. In several studies, the incidence of a tracheoarterial fistula was less than 1% with both short-term and long-term tracheostomies.]
Which lung cancer can look like pneumonia, grows along alveolar walls, and is multifocal?
Bronchoalveolar cancer
[UpToDate: Bronchioloalveolar carcinoma (BAC) can have a highly variable clinical presentation, which ranges from a small solitary nodule or limited number of nodules, to more extensive miliary disease, or diffuse parenchymal infiltrates that are similar in appearance to a bacterial pneumonia.
When disease is more extensive, BAC patients can present with lobar consolidation that resembles bacterial pneumonia. CT scans typically show air bronchograms or even the CT angiogram sign, which is observed when the massive accumulation of mucus in the airspaces delineates the nearby vasculature. By the new classification, these are most commonly mucinous adenocarcinomas. The diagnosis of BAC may not be considered until the clinical symptoms and radiographic abnormalities fail to respond to antibacterial treatment. Unfortunately, this so-called “pneumonic” form of BAC has been associated with a particularly poor prognosis.]
What types of mediastinal masses are located in the posterior mediastinum?
- Enteric cysts
- Neurogenic tumors
- Lymphoma
[UpToDate: Neurogenic tumors represent more than 60% of posterior mediastinal masses. These lesions are classified based upon their neural cell of origin.
Schwannomas and neurofibromas are benign lesions that arise from the intercostals nerve sheath and make up 90% of adult neurogenic tumors.
Neuroblastomas and ganglioneuroblastomas are malignant tumors that occur most commonly in children and originate from the sympathetic ganglia.
Ganglioneuromas are benign lesions that arise from the sympathetic ganglia, and are most common in young adults. Lesions that arise from para-ganglionic cells include pheochromocytomas and paragangliomas.
Some neurogenic tumors are “dumbbell shaped” and arise near intervertebral foramen, and have a posterior mediastinal and intraspinal component. Resection usually requires a combined approach with neurosurgery and thoracic surgery.]
What percent of symptomatic mediastinal masses are malignant?
50%
[UpToDate: Patients with mediastinal masses can present in a variety of ways. A mediastinal mass is often an incidental diagnosis when patients undergo an evaluation for an unrelated condition or symptom. In some cases, patients present with complaints secondary to local mass effect on adjacent structures, such as respiratory symptoms due to airway compression or swelling due to compression of vascular structures. Other patients develop systemic symptoms that result from the mediastinal mass, which is discovered on subsequent work-up.
Benign or malignant mediastinal masses can develop from structures that normally are in the mediastinum or that pass through the mediastinum during development, as well as from metastases of malignancies that arise elsewhere in the body. A combination of clinical factors and imaging features often narrow the differential diagnosis when a mediastinal mass is detected. In some instances, the clinical and imaging features can be enough to guide therapy, which often includes surgical resection that provides a definitive diagnosis. Blood tumor markers can sometimes also support a specific diagnosis. In other cases, obtaining tissue via biopsy can be necessary to confirm a clinical suspicion prior to proceeding with therapy.]
What is the most common malignant chest wall tumor?
Chondrosarcoma
[UpToDate: Chondrosarcoma is the most common malignant chest wall tumor. It is located on the anterior chest wall (costochondral arches or sternum) and can arise from a degenerated chondroma. Presentation is usually as a slowly growing painful mass with a hard, fixed chest wall lesion; 10% of patients have lung metastases at presentation. Wide excision is recommended because of an increased risk of recurrence and metastasis following incomplete resection. Radiation therapy is recommended for unresectable or incompletely resected tumors. Five-year survival rates are between 70% and 90%.]
What is the treatment for laryngeal edema following tracheal surgery?
- Reintubation
- Racemic epinephrine
- Steroids
[UpToDate: We believe that the risk for post-extubation stridor is more important than the number of doses administered when deciding whether giving glucocorticoids prior to extubation may be beneficial. This is supported by a trial that randomly assigned 71 patients with a cuff leak of less than 24% of the tidal volume administered by the ventilator to receive either a saline placebo or a single dose of 40 mg of methylprednisolone four hours prior to extubation. The group that received the methylprednisolone had significantly decreased rates of post-extubation stridor (16% vs 39%) and reintubation (8% vs 30%) than the group that received the placebo.
We suggest that patients whose extubation is delayed due to a reduced cuff leak receive a short course of glucocorticoid therapy before extubation. Methylprednisolone (20 mg) administered every four hours for a total of four doses prior to extubation is an acceptable regimen. Alternatively, a single dose of 40 mg of methylprednisolone administered four hours prior to extubation may be used.
We limit glucocorticoid therapy to those patients who have a reduced cuff leak, since the overall incidence of postextubation laryngeal edema requiring reintubation is low (<5%). We believe this approach focuses therapy on those who are most likely to benefit and avoids unnecessarily prolonging mechanical ventilation for glucocorticoid therapy.]
What measure can be taken to avoid a tracheo-innominate artery fistula when performing a tracheostomy?
Keep tracheostomy above 3rd tracheal ring
[UpToDate: Massive hemorrhage due to a tracheoarterial fistula is the most devastating complication. Tracheoarterial fistula (most often a tracheoinnominate artery fistula) was more common in the past from low-positioned tracheostomy tubes and is now rarely encountered with several studies reporting an incidence of less than 1% with both short-term and long-term tracheostomies.
The development of a tracheoarterial fistula is a life-threatening complication with a reported survival of 14%. Tracheoarterial fistulas are due to erosion from the tube tip or cuff into the anterior wall of the trachea resulting in a fistulous communication with the innominate artery as it passes anteriorly across the trachea. Patients may develop a “sentinel” bleed followed by massive hemoptysis. Diagnosis is dependent upon a high index of suspicion and when suspected, immediate action should be undertaken to stop the bleeding since diagnostic modalities such as angiography or bronchoscopy may lead to delay and death.]
What percent of patients with myasthenia gravis have a thymoma?
10%
[50% of patients with thymomas have myasthenia gravis.]
[UpToDate: Myasthenia gravis is an autoimmune disorder caused by interference with acetylcholine receptors of voluntary muscle at the neuromuscular junction. Common symptoms include diplopia, ptosis, dysphagia, weakness, and fatigue.
Up to one-half of patients with thymoma have symptoms consistent with myasthenia gravis. Myasthenia gravis is common with all types of thymoma, but is rare in thymic carcinoma. Men and women are equally affected.
Patients with thymoma and myasthenia gravis usually present with less advanced disease than those without myasthenia gravis, possibly because neuromuscular symptoms may lead to an earlier diagnosis. In patients with thymoma and myasthenia gravis, thymectomy usually results in an attenuation of the severity of myasthenia gravis, although some symptoms persist in most patients.
Patients who have detectable antibodies to the acetylcholine receptor (AChR) or to the muscle-specific receptor tyrosine kinase (MuSK) are considered to have seropositive myasthenia gravis, while those lacking both AChR and MuSK antibodies on standard assays are considered to have seronegative myasthenia. About half of patients with purely ocular myasthenia are seropositive, compared with approximately 90% of those with generalized disease. Another important consideration is that about 10-15% of patients with myasthenia gravis have an underlying thymoma.]
Which cell type is responsible for surfactant production in the lungs?
Type 2 pneumocytes
What is the 5-year survival rate of lung cancer following resection for cure?
30%
[UpToDate: The most important prognostic factor in patients with SCLC is the extent of disease (stage) at presentation. For patients with limited stage disease, median survivals range from 15-20 months, and the reported five-year survival rate is 10-13%. In contrast, for patients with extended stage disease, the median survival is 8-13 months, and the five-year survival rate is 1-2%.]
[National Cancer Institute’s SEER database:
NSCLC - This data is based on people who were diagnosed with NSCLC between 1998 and 2000. Although they are based on people diagnosed several years ago, they are the most recent rates published for the current AJCC staging system.
Stage IA NSCLC is about 49%
Stage IB NSCLC is about 45%.
Stage IIA NSCLC is about 30%
Stage IIB NSCLC is about 31%
Stage IIIA NSCLC is about 14%
Stage IIIB NSCLC is about 5%
Stage IV NSCLC is about 1%
SCLC - This data is based on people who were diagnosed with SCLC between 1988 and 2001. These survival rates are based on the TNM staging system in use at the time, which has since been modified slightly for the latest version. Because of this, the survival numbers may be slightly different for the latest staging system. 5-year relative survival rate:
Stage I SCLC is about 31%
Stage II SCLC is about 19%
Stage III SCLC is about 8%
Stage IV SCLC is about 2%]
What percent of lung coin lesions are malignant?
- Overall: 10%
- Age less than 50: <5% malignant
- Age greater than 50: >50% malignant
[UpToDate: Clinical features associated with an increased probability of malignancy include advanced patient age and underlying risk factors. However, young age and the absence of risk factors do not preclude a diagnosis of malignancy.
The probability of malignancy rises with increasing patient age. One study reported a higher frequency of malignant nodules in patients >50 years of age compared with patients
- 35 to 39 years: 3%
- 40 to 49 years: 15%
- 50 to 59: 43%
- ≥60 years: >50%
Risk factors – The probability of malignancy is always higher when a nodule occurs in a patient with a history of smoking, especially current smokers, because of the strong association between cigarette smoking and lung cancer. Other risk factors for lung cancer including family history, female sex, emphysema, prior malignancy, and asbestos exposure should also be considered when evaluating a patient with a nodule.]
What vessel runs along the right side of the thorax, crosses the midline at T4-5, and dumps into the left subclavian vein at the junction with the internal jugular vein?
Thoracic duct
What percent of patients with thymomas have myasthenia gravis?
50%
[10% of patients with myasthenia gravis have a thymoma.]
[UpToDate: Myasthenia gravis is an autoimmune disorder caused by interference with acetylcholine receptors of voluntary muscle at the neuromuscular junction. Common symptoms include diplopia, ptosis, dysphagia, weakness, and fatigue.
Up to one-half of patients with thymoma have symptoms consistent with myasthenia gravis. Myasthenia gravis is common with all types of thymoma, but is rare in thymic carcinoma. Men and women are equally affected.
Patients with thymoma and myasthenia gravis usually present with less advanced disease than those without myasthenia gravis, possibly because neuromuscular symptoms may lead to an earlier diagnosis. In patients with thymoma and myasthenia gravis, thymectomy usually results in an attenuation of the severity of myasthenia gravis, although some symptoms persist in most patients.
Patients who have detectable antibodies to the acetylcholine receptor (AChR) or to the muscle-specific receptor tyrosine kinase (MuSK) are considered to have seropositive myasthenia gravis, while those lacking both AChR and MuSK antibodies on standard assays are considered to have seronegative myasthenia. About half of patients with purely ocular myasthenia are seropositive, compared with approximately 90% of those with generalized disease. Another important consideration is that about 10-15% of patients with myasthenia gravis have an underlying thymoma.]
Which type(s) of bronchial adenoma(s) grow slowly and do not metastasize?
- Mucoepidermoid adenomas
- Mucous gland adenomas
[Treatment is resection.]
[UpToDate: Mucoepidermoid carcinoma (MEC) is the most common malignant salivary gland tumor in adults and children. It consists of a mixture of mucin-producing columnar cells, epidermoid (squamous) cells, and polygonal intermediate cells.
While tumor stage is the most important prognostic feature for mucoepidermoid carcinoma, histologic grading has prognostic significance. Low-grade lesions are typically cystic; higher grade lesions become progressively more solid in growth and more difficult to classify correctly.
The WHO system assigns points to individual histologic features, which contribute to a final score. The Armed Forces Institute of Pathology system separates patients into three groups; low-grade tumors have scores of 0-4 points, intermediate-grade tumors 5-6 points, and high-grade mucoepidermoid carcinoma ≥7 points. In one study, there were no locoregional recurrences or distant metastases among patients with low-grade MEC after at least three years of follow-up. In contrast, 45% of patients with high-grade and 67% with intermediate-grade MEC experienced a recurrence or metastases.
In addition to tumor grade, age greater than 40 years, tumor fixation, and T and N stages were individually found to be independent prognostic features. Most reports show that mucoepidermoid carcinomas arising in the submandibular gland tend to behave aggressively, regardless of grade. In contrast, mucoepidermoid carcinoma arising in the pediatric age group tends to have a favorable prognosis.
A translocation involving (11;19)(q21;p13), which produces a unique fusion product, MECT1-MAML2, occurs commonly in mucoepidermoid carcinoma and may be prognostically favorable. Epidermal growth factor receptor (EGFR) is overexpressed in about two-thirds of cases, in contrast to human epidermal growth factor receptor 2 (HER2), which is expressed in less than 5%. Herceptin, a monoclonal antibody that targets HER2 overexpressing cells, appears to have low activity, even among HER2+ cases of salivary gland tumor.]
What percent of patients with thymomas are symptomatic?
50%
[UpToDate: Thymomas and thymic carcinomas typically present in one of three major ways:
- As an incidental finding identified on imaging in an asymptomatic patient.
- Because of local (thoracic) symptoms
- Due to symptoms from a paraneoplastic syndrome.]
Arterio-venous malformations (AVMs) are connections between the pulmonary arteries and pulmonary veins and usually occur where in the lungs?
Lower lobes
[UpToDate: Pulmonary arteriovenous malformations (AVMs) are abnormal connections between pulmonary arteries and pulmonary veins. They allow blood to bypass the pulmonary capillaries, thus creating an extracardiac right-to-left shunt. Radiographically, pulmonary AVMs appear as round, oval, or scalloped homogeneous nodules or masses with feeding arteries and draining veins. They are most common in the lower lobes and in the periphery of the lung. It is important to measure the diameter of the feeding artery, since embolization of the arteriovenous malformation is possible only if the diameter exceeds 3 mm.]
What is the treatment for a non-seminoma mediastinal germ cell tumor?
- Chemotherapy (cisplatin, bleomycin, VP-16)
- Surgery for residual disease
[UpToDate: For patients with a mediastinal nonseminomatous GCT, we recommend four cycles of chemotherapy as the initial therapy, rather than surgery or RT (Grade 1A). We suggest VIP rather than BEP because of the increased risks of bleomycin pulmonary toxicity should surgery eventually be required.
For patients with a residual mediastinal mass following initial chemotherapy, we recommend complete surgical resection if technically feasible (Grade 1A). If viable malignancy is identified, two additional cycles of VIP chemotherapy should be given.]
What kind of pleural fluid has <1,000 WBC, a pH of 7.45-7.55, a pleural fluid protein to serum ratio <0.5, and a pleural fluid LDH to serum ratio <0.6?
Transudative pleural fluid
[UpToDate: Transudates result from imbalances in hydrostatic and oncotic pressures in the chest, as occur with CHF and nephrosis, or conditions external to the pleural space. Examples of the latter include movement of fluid from the peritoneal, cerebrospinal, or retroperitoneal spaces, or from iatrogenic causes, such as crystalloid infusion through a central venous catheter that has migrated into the mediastinum or pleural space. Nevertheless, transudates have a limited number of diagnostic possibilities that can usually be discerned from the patient’s clinical presentation.
According to the traditional Light’s Criteria Rule, if at least one of the following three criteria (ie, component tests of the rule) is fulfilled, the fluid is defined as an exudate:
- Pleural fluid protein/serum protein ratio greater than 0.5, or
- Pleural fluid LDH/serum LDH ratio greater than 0.6, or
- Pleural fluid LDH greater than two-thirds the upper limits of the laboratory’s normal serum LDH]
Where do lung abscesses usually occur?
Superior segment of the right lower lobe
[UpToDate: Most patients with lung abscesses, and nearly all with lung abscesses due to anaerobic bacteria, present with indolent symptoms that evolve over a period of weeks or months.
Anaerobic infection: The characteristic features suggest pulmonary infection, including fever, cough, and sputum production. Evidence of chronic systemic disease is usually present, with night sweats, weight loss, and anemia. Patients may seek medical attention for these systemic symptoms, hemoptysis, or pleurisy. Nearly all patients have fever, but virtually none have shaking chills or true rigors. Most patients are aware of putrid or sour-tasting sputum. Lung abscesses due to S. milleri behave like anaerobic infections but do not have putrid sputum unless the organism occurs in a mixed infection including anaerobes.
Typical findings on physical examination are gingival crevice disease, the stigma of associated conditions that compromise consciousness or cause dysphagia, fever, and abnormal lung sounds reflecting a pleural effusion and/or parenchymal disease. Chest radiographs usually show infiltrates with a cavity, frequently in a segment of the lung that is dependent in the recumbent position (eg, the superior segment of a lower lobe or a posterior segment of the upper lobes). The approach should include evaluation of the expectorated secretions for evidence of putrid odor.
Although the majority of lung abscesses are caused by anaerobic bacteria, aerobic bacteria such as microaerophilic streptococci (eg, S. milleri), Staphylococcus aureus, and Klebsiella pneumoniae may also cause lung abscesses.]
What is the most common mediastinal neurogenic tumor?
Neurolemmoma (Schwannoma)
[UpToDate: Neurogenic tumors of the mediastinum represent 19-39% of all mediastinal tumors and develop from mediastinal peripheral nerves, sympathetic and parasympathetic ganglia, and embryonic remnants of the neural tube. They are most frequent in the posterior compartment of the mediastinum, where they can cause neurologic symptoms by compression
A variety of benign and malignant tumors of peripheral nerve origin can occur in the mediastinum, among which benign schwannoma (neurilemmoma) is the most common. Mediastinal benign schwannoma originates from Schwann cells and affects patients of both sexes predominantly in the third and fourth decade of life. These tumors can be multiple in patients with neurofibromatosis.]
Spontaneous pneumothorax usually occurs on which side?
Right side
[Note: Unable to corroborate this.]
What percent of lung cancer is small cell carcinoma?
20%
[It is neuroendocrine in origin.]
[UpToDate: Small cell lung cancer (SCLC) is a neuroendocrine tumor that represents about 15% of all lung cancers. SCLC occurs predominantly in smokers.
SCLC is distinguished clinically from most types of non-small cell lung cancer (NSCLC) by its rapid doubling time, high growth fraction, and the early development of metastases. Large cell neuroendocrine carcinoma, a rare form of lung cancer, and extrapulmonary small cell carcinomas are generally treated with the same chemotherapy regimens used for SCLC.
SCLC usually presents with disseminated disease, and treatment strategies have focused on systemic therapy. Although SCLC is highly responsive to both chemotherapy and radiotherapy (RT), it commonly relapses within months despite treatment.]
Massive hemoptysis is usually the result of bleeding from where?
High-pressure bronchial arteries
[UpToDate: Before assuming that the source of bleeding is the lower respiratory tract, the possibility that the blood may be coming from a non-pulmonary source, such as the upper airway or the gastrointestinal tract, should be considered. This distinction can be difficult and may require an otolaryngological or gastrointestinal evaluation. Characteristics of the expectorated material that suggest that a gastrointestinal source is unlikely include an alkaline pH, foaminess, and/or the presence of pus.
There are numerous causes of bleeding from the lower respiratory tract. Three etiologies accounted for 90% of the cases of massive hemoptysis through the 1960s: tuberculosis, bronchiectasis, and lung abscess. Each of these causes has since decreased in frequency, although other etiologies have increased. There are no more recent large series examining the prevalence of the causes of massive hemoptysis in general hospital settings.
Massive hemoptysis due to active TB can occur in the setting of cavitary or noncavitary disease. Most patients have sputum smears that stain positive for acid-fast bacilli. The cause of the bleeding is usually bronchiolar ulceration with necrosis of adjacent blood vessels. This type of bleeding usually is from the bronchial arterial circulation. Less often, active TB may cause sudden rupture of a Rasmussen’s aneurysm. This is an aneurysm of the pulmonary artery that slowly expands because of inflammatory erosion of the external vessel wall until it bursts. There is some uncertainty about whether similar aneurysms can also arise from bronchial arteries.]
Empyema is usually secondary to what?
Pneumonia and subsequent parapneumonic effusion (staph, strep)
[UpToDate: Parapneumonic effusions are pleural effusions that form in the pleural space adjacent to a bacterial pneumonia. They are found in at least 40% of bacterial pneumonias. The usual parapneumonic effusion is small and resolves with appropriate antibiotic therapy. However, if bacteria invade the pleural space, a complicated parapneumonic effusion or empyema may result, which will require antibiotic therapy plus additional interventions. Infected pleural effusions can also rarely develop without the presence of an adjacent pneumonia.]
Lung squamous cell carcinoma usually occurs where?
Centrally
[UpToDate: Squamous cell carcinoma was the most frequent histologic type of lung tumor in nearly all studies done prior to the mid-1980s. Now, adenocarcinoma is more common than squamous cell carcinoma, particularly in women.
The diagnosis of squamous cell carcinoma is predicated upon the presence of keratin production by tumor cells and/or intercellular desmosomes (referred to as “intercellular bridges”), or by immunohistochemistry consistent with squamous cell carcinoma (ie, expression of p40, p63, CK5, or CK5/6, desmoglein). While variants of squamous cell carcinoma in the 2004 World Health Organization (WHO) classification system included papillary, clear cell, small cell, and basaloid carcinoma, these have since been replaced with the categories of non-keratinizing, keratinizing, and basaloid subtypes, with clear cell change now regarded as a cytologic feature. Tumors are non-keratinizing if there is no keratinization, keratinizing if any keratinization is present, and basaloid if basaloid features comprise more than 50% of the tumor. For tumors that are non-keratinizing, immunohistochemistry is required to distinguish between squamous carcinoma, solid type adenocarcinoma, and large cell carcinoma with a null phenotype. For such tumors, diffuse positive staining with a squamous marker should be present to confirm a squamous phenotype.
Most squamous cell carcinomas (60-80%) arise in the proximal portions of the tracheobronchial tree through a squamous metaplasia-dysplasia-carcinoma in situ sequence (squamous carcinoma in situ), although they are increasingly presenting as peripheral lesions. Central and peripheral squamous cell carcinomas may show extensive central necrosis with resulting cavitation. A small subset of central, well differentiated squamous cell carcinomas occur as exophytic, endobronchial, papillary lesions. Patients with this unusual variant of squamous cell carcinoma typically present with persistent cough, recurrent hemoptysis, or relapsing pulmonary infections due to airway obstruction. Most patients with exophytic endobronchial squamous cell carcinoma have low-stage disease at diagnosis, with a correspondingly good prognosis; five-year survival rates are greater than 60%.]
What is the most common germ cell tumor in the mediastinum?
Teratoma
[UpToDate: Benign teratomas comprise two-thirds of all mediastinal germ cell tumors and have an equal gender distribution. These tumors are often found incidentally but can cause pain or other symptoms due to compression of adjacent structures. There have been reports of paraneoplastic encephalitis due to anti-N-methyl-D-aspartate receptor antibodies in patients with benign ovarian or mediastinal teratomas. Alpha-fetoprotein is normal with teratoma. Teratomas can contain elements of fat, fluid, and bone, and, if the imaging is convincing that teratoma is the most likely diagnosis, biopsy is not necessary. The treatment is surgical resection, which should be undertaken when a teratoma is identified to definitively confirm the diagnosis and prevent the development of local symptoms due to tumor growth. Teratomas have the potential for malignant degeneration and can be very aggressive; their prognosis is generally very poor.]
What is the treatment for myasthenia gravis?
- Anticholinesterase inhibitors (neostigmine)
- Steroids
- Plasmapheresis
- Thymectomy
[UpToDate: The four basic therapies for myasthenia gravis (MG) include symptomatic treatments (anticholinesterase agents), chronic immunotherapies (glucocorticoids and other immunosuppressive drugs), rapid immunotherapies (plasma exchange and intravenous immune globulin [IVIG]), and thymectomy. The time of onset of clinical effect of each of these therapies for MG varies considerably.
We recommend treatment with acetylcholinesterase inhibitors as the first line of treatment for symptomatic MG (Grade 1B). Pyridostigmine is the most widely used choice. For adults and older adolescents, a typical starting dose is 30 mg three times a day. For children and younger adolescents, the initial dose is 0.5 to 1 mg/kg every four to six hours. The dose of pyridostigmine is then titrated by its effect.
Most patients with MG will need some form of immunotherapy in addition to pyridostigmine. We recommend adding immunotherapy for patients who remain significantly symptomatic on pyridostigmine, or who become symptomatic after a temporary response to pyridostigmine (Grade 1B). Glucocorticoids, azathioprine, mycophenolate mofetil, and cyclosporine are the most widely used. This approach is discussed in greater detail separately.
Plasmapheresis (with plasma exchange) and IVIG work quickly but have a short duration of action. In addition to treatment of myasthenic crisis, these rapid therapies are useful in presurgical treatment of moderate to severe MG. They are also used as a “bridge” when initiating slower acting immunotherapies, and as periodic adjuvants to other immunotherapeutic medications in refractory MG.
We suggest thymectomy for patients without thymoma below age 60 years who have generalized MG and either have AChR antibodies, or have no detectable AChR or MuSK antibodies (ie, seronegative MG) (Grade 2C). We suggest not performing thymectomy in patients with MuSK antibody-associated MG without thymoma (Grade 2C).
Attempted surgical excision is the treatment of choice for nonmetastatic thymoma and thymic carcinoma.]
Which type(s) of bronchial adenoma come(s) from the submucosal glands and spread(s) along perineural lymphatics, well beyond the endoluminal component?
Adenoid cystic adenoma
[UpToDate: Adenoid cystic carcinoma (ACC) was previously considered to be the most common form of malignant minor salivary gland tumor. Many of these cases subsequently have been reclassified as polymorphous low-grade adenocarcinoma (PLGA). ACC arises in both major and minor salivary glands. The tumor is locally aggressive, with recurrences often arising after many years.
Three basic growth patterns are commonly seen: tubular, cribriform, and solid. These patterns are often mixed. The biologic aggressiveness of ACC correlates with the amount of the solid component within the tumor. The solid areas generally contain cells with larger, more pleomorphic nuclei, increased mitotic activity, and often, foci of necrosis. A grading scheme attempts to integrate the varied histologic components: grade 1 tumors are composed entirely of tubules or cribriform areas, while the presence of a solid component defines higher-grade tumors. A 30% solid component serves as the breakpoint between grade 2 and 3 tumors.
In a study of 129 cases, clinical stage, solid growth pattern, and p53 expression were found by multivariate analysis to be the most important prognostic features in head and neck ACC. Increased proliferative activity has also been reported as an adverse prognostic factor. ACC frequently demonstrates bone and perineural invasion. As with other tumors that commonly invade perineural spaces, neural cell adhesion molecule (NCAM), nerve growth factor (NGF) and its receptor, and TrkA are commonly expressed in adenoid cystic carcinoma, and may provide the molecular basis underlying its behavior.]
Which mediastinal neurogenic tumor can produce catecholamines, associated with von recklinghausen’s disease (Neurofibromatosis 1)?
Paraganglioma
[UpToDate: Paragangliomas are rare neuroendocrine tumors that arise from the extra-adrenal autonomic paraganglia, small organs consisting mainly of neuroendocrine cells that are derived from the embryonic neural crest and have the ability to secrete catecholamines.
Paragangliomas are closely related to pheochromocytomas (which are sometimes referred to as intra-adrenal paragangliomas) and are indistinguishable at the cellular level. Sympathetic paragangliomas usually secrete catecholamines and are located in the sympathetic paravertebral ganglia of thorax, abdomen, and pelvis. In contrast, most parasympathetic paragangliomas are nonfunctional and located along the glossopharyngeal and vagal nerves in the neck and at the base of the skull. Catecholamine-secreting paragangliomas often present clinically like pheochromocytomas with hypertension, episodic headache, sweating, and tachycardia. However, the distinction between pheochromocytoma and paraganglioma is an important one because of implications for associated neoplasms, risk for malignancy, and genetic testing.
Even with modern genetic testing, the majority of paragangliomas appear to be sporadic. However, approximately one-third to one-half are associated with an inherited syndrome. Some hereditary paragangliomas, particularly those arising in the head and neck, have been linked to mutations in the genes encoding different subunits of the succinate dehydrogenase (SDH) enzyme complex. In addition, susceptibility to pheochromocytomas and paragangliomas is an established component of four genetic syndromes, multiple endocrine neoplasia types 2A and 2B (MEN2), neurofibromatosis type 1 (NF1), von Hippel Lindau (VHL), and Carney-Stratakis dyad.]
What are the staging criteria for “N” in the TNM staging system for lung cancer?
- N1: Ipsilateral hilum nodes
- N2: Ipsilateral mediastinal or subcarinal nodes (unresectable)
- N3: Contralateral mediastinal or supra clavicle nodes (unresectable)
- N4: Distant metastasis
What types of mediastinal masses are located in the middle mediastinum?
- Bronchogenic cysts
- Pericardial cysts
- Enteric cysts
- Lymphoma
[UpToDate: Lymphadenopathy is the most common lesion presenting as a mass in the middle compartment of the mediastinum. The most common causes include lymphoma, sarcoid, and metastatic lung cancer. Mediastinoscopy is a very useful technique to biopsy lymphadenopathy in this region.
Cystic masses comprise approximately 20% of middle mediastinal masses.
Bronchogenic cysts are the most common cystic lesion, and are felt to be secondary to abnormal lung budding during development. Bronchogenic cysts are more common in men, in the right paratracheal region and in the subcarinal location. These lesions are sometimes identified because patients have symptoms of substernal pain, cough, recurrent infection symptoms, or dyspnea.
Enteric cysts are the third most common benign esophageal mass, after leiomyomas and polyps, and are usually asymptomatic. Three criteria are required to establish their diagnosis: esophageal attachment, the presence of two layers of muscularis propria, and epithelium characteristic of the gastrointestinal tract.
Pericardial cysts occur with an incidence of 1 in 100,000 patients. Seventy percent arise in the right cardiophrenic angle. Symptoms can include shortness of breath, right heart failure secondary to compression, infection, and bleeding.
In general, bronchogenic and enteric cysts are resected to establish a definitive diagnosis and to decrease the risk of infection or malignant degeneration. Pericardial cysts can typically be observed if asymptomatic, but resection can be utilized if there are symptoms or if the diagnosis is not completely established by imaging. Simple drainage is generally not recommended because these cysts typically recur without complete resection.]
What is the treatment for tracheo-innominate artery fistula following tracheostomy?
Place finger in tracheostomy hole and hold pressure then median sternotomy with ligation and resection of innominate artery
[UpToDate: Fistula formation between a blood vessel and the tracheobronchial tree can occur when there is chronic vascular inflammation (eg, aortic aneurysm) or an indwelling vascular or tracheobronchial medical device. Although an uncommon cause of hemoptysis, fistulas between the aorta and the airway (especially the left bronchopulmonary tree) are frequently associated with aneurysms of the thoracic aorta and are fatal if not diagnosed and surgically treated. Tracheo-innominate fistulas are a rare but potentially life-threatening complication of tracheostomy, occurring most often if the tracheostomy tube is placed too low. The tube can erode directly into the innominate artery, which crosses the anterolateral surface of the trachea at the level of the upper sternum. Bronchial stents are another source of fistula formation.]
What is the single best test for T and N status of lung cancer?
Chest and abdominal CT
[UpToDate: CT and (in some cases) PET provide a non-invasive assessment of tumor size, mediastinal node enlargement, and potential intra- or extra-thoracic metastases. Although confirmation by tissue biopsy must be pursued, these imaging tests provide the basis for the initial assessment of the TNM stage of disease and help guide the clinician in choosing the optimal site(s) for tissue sampling.]
What is the 5-year survival rate for atypical lung carcinoid tumors?
60%
[90% 5-year survival for typical carcinoid tumors]
[UpToDate: Atypical bronchial NETs have a worse prognosis than do typical tumors. Five-year survival rates range widely from 30%-95%; the corresponding rates at 10 years are 35%-56%. Atypical tumors have a greater tendency to both metastasize (16% and 23% in three large series) and recur locally (3% and 25% in the same series). Distant metastases to the liver or bone are more common than local recurrence. Most series report an adverse influence of nodal metastases on prognosis that is more profound than for typical tumors. This is best illustrated by the experience at the Mayo Clinic. 19 of 23 patients with typical bronchial carcinoids and lymph node involvement (83%) remained alive and well, while four failed distantly, two of whom died. In contrast, only 4 of the 11 patients with atypical tumors and lymph node involvement were alive without disease, while seven developed distant metastases and six died.]
What are the left-sided structures when looking into the middle mediastinum with mediastinoscopy?
- Recurrent laryngeal nerve
- Esophagus
- Aorta
- Main pulmonary artery
80% of lung cancers are what type?
Non-small cell carcinoma
[UpToDate: Worldwide, lung cancer occurred in approximately 1.8 million patients in 2012 and caused an estimated 1.6 million deaths. In the United States, lung cancer occurs in about 225,000 patients and causes over 160,000 deaths annually.
Both the absolute and relative frequency of lung cancer has risen dramatically. Around 1953, lung cancer became the most common cause of cancer deaths in men, and in 1985, it became the leading cause of cancer deaths in women. Lung cancer deaths have begun to decline in both men and women, reflecting a decrease in smoking.
The term lung cancer, or bronchogenic carcinoma, refers to malignancies that originate in the airways or pulmonary parenchyma. Approximately 95% of all lung cancers are classified as either small cell lung cancer (SCLC) or non-small cell lung cancer (NSCLC). This distinction is essential for staging, treatment, and prognosis. Other cell types comprise about 5% of malignancies arising in the lung.
Lung cancer is the leading cause of cancer deaths worldwide in both men and women. Non-small cell lung cancer (NSCLC) accounts for the majority (approximately 85%) of lung cancers with the remainder as mostly small cell lung cancer (SCLC).
Distinguishing among the different histologic subtypes of NSCLC is increasingly important to guide subsequent testing for specific mutations and to guide treatment selection, including the identification of patients who are more likely to respond to newer targeted therapies. Adenocarcinoma, squamous carcinoma, adenosquamous carcinoma, and large cell carcinoma are the four major histological subtypes of NSCLC. The four subtypes of NSCLC are histologically characterized by the absence of the pathologic features of small cell lung cancer (SCLC; eg, small cell size, nuclear molding, “salt and pepper” chromatin pattern, and nuclear crush artifact) together with the following:
- Adenocarcinoma – Neoplastic gland formation or intracytoplasmic mucin
- Squamous cell carcinoma – The presence of keratin production by tumor cells and/or intercellular desmosomes (“intercellular bridges”)
- Adenosquamous carcinoma – Greater than 10% malignant glandular and squamous components
- Large cell carcinoma – The absence of glandular or squamous differentiation features (ie, poorly differentiated NSCLC).
Small cell lung cancer (SCLC) typically arises in the central airways of smokers, and due to its short doubling time and biological aggressiveness, patients have only a brief period of pre-diagnosis symptoms. Despite this, 60-70% of patients present with overt metastatic disease. SCLC is distinguished from NSCLC by its rapid doubling time, high growth fraction, and the early development of widespread metastases. Although SCLC is highly responsive to chemotherapy and radiotherapy, the disease usually relapses within two years despite treatment. Overall, only 10-15% of patients with limited stage SCLC and 1-2% of patients with extensive stage SCLC survive beyond five years.]
What are the two preferred chemotherapy agents for small cell lung cancer?
Cisplatin and Etoposide
[UpToDate: Small cell lung cancer (SCLC) usually presents with disseminated disease. SCLC is sensitive to cytotoxic chemotherapy, and the use of platinum-based combination regimens has resulted in a significant improvement in survival.
For patients with extensive stage SCLC, we recommend combination chemotherapy with a platinum-based regimen (Grade 1A).
We suggest a two-drug combination of etoposide plus either carboplatin or cisplatin (Grade 2B). Regimens substituting irinotecan, topotecan, or epirubicin for etoposide are reasonable alternatives.
Initial therapy is usually limited to four to six cycle of induction chemotherapy.
The use of maintenance chemotherapy, three- or four-drug combinations, and alternating or sequential non-cross-resistant regimens have not been shown to offer substantial benefits compared with a two-drug combination; thus, these approaches are not routinely utilized.
Most clinicians in the United States use carboplatin plus etoposide to treat patients with ES-SCLC based upon its better toxicity profile, while cisplatin plus etoposide is preferred for those with LS-SCLC because of the possibility of a higher response rate.
Cisplatin-based regimens have been compared with carboplatin-based combinations in four randomized trials. A meta-analysis that included individual patient data from these four trials found no statistically significant difference between cisplatin and carboplatin-based combinations in terms of overall survival, progression-free survival, or objective response rate (median overall survival 9.6 versus 9.4 months, 5.5 versus 5.3 months, and 67% versus 66%, respectively).
What percent of myasthenia gravis patients improve with thymectomy?
80%
[UpToDate: The benefit of thymectomy for patients with nonthymomatous MG is supported by the results of the multicenter, assessor-blinded MGTX trial. The trial enrolled 126 subjects (ages 16 to 65 years, median age approximately 33 years) with generalized acetylcholine receptor (AChR) antibody-associated MG and disease duration of
The time-weighted average Quantitative Myasthenia Gravis score (with higher scores indicating more severe weakness) over a three-year period was significantly lower for the thymectomy group compared with the prednisone-alone group (6.15 versus 8.99, estimated difference 2.85).
The average requirement for alternate-day prednisone over three years was significantly lower for the thymectomy group (44 vs 60 mg, estimated difference 16 mg).
The proportion of subjects requiring immunosuppression with azathioprine was significantly lower for the thymectomy group (17% vs 48%, estimated difference 31%).
The proportion of subjects hospitalized for MG exacerbations was significantly lower for the thymectomy group (9% vs 37%, estimated difference 28%).
The proportion of subjects who achieved minimal manifestation status (ie, no symptoms or functional limitations from MG but may have some weakness on examination of some muscles) was significantly greater in the thymectomy group at 12 months (67% vs 37%) and at 36 months (67% vs 47%).
What percent of lung carcinoid tumors have symptoms at the time of diagnosis (I.E. cough, hemoptysis)?
50%
[UpToDate: The majority of tumors arise in the proximal airways, and most are symptomatic from an obstructing tumor mass or bleeding due to hypervascularity. Patients may have a cough or wheeze, hemoptysis, chest pain, or recurrent pneumonia in the same pulmonary segment or lobe due to bronchial obstruction. Due to misdiagnosis, the diagnosis of a bronchial neuroendocrine tumor (NET) is often delayed, and patients may receive several courses of antibiotics to treat recurrent pneumonia before the carcinoid is diagnosed.
On chest x-ray, most tumors appear as round or ovoid opacities that range in size from 2-5 cm and may be associated may be a hilar or perihilar mass. If a central tumor results in bronchial obstruction, atelectasis and mucoid impaction may be visible radiographically. Cavitation is rare. Pleural effusions are unusual but may occur with postobstructive pneumonia.
Approximately one-fourth of cases present in the periphery as an asymptomatic solitary pulmonary nodule. These tumors are frequently discovered on a routine chest x-ray, most commonly as a solitary pulmonary nodule.]
Where does the phrenic nerve travel with respect to the hilum?
It runs anterior to the hilum
What is the most common site for a mediastinal tumor?
Anterior mediastinum
[Thymoma is most common anterior mediastinal mass.]
[UpToDate: The anterior mediastinum is the most common location where mediastinal masses occur in adults. The most commonly found anterior mediastinal masses are often referred to as “the terrible T’s”: thymoma, teratoma/germ cell tumor, (terrible) lymphoma, and thyroid tissue.
Thymomas account for about 20% of mediastinal neoplasms. Most thymoma patients are between 40 and 60 years of age, and there is a similar incidence in men and women. There are no known risk factors, although there is a strong association with myasthenia gravis and other paraneoplastic syndromes.
Benign teratomas have an equal gender distribution, and comprise two thirds of all mediastinal GCTs. Teratomas can contain elements of fat, fluid, and bone. Treatment is surgery, and biopsy is not needed if imaging is convincing that teratoma is the most likely diagnosis. These tumors are often found incidentally, but can cause pain or other symptoms due to compression of adjacent structures. There have been reports of paraneoplastic encephalitis due to anti-N-methyl-D-aspartate receptor antibodies in patients with benign ovarian or mediastinal teratomas.
Teratomas should generally be resected when identified to definitively confirm the diagnosis and prevent the development of local symptoms due to tumor growth. Although teratomas are benign, these lesions have the potential for malignant degeneration. Teratomas with malignant degeneration can be very aggressive, and their prognosis is generally very poor.
Ninety percent of malignant mediastinal GCTs in adults occur in males and are most frequent in the third decade of life. Patients require physical examination and a scrotal ultrasound to ensure that the mediastinal findings do not represent metastatic disease secondary to a testicular primary. In addition to the initial chest CT, these patients require an abdominal CT scan for staging purposes.
Tumor markers are useful both diagnostically and to follow the results of treatment; all patients with a mediastinal mass that could be a GCT should have AFP and beta-HCG measured prior to any therapy. AFP is normal in teratoma and “pure” seminomas. Beta-HCG is mildly elevated in 10% of patients with seminomas. 90% of non-seminomatous GCTs have elevated AFP and/or beta-HCG.]
What percent of asymptomatic mediastinal masses are benign?
90%
[UpToDate: Patients with mediastinal masses can present in a variety of ways. A mediastinal mass is often an incidental diagnosis when patients undergo an evaluation for an unrelated condition or symptom. In some cases, patients present with complaints secondary to local mass effect on adjacent structures, such as respiratory symptoms due to airway compression or swelling due to compression of vascular structures. Other patients develop systemic symptoms that result from the mediastinal mass, which is discovered on subsequent work-up.
Benign or malignant mediastinal masses can develop from structures that normally are in the mediastinum or that pass through the mediastinum during development, as well as from metastases of malignancies that arise elsewhere in the body. A combination of clinical factors and imaging features often narrow the differential diagnosis when a mediastinal mass is detected. In some instances, the clinical and imaging features can be enough to guide therapy, which often includes surgical resection that provides a definitive diagnosis. Blood tumor markers can sometimes also support a specific diagnosis. In other cases, obtaining tissue via biopsy can be necessary to confirm a clinical suspicion prior to proceeding with therapy.]
Which cell type is responsible for gas exchange in the lungs?
Type 1 pneumocytes
What are the anterior structures when looking into the middle mediastinum with mediastinoscopy?
- Innominate vein
- Innominate artery
- Right pulmonary artery
Asbestos exposure increases lung cancer risk by how much?
90x
[UpToDate: Although some investigators have questioned the causal relationship between asbestosis and bronchogenic carcinoma, most studies have demonstrated a clear association between the two entities. As an example, a Dutch cohort study of 58,279 men, in which 524 cases of lung cancer developed, found that asbestos exposure was associated with a relative risk of lung cancer of 3.5 after adjustment for age, smoking habits, and intake of vitamin C, beta-carotene, and retinol.
The increased risk of lung cancer associated with asbestos is greatly magnified by coexisting exposure to tobacco smoke. In one report, for example, the risk of dying of lung cancer in asbestos workers increased 16-fold if they smoked more than 20 cigarettes per day and 9-fold if they smoked fewer than 20 cigarettes per day, compared to asbestos workers without a regular smoking history.
The risk of lung cancer associated with combined exposure to asbestos and cigarette smoke appears to be multiplicative. In the same report noted above:
Asbestos exposure in the absence of a smoking history was associated with a 6-fold relative risk
Cigarette smoking without a history of asbestos exposure was associated with an 11-fold increase in risk
The relative risk for cigarette smokers with a history of asbestos exposure was 59
For any given individual, the relative risk depends upon the magnitude of the exposure both to cigarette smoke and to asbestos. The type of asbestos fiber affects the risk of lung cancer as well; the risk appears to be considerably higher for workers exposed to amphibole fibers than for those exposed to chrysotile fibers. However, an analysis of 35-year prospective cohort data suggested a significant exposure–response relationship between exposure to chrysotile asbestos and increased risk for lung cancer mortality.
Asbestos exposure increases the incidence of other neoplasms as well. Other malignancies that have been linked to asbestos include cancers of the larynx, oropharynx, kidney, esophagus, and biliary system. Asbestos is the only known risk factor for malignant mesothelioma.]
What is the treatment for a bronchiogenic cyst?
Resection
[UpToDate: Bronchogenic cysts arise from anomalous budding of the foregut during development and represent part of the spectrum of bronchopulmonary foregut malformations. They can occur at any point throughout the tracheobronchial tree. Cervical, intrapleural, cutaneous, esophageal, cardiac, and subdiaphragmatic retroperitoneal bronchogenic cysts are unusual occurrences but have been reported. These lesions, although rare, are among the most common lower respiratory tract malformations.
Affected patients typically present during the second decade of life with recurrent coughing, wheezing (which may simulate asthma), and pneumonia, but they may become symptomatic in infancy or adulthood. Newborns with rapidly enlarging central cysts can develop respiratory distress, cyanosis, and feeding difficulty. Bronchogenic cysts also may be detected as neck masses or incidental findings on chest radiographs.
Bronchogenic cysts appear on chest radiograph as round water-density masses that may have air-fluid levels associated with previous or current infection. CT typically shows sharply marginated cystic mediastinal masses of soft tissue or water attenuation. Lesions that appear solid on CT usually can be characterized as cystic by MRI. The radiographic appearance of bronchogenic cysts and other developmental anomalies of the lung is discussed in detail separately.
Gross pathologic examination demonstrates unilocular cysts that are filled with thick, clear fluid and do not communicate with the tracheobronchial tree. On histologic examination, the cyst is lined by respiratory epithelium with occasional foci of squamous metaplasia; the wall resembles that of larger airways and contains smooth muscle, glands, and cartilage. The presence of cartilage plates is the most reliable diagnostic criterion.
The management of a bronchogenic cyst consists of surgical excision by partial or total lobectomy. This procedure is curative. Controversy exists regarding the need for resection when patients are asymptomatic. We recommend surgery in all cases because of the likelihood of eventual development of symptoms and the potential for serious illness. In addition, malignant degeneration may occur with this disorder, as in other congenital cystic anomalies. Although surgical excision is typically straightforward, operative complications have been reported. The prenatal ultrasound identification of large cysts compressing cardiovascular structures warrants in utero thoracentesis to prevent fetal hydrops.]
What is the treatment for Arterio-venous malformations (AVMs) in the lungs?
Embolization
[UpToDate: Not all pulmonary arteriovenous malformations (PAVMs) require intervention. When indicated, embolotherapy is the mainstay of treatment as most PAVMs (>99%) can be successfully treated with this therapy. Although many interventional radiologists at local institutions have treated one or more PAVM, we believe that most PAVMs are best managed by referral to a center that has expertise in PAVM treatment, usually hereditary hemorrhagic telangiectasia (HHT) centers www.cureHHT.org. This affords the best opportunity to treat all appropriate PAVMs in the least number of sessions and minimize the chance of reperfusion, especially for patients with PAVMs that are large, complex, and multiple.]
What is the 5-year survival rate for typical lung carcinoid tumors?
90%
[60% 5-year survival for atypical carcinoid tumors]
[UpToDate: Typical bronchial NETs have an excellent prognosis following surgical resection. Reported five-year survival rates are 87%-100%; the corresponding rates at 10 years are 82%-87%. A contemporary large series with long-term follow-up and expert pathology review reported a 3% (9 of 291) recurrence rate for resected typical bronchial NETs.
The prognostic impact of nodal involvement for typical bronchial NETs is controversial, but most studies show a worse outcome compared with cases without nodal involvement. Besides nodal involvement, incomplete resection is the only widely accepted feature with negative prognostic significance. A nomogram to predict survival for typical bronchial carcinoid tumors has been developed that is based upon age; gender; prior malignancy; tumor site (central versus peripheral); Tumor, Nodes, Metastasis (TNM) stage; and performance status.]
Injury at what level of the thorax results in a left-sided chylothorax?
Above T5-T6
[UpToDate: Generally, the thoracic duct ascends from the cisterna chyli (sac at the lower end of the thoracic duct into which the intestinal and two lumbar lymphatic trunks drain), which lies just anterior to the first or second lumbar vertebra, and passes through the aortic hiatus of the diaphragm to enter the posterior mediastinum, although wide anatomic variation exists. The thoracic duct continues cephalad in a rightward position between the aorta and azygos vein until it reaches the approximate level of the fifth thoracic vertebra, where it crosses over the vertebral column behind the esophagus and continues in the left posterior mediastinum. The thoracic duct in this region is 2 to 3 mm in diameter and passes behind the aortic arch adjacent to the left side of the esophagus and behind the left subclavian artery. It then arches over the subclavian artery in the anterolateral superior mediastinum, descending to empty into the venous circulation in the region of the left jugular and subclavian veins.
In some patients, two thoracic ducts exist within the mediastinum, and occasionally a single thoracic duct may empty into right-sided venous structures.
The anatomy of the thoracic duct determines the location of the effusion seen with duct injury or obstruction. Because the thoracic duct crosses the mediastinum at the fifth thoracic vertebral body, lymphatic injury or obstruction below this level generally results in a right–sided pleural effusion. In contrast, disease above this level usually leads to a left-sided effusion.]
What is the treatment for a lung abscess?
Antibiotics alone will be successful in 95% of cases, CT-guided drainage if that fails
[surgery if above fails or if cannot rule out cancer (Greater than 6 cm, failure to resolve after 6 weeks)]
[UpToDate: An early study of 1560 cases of lung abscess after the introduction of sulfonamides showed that these drugs had no important effect on the outcome of the infection. Resectional surgery and penicillin were commonly used for the treatment of lung abscess in the early 1950s, and the relative merits of surgery versus antibiotics were often debated. Antibiotics then became favored, using penicillin as the initial agent with tetracycline for those who did not respond. Patients who had persistent cavities at four to six weeks were defined as having “delayed closure,” and these patients were candidates for surgical resection. An important study from Philadelphia General Hospital in the 1960s showed that even patients with delayed closure eventually responded when antibiotics were simply continued. Since that time, surgery has been limited to only approximately 5% to 10% of cases in most series.
Standard treatment for an anaerobic lung infection is clindamycin (600 mg intravenously [IV] every eight hours, followed by 150 to 300 mg orally four times daily) based upon two published trials that demonstrated superiority of this agent compared with parenteral penicillin in the number of patients who responded and the speed of defervescence following the inception of treatment.]
What type of benign lung lesion has calcifications and can appear as a popcorn lesion on chest CT?
Hamartoma
[UpToDate: Hamartomas cause approximately 10% of benign nodules found in the lung. They typically present in middle age, grow slowly over years, and are histologically heterogeneous. Cartilage (with scattered calcification), fat, muscle, myxomatous tissue, and fibroblastic tissue may all exist. The characteristic appearance of a hamartoma on a chest radiograph is a SPN with “popcorn” calcification, although this pattern is observed in less than 10% of cases. High-resolution CT scanning of the lesion is particularly useful because it may demonstrate focal areas of fat, or calcification alternating with fat, which are virtually diagnostic of a hamartoma. Less common benign neoplasms such as fibromas, leiomyomas, hemangiomas, amyloidoma, and pneumocytoma do not have characteristic features on imaging.]
Which lung cancer is associated with ACTH and ADH paraneoplastic syndromes?
Small cell lung cancer
[Small cell ACTH is the most common paraneoplastic syndrome]
[UpToDate: The syndrome of inappropriate antidiuretic hormone secretion (SIADH) is frequently caused by SCLC and results in hyponatremia. Approximately 10% of patients who have SCLC exhibit SIADH. SCLC accounts for approximately 75% of all malignancy-related of SIADH.
The severity of symptoms is related to the degree of hyponatremia and the rapidity of the fall in serum sodium. Symptoms include anorexia, nausea, and vomiting. Cerebral edema can occur when the onset of hyponatremia is rapid. Symptoms caused by cerebral edema may include irritability, restlessness, personality changes, confusion, coma, seizures, and respiratory arrest.
The treatment of SIADH focuses on treating the malignancy. In the majority of patients with SCLC, the hyponatremia will resolve within weeks of starting chemotherapy. Chronic hyponatremia or that of unclear duration may be treated with normal saline infusion to euvolemia, fluid restriction and demeclocycline, or a vasopressin-receptor antagonist. Acute and severe hyponatremia may be carefully treated with hypertonic (3%) saline infusion for a correction of 1-2 mmol per liter per hour with a correction of not more than 8-10 mmol per liter in 24 hours.
Ectopic production of adrenal corticotropin (ACTH) can cause Cushing’s syndrome. Patients typically present with muscle weakness, weight loss, hypertension, hirsutism, and osteoporosis. Hypokalemic alkalosis and hyperglycemia are usually present.
Cushing’s syndrome is relatively common in patients with SCLC and with carcinoid tumors of the lung, as well as extrathoracic malignancies. Patients with Cushing’s syndrome and SCLC appear to have a worse prognosis than patients with SCLC without Cushing’s syndrome.]
Where does the vagus nerve travel with respect to the hilum?
It runs posterior to the hilum
[The phrenic nerve travels anterior to the hilum.]
What has the strongest influence on survival of a lung cancer patient?
Nodal involvement
[UpToDate: Prognosis of NSCLC - The TNM stage at presentation in patients with NSCLC is the factor that has the greatest impact on prognosis. The most extensive data relating stage to prognosis come from a validation series of over 31,000 cases from the Surveillance, Epidemiology and End Results (SEER) database used to validate the 7th TNM staging system. Survival decreased progressively with more advanced disease from a median of 59 months for patients with stage IA disease to four months for those with stage IV disease
Prognosis of SCLC - The most important prognostic factor in patients with SCLC is the extent of disease (stage) at presentation. For patients with limited stage disease, median survivals range from 15 to 20 months, and the reported five-year survival rate is 10-13%. In contrast, for patients with extended stage disease, the median survival is 8-13 months, and the five-year survival rate is 1-2%.]
Whiteout on chest xray with no midline shift should be investigated with which follow-up test?
Chest CT
[UpToDate: Computed tomography (CT) detects small pleural effusions, ie, less than 10 mL and possibly as little as 2 mL of liquid in the pleural space. Thickening of the visceral and parietal pleura as well as enhancement of the visceral and parietal pleura after injection of intravenous contrast material (the “split pleura sign”) suggest the presence of inflammation and thus an exudative, rather than transudative, effusion. The administration of intravenous contrast material in patients with pleural abnormalities is important, since it facilitates the differential diagnosis of pleural effusions.
Other uses of CT scanning in the evaluation of pleural disease include:
- Facilitating measurement of pleural thickness
- Distinguishing an empyema from a lung abscess
- Visualization of small pneumothoraces in supine patients
- Visualization of underlying lung parenchymal processes that are obscured on the chest radiograph by a large pleural effusion
- Determination of the exact location of pleural masses and characterization of their composition
- Occasionally identifying peripheral bronchopleural fistulae
- Occasionally identifying a diaphragmatic defect in a cirrhotic patient with hepatic hydrothorax
- Identification of lung parenchymal or upper abdominal abnormalities that may provide a clue to the etiology of the pleural effusion (eg, lung mass, apical cavities, aortic dissection, infradiaphragmatic abscess, liver cirrhosis with ascites leading to hepatic hydrothorax)
- Guidance for thoracentesis and tube thoracostomy of loculated empyemas.]
What side of the thorax does the azygous vein travel on and what does it empty into?
It runs along the right side of the thorax and empties into the superior vena cava
What percent of thymomas are malignant?
50%
[UpToDate: The Masaoka staging system is the most useful for treatment planning and prognostic purposes. A chest CT scan with intravenous contrast can often show whether the thymoma appears well circumscribed or if it infiltrates surrounding structures. Pre-operative biopsy is not necessary if the lesion is well circumscribed and the patient does not have systemic symptoms that suggest another diagnosis. Masses that appear to infiltrate surrounding structures are more likely to be malignant. If the mass appears to have local infiltration of surrounding structures or the patient has systemic symptoms or other findings that suggest an alternative diagnosis, biopsy should precede definitive resection. Fine needle aspiration should not be used, because distinguishing a thymoma from lymphoma can be difficult histologically. Overall, 15% of thymomas are malignant.]
What is the most common late complication after tracheal surgery?
Granulation tissue formation
[This can cause airway narrowing. The most common early complication of tracheal surgery is laryngeal edema.]
[UpToDate: Endotracheal intubation can induce vocal cord granuloma formation, presumed to be a sequela of inflammation and ulceration and may occur in up to 30-40% of patients intubated for longer than three or four days but symptoms may not be apparent until a few weeks (eg, four weeks) after extubation. The duration of intubation and severity of initial laryngeal injury do not appear to predict granuloma formation. Hoarseness that persists longer than 7-10 days following extubation may indicate the presence of a laryngeal granuloma and should prompt fiberoptic laryngoscopy for diagnosis. Granulomas may also be appreciated on computed tomography. Laryngeal granulomas often require surgical removal but some resolve spontaneously; subspecialty consultation is usually necessary for management.]
Aside from the brain, where does lung cancer commonly metastasize?
Supraclavicular nodes, other lung, bone, liver, and adrenals
What are the right-sided structures when looking into the middle mediastinum with mediastinoscopy?
- Azygous
- Superior vena cava
What is the most common malignant germ cell tumor of the mediastinum?
Seminoma
[UpToDate: Mediastinal seminomas constitute approximately one-third of malignant mediastinal GCTs and 2-4% of mediastinal masses. Seminomas are slightly more common than nonseminomatous germ cell tumors. Management of seminomas involves chemotherapy with or without radiation therapy, with surgical excision only if residual mass is present after therapy.
Mediastinal seminomas occur predominantly in men between the ages of 20 and 40. Although it is uncommon for testicular seminoma to metastasize to the mediastinum in the absence of retroperitoneal lymph node involvement, all men with mediastinal seminoma should undergo careful testicular palpation and ultrasonography. Orchiectomy is generally indicated in the event of suspicious findings. Mediastinal dysgerminomas (the female counterpart to seminomas) are rare in women with histologically normal ovaries.
In order for a GCT to be classified as a seminoma in men or a dysgerminoma in women, no other histologic element of a GCT can be present and serum alpha-fetoprotein (AFP) must be normal (unless liver disease or another medical condition exists to explain the AFP elevation). Tumors consisting of a mixture of seminoma and other tumor types are termed mixed GCTs and are treated as nonseminomatous GCTs.]
What kind of pleural fluid has >1,000 WBCs, pH <7.45, a pleural fluid protein to serum ratio >0.5, and a pleural fluid LDH to serum ration >0.6?
Exudative pleural fluid
[UpToDate: Exudative effusions present more of a diagnostic challenge. Disease in virtually any organ can cause exudative pleural effusions by a variety of mechanisms, including infection, malignancy, immunologic responses, lymphatic abnormalities, noninfectious inflammation, iatrogenic causes, and movement of fluid from below the diaphragm.
Exudates result primarily from pleural and lung inflammation (resulting in increased capillary and pleural membrane permeability) or from impaired lymphatic drainage of the pleural space (resulting in decreased removal of protein and other large molecular weight constituents from the pleural space). Exudates can also result from movement of fluid from the peritoneal space, as seen with acute or chronic pancreatitis, chylous ascites, and peritoneal carcinomatosis.
According to the traditional Light’s Criteria Rule, if at least one of the following three criteria (ie, component tests of the rule) is fulfilled, the fluid is defined as an exudate:
- Pleural fluid protein/serum protein ratio greater than 0.5, or
- Pleural fluid LDH/serum LDH ratio greater than 0.6, or
- Pleural fluid LDH greater than two-thirds the upper limits of the laboratory’s normal serum LDH]
What is the single most common site of metastasis from lung cancer?
The brain
What are the 3 phases of empyema?
- Exudative phase (1st week)
- Fibro-proliferative phase (2nd week)
- Organized phase (3rd week)
What is the treatment for chylothorax secondary to trauma if conservative treatment fails?
Ligation of thoracic duct on right side low in mediastinum
[80% successful]
[UpToDate: For the majority of patients with traumatic chylothorax (eg, nonsurgical or postoperative), we suggest initial conservative management rather than surgical intervention (Grade 2C). Conservative management includes chest tube drainage and dietary modifications with total parenteral nutrition or a high protein-reduced fat diet with MCT supplementation. Close attention to fluid and electrolyte management, nutrition, and the daily volume of pleural drainage is needed.
For patients with a traumatic chylothorax (eg, nonsurgical or postoperative) who fail to respond to chest tube drainage and dietary modifications, pleurodesis may control the chylothorax allowing chest tube removal in 80% of patients. Selecting patients for pleurodesis based on pleural fluid drainage <500 mL/day may improve success rates. Thoracic duct embolization or disruption where available are additional approaches.
For patients with a traumatic chylothorax (eg, nonsurgical or postoperative) and large volume drainage of chylous fluid (>1 L per day) who can tolerate surgery, we recommend early thoracic duct ligation (eg, within 3 to 7 days) (Grade 1B). Pleurodesis may be performed at the time of thoracic duct ligation via mechanical abrasion or insufflation of talc. Thoracic duct embolization or disruption where available are additional approaches.
For patients with a traumatic chylothorax (eg, nonsurgical or postoperative) and continued pleural drainage after 14 days of conservative therapy, failed pleurodesis, and/or failed thoracic duct embolization or disruption, we recommend thoracic duct ligation (Grade 1B). A longer duration of conservative therapy is associated with nutritional depletion and high mortality rates. Earlier surgical intervention is indicated for patients who appear unlikely to respond to conservative measures or with initially compromised nutritional status. Pleurodesis may be performed at the time of thoracic duct ligation via mechanical abrasion or insufflation of talc.]
Do mediastinal germ cell tumors need to be biopsied?
Yes
[UpToDate: A tissue diagnosis is required for definitive diagnosis prior to treatment, unless the patient requires emergent treatment because of severe symptoms and the diagnosis is obvious by tumor markers and the distribution of disease. Unlike testis cancer, extragonadal germ cell tumors (GCTs) are typically diagnosed based upon a needle or open biopsy.]
Which lung cancer is associated with PTH-related peptide paraneoplastic syndrome?
Squamous cell carcinoma
[UpToDate: Hypercalcemia in patients with lung cancer may arise from a bony metastasis or less commonly tumor secretion of a parathyroid hormone-related protein (PTHrP), calcitriol or other cytokines, including osteoclast activating factors.
In one study of 1149 consecutive lung cancers, 6% had hypercalcemia. Among those with hypercalcemia, squamous cell carcinoma, adenocarcinoma, and SCLC were responsible in 51%, 22%, and 15% of cases, respectively. Most patients with hypercalcemia have advanced disease (stage III or IV) and a median survival of a few months.
Symptoms of hypercalcemia include anorexia, nausea, vomiting, constipation, lethargy, polyuria, polydipsia, and dehydration. Confusion and coma are late manifestations, as are renal failure and nephrocalcinosis. Symptomatic patients who have serum calcium of 12 mg/dL (3 mmol/L) or higher require treatment that includes hydration and bisphosphonate.]
What is the most common type of mediastinal tumor in adults and children and usually occurs in the posterior mediastinum?
Neurogenic tumors
[UpToDate: Neurogenic tumors represent more than 60% of posterior mediastinal masses. These lesions are classified based upon their neural cell of origin.
Schwannomas and neurofibromas are benign lesions that arise from the intercostals nerve sheath and make up 90% of adult neurogenic tumors.
Neuroblastomas and ganglioneuroblastomas are malignant tumors that occur most commonly in children and originate from the sympathetic ganglia.
Ganglioneuromas are benign lesions that arise from the sympathetic ganglia, and are most common in young adults. Lesions that arise from para-ganglionic cells include pheochromocytomas and paragangliomas.
Some neurogenic tumors are “dumbbell shaped” and arise near intervertebral foramen, and have a posterior mediastinal and intraspinal component. Resection usually requires a combined approach with neurosurgery and thoracic surgery.]
Whiteout on chest xray with a midline shift toward the whiteout is most likely due to what?
Collapsed lung
[Requires bronchoscopy to remove plug]
[UpToDate: Obstruction of the right or left mainstem bronchus can lead to atelectasis of the entire right or left lung, respectively. On the frontal view of a chest radiograph, a totally collapsed lung causes opacification of the hemithorax with ipsilateral cardiomediastinal shift. The ipsilateral cardiomediastinal shift distinguishes the atelectasis from a massive pleural effusion, since the latter causes a contralateral cardiomediastinal shift. On the lateral view of a chest radiograph, the cardiac silhouette, one hemidiaphragm, and one hilum are obscured.
The complete opacification and loss of volume of the atelectatic lung, as well as the rotational shift of the cardiomediastinal structures toward the atelectatic lung, are better seen on a CT scan than on a chest radiograph. The cause of the obstruction can be elucidated on a CT scan as well.]
What are the staging criteria for “T” in the TNM staging system for lung cancer? (I.E What is T1 vs T2 vs T3 vs T4?)
- T1: Less than 3cm
- T2: Greater than 3cm and greater than 2cm from the carina
- T3: Invasion of the chest wall, pericardium, diaphragm, or or less than 2cm from the carina
- T4: Involvement of mediastinum, esophagus, trachea, vertebra, heart, great vessels, malignant effusion (all indicate unresectability)
Massive hemoptysis is most commonly secondary to what?
Infection (death occurs due to asphyxiation)
[UpToDate: There are numerous causes of bleeding from the lower respiratory tract. Three etiologies accounted for 90% of the cases of massive hemoptysis through the 1960s: tuberculosis, bronchiectasis, and lung abscess. Each of these causes has since decreased in frequency, although other etiologies have increased. There are no more recent large series examining the prevalence of the causes of massive hemoptysis in general hospital settings.]
What is the overall 5-year survival rate of lung cancer?
10%
[UpToDate: The most important prognostic factor in patients with SCLC is the extent of disease (stage) at presentation. For patients with limited stage disease, median survivals range from 15-20 months, and the reported 5-year survival rate is 10-13%. In contrast, for patients with extended stage disease, the median survival is 8-13 months, and the 5-year survival rate is 1-2%.]
[National Cancer Institute’s SEER database:
NSCLC - This data is based on people who were diagnosed with NSCLC between 1998 and 2000. Although they are based on people diagnosed several years ago, they are the most recent rates published for the current AJCC staging system.
- Stage IA NSCLC is about 49%
- Stage IB NSCLC is about 45%.
- Stage IIA NSCLC is about 30%
- Stage IIB NSCLC is about 31%
- Stage IIIA NSCLC is about 14%
- Stage IIIB NSCLC is about 5%
- Stage IV NSCLC is about 1%
SCLC - This data is based on people who were diagnosed with SCLC between 1988 and 2001. These survival rates are based on the TNM staging system in use at the time, which has since been modified slightly for the latest version. Because of this, the survival numbers may be slightly different for the latest staging system. 5-year relative survival rate:
- Stage I SCLC is about 31%
- Stage II SCLC is about 19%
- Stage III SCLC is about 8%
- Stage IV SCLC is about 2%]
What allows for direct air exchange between alveoli?
The Pores of Kohn
What is the most common benign adult lung tumor?
Hamartoma
[UpToDate: Hamartomas cause approximately 10% of benign nodules found in the lung. They typically present in middle age, grow slowly over years, and are histologically heterogeneous. Cartilage (with scattered calcification), fat, muscle, myxomatous tissue, and fibroblastic tissue may all exist. The characteristic appearance of a hamartoma on a chest radiograph is a SPN with “popcorn” calcification, although this pattern is observed in less than 10% of cases. High-resolution CT scanning of the lesion is particularly useful because it may demonstrate focal areas of fat, or calcification alternating with fat, which are virtually diagnostic of a hamartoma. Less common benign neoplasms such as fibromas, leiomyomas, hemangiomas, amyloidoma, and pneumocytoma do not have characteristic features on imaging.]
What types of mediastinal masses are located in the anterior mediastinum?
- Thymoma
- Thyroid cancer (goiter)
- T-cell lymphoma
- Teratoma (and other germ cell tumors)
- Parathyroid adenomas
[UpToDate: The anterior mediastinum is the most common location where mediastinal masses occur in adults. The most commonly found anterior mediastinal masses are often referred to as “the terrible T’s”: thymoma, teratoma/germ cell tumor, (terrible) lymphoma, and thyroid tissue.
Thymomas account for about 20% of mediastinal neoplasms. Most thymoma patients are between 40 and 60 years of age, and there is a similar incidence in men and women. There are no known risk factors, although there is a strong association with myasthenia gravis and other paraneoplastic syndromes.
Benign teratomas have an equal gender distribution, and comprise two thirds of all mediastinal GCTs. Teratomas can contain elements of fat, fluid, and bone. Treatment is surgery, and biopsy is not needed if imaging is convincing that teratoma is the most likely diagnosis. These tumors are often found incidentally, but can cause pain or other symptoms due to compression of adjacent structures. There have been reports of paraneoplastic encephalitis due to anti-N-methyl-D-aspartate receptor antibodies in patients with benign ovarian or mediastinal teratomas.
Teratomas should generally be resected when identified to definitively confirm the diagnosis and prevent the development of local symptoms due to tumor growth. Although teratomas are benign, these lesions have the potential for malignant degeneration. Teratomas with malignant degeneration can be very aggressive, and their prognosis is generally very poor.
Ninety percent of malignant mediastinal GCTs in adults occur in males and are most frequent in the third decade of life. Patients require physical examination and a scrotal ultrasound to ensure that the mediastinal findings do not represent metastatic disease secondary to a testicular primary. In addition to the initial chest CT, these patients require an abdominal CT scan for staging purposes.
Tumor markers are useful both diagnostically and to follow the results of treatment; all patients with a mediastinal mass that could be a GCT should have AFP and beta-HCG measured prior to any therapy. AFP is normal in teratoma and “pure” seminomas. Beta-HCG is mildly elevated in 10% of patients with seminomas. 90% of non-seminomatous GCTs have elevated AFP and/or beta-HCG.]
