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Surgery_Schwartz_4502 | Surgery_Schwartz | However, with the advancement of endovascular tech-niques, bronchial artery embolization in select centers with experience in these techniques has been effective.11 In patients with malignant pleural effusion, poor expan-sion of the lung (because of entrapment by tumor or adhe-sions) generally predicts a poor result with pleurodesis and is the primary indication for placement of indwelling pleu-ral catheters. These catheters have dramatically changed the management of end-stage cancer treatment because they substantially shorten the amount of time patients spend in the hospital during their final weeks of life.Brunicardi_Ch19_p0661-p0750.indd 66201/03/19 7:00 PM | Surgery_Schwartz. However, with the advancement of endovascular tech-niques, bronchial artery embolization in select centers with experience in these techniques has been effective.11 In patients with malignant pleural effusion, poor expan-sion of the lung (because of entrapment by tumor or adhe-sions) generally predicts a poor result with pleurodesis and is the primary indication for placement of indwelling pleu-ral catheters. These catheters have dramatically changed the management of end-stage cancer treatment because they substantially shorten the amount of time patients spend in the hospital during their final weeks of life.Brunicardi_Ch19_p0661-p0750.indd 66201/03/19 7:00 PM |
Surgery_Schwartz_4503 | Surgery_Schwartz | CHAPTER 19663CHEST WALL, LUNG, MEDIASTINUM, AND PLEURAEpiglottisAryepiglottic m.Transverse, obliquearytenoid mm.Lateralcricoarytenoid m.Posteriorcricoarytenoid m.Thyroid cartilage facetRecurrentlaryngeal n.Internallaryngeal n.Thyroepiglottic m.Thyroarytenoid m.Cricothyroid m.(cut)Inferiorthyroid a.Branch from internal thoracic a. Superior bronchial a.Middle bronchial a.1Lateral longitudinalanastomosis32Figure 19-2. Arterial blood supply to the larynx and upper trachea. a. = artery.Figure 19-1. Anatomy of the larynx and upper trachea. m. = muscle; n. = nerve.and stenosis; full-thickness injury can result in fistulae between the innominate artery anteriorly and the esophagus posteriorly. Avoidance requires careful cuff management to keep pressures as low as possible; in circumstances of prolonged ventilatory support and high airway pressure, cuff pressure monitoring (to maintain pressures <20 mmHg) is advisable.Historically, clinically significant tracheal stenosis after | Surgery_Schwartz. CHAPTER 19663CHEST WALL, LUNG, MEDIASTINUM, AND PLEURAEpiglottisAryepiglottic m.Transverse, obliquearytenoid mm.Lateralcricoarytenoid m.Posteriorcricoarytenoid m.Thyroid cartilage facetRecurrentlaryngeal n.Internallaryngeal n.Thyroepiglottic m.Thyroarytenoid m.Cricothyroid m.(cut)Inferiorthyroid a.Branch from internal thoracic a. Superior bronchial a.Middle bronchial a.1Lateral longitudinalanastomosis32Figure 19-2. Arterial blood supply to the larynx and upper trachea. a. = artery.Figure 19-1. Anatomy of the larynx and upper trachea. m. = muscle; n. = nerve.and stenosis; full-thickness injury can result in fistulae between the innominate artery anteriorly and the esophagus posteriorly. Avoidance requires careful cuff management to keep pressures as low as possible; in circumstances of prolonged ventilatory support and high airway pressure, cuff pressure monitoring (to maintain pressures <20 mmHg) is advisable.Historically, clinically significant tracheal stenosis after |
Surgery_Schwartz_4504 | Surgery_Schwartz | of prolonged ventilatory support and high airway pressure, cuff pressure monitoring (to maintain pressures <20 mmHg) is advisable.Historically, clinically significant tracheal stenosis after tracheostomy occurred in 3% to 12% of cases, with severe stenosis in 1% to 2%.2 With the use of low-pressure cuffs, the estimated incidence has decreased to 4.9 cases per million patients per year. Intubation-related risk factors include pro-longed intubation; high tracheostomy through the first tracheal ring or cricothyroid membrane; transverse rather than vertical incision on the trachea; oversized tracheostomy tube; prior tra-cheostomy or intubation; and traumatic intubation. Stenosis is also more common in older patients, in women, after radiation, or after excessive corticosteroid therapy, and in the setting of concomitant diseases such as autoimmune disorders, severe reflux disease, or obstructive sleep apnea and the setting of severe respiratory failure. However, even a properly placed | Surgery_Schwartz. of prolonged ventilatory support and high airway pressure, cuff pressure monitoring (to maintain pressures <20 mmHg) is advisable.Historically, clinically significant tracheal stenosis after tracheostomy occurred in 3% to 12% of cases, with severe stenosis in 1% to 2%.2 With the use of low-pressure cuffs, the estimated incidence has decreased to 4.9 cases per million patients per year. Intubation-related risk factors include pro-longed intubation; high tracheostomy through the first tracheal ring or cricothyroid membrane; transverse rather than vertical incision on the trachea; oversized tracheostomy tube; prior tra-cheostomy or intubation; and traumatic intubation. Stenosis is also more common in older patients, in women, after radiation, or after excessive corticosteroid therapy, and in the setting of concomitant diseases such as autoimmune disorders, severe reflux disease, or obstructive sleep apnea and the setting of severe respiratory failure. However, even a properly placed |
Surgery_Schwartz_4505 | Surgery_Schwartz | in the setting of concomitant diseases such as autoimmune disorders, severe reflux disease, or obstructive sleep apnea and the setting of severe respiratory failure. However, even a properly placed tra-cheostomy can lead to tracheal stenosis because of scarring and local injury. Mild ulceration and stenosis are frequently seen after tracheostomy removal. Use of the smallest tracheostomy tube possible, rapid downsizing, and a vertical tracheal incision minimize the risk for posttracheostomy stenosis.Stridor and dyspnea on exertion are the primary symp-toms of tracheal stenosis. In the setting of postintubation injury, a significant portion of the cartilaginous structural support to the airway is destroyed by regional ischemic necrosis; during healing, a weblike fibrous growth develops and narrows the airway (Fig. 19-3). In contrast, stenosis caused by tracheostomy is most commonly due to an excess of granulation tissue forma-tion around the tracheal stoma site. Time to onset of | Surgery_Schwartz. in the setting of concomitant diseases such as autoimmune disorders, severe reflux disease, or obstructive sleep apnea and the setting of severe respiratory failure. However, even a properly placed tra-cheostomy can lead to tracheal stenosis because of scarring and local injury. Mild ulceration and stenosis are frequently seen after tracheostomy removal. Use of the smallest tracheostomy tube possible, rapid downsizing, and a vertical tracheal incision minimize the risk for posttracheostomy stenosis.Stridor and dyspnea on exertion are the primary symp-toms of tracheal stenosis. In the setting of postintubation injury, a significant portion of the cartilaginous structural support to the airway is destroyed by regional ischemic necrosis; during healing, a weblike fibrous growth develops and narrows the airway (Fig. 19-3). In contrast, stenosis caused by tracheostomy is most commonly due to an excess of granulation tissue forma-tion around the tracheal stoma site. Time to onset of |
Surgery_Schwartz_4506 | Surgery_Schwartz | and narrows the airway (Fig. 19-3). In contrast, stenosis caused by tracheostomy is most commonly due to an excess of granulation tissue forma-tion around the tracheal stoma site. Time to onset of symptoms after extubation or tracheostomy decannulation usually ranges from 2 to 12 weeks, but symptoms can appear immediately or as long as 1 to 2 years later. Frequently, patients are misdiag-nosed as having asthma or bronchitis, and treatment for such illnesses can persist for some time before the correct diagnosis is discovered. Generally, symptom intensity is related to the degree of stenosis and to the patient’s underlying pulmonary disease.Brunicardi_Ch19_p0661-p0750.indd 66301/03/19 7:00 PM 664SPECIFIC CONSIDERATIONSPART IIFigure 19-3. Diagram of the principal postintubation lesions. A. A circumferential lesion at the cuff site after the use of an endotracheal tube. B. Potential lesions after the use of tracheostomy tubes. Anterolateral stenosis can be seen at the stomal level. | Surgery_Schwartz. and narrows the airway (Fig. 19-3). In contrast, stenosis caused by tracheostomy is most commonly due to an excess of granulation tissue forma-tion around the tracheal stoma site. Time to onset of symptoms after extubation or tracheostomy decannulation usually ranges from 2 to 12 weeks, but symptoms can appear immediately or as long as 1 to 2 years later. Frequently, patients are misdiag-nosed as having asthma or bronchitis, and treatment for such illnesses can persist for some time before the correct diagnosis is discovered. Generally, symptom intensity is related to the degree of stenosis and to the patient’s underlying pulmonary disease.Brunicardi_Ch19_p0661-p0750.indd 66301/03/19 7:00 PM 664SPECIFIC CONSIDERATIONSPART IIFigure 19-3. Diagram of the principal postintubation lesions. A. A circumferential lesion at the cuff site after the use of an endotracheal tube. B. Potential lesions after the use of tracheostomy tubes. Anterolateral stenosis can be seen at the stomal level. |
Surgery_Schwartz_4507 | Surgery_Schwartz | A. A circumferential lesion at the cuff site after the use of an endotracheal tube. B. Potential lesions after the use of tracheostomy tubes. Anterolateral stenosis can be seen at the stomal level. Circumferential stenosis can be seen at the cuff level (lower than with an endotracheal tube). The segment in between is often inflamed and malacotic. C. Damage to the subglottic larynx. D. Tracheoesophageal fistula occurring at the level of the tracheostomy cuff; circumferential damage is usual at this level. E. Tracheoinnominate artery fistula. (Adapted with permission from Grillo H. Surgical treatment of postintubation tracheal injuries. J Thorac Cardiovasc Surg. 1979 Dec;78(6):860-875.)Acute Management. A comprehensive bronchoscopic evalua-tion is critical in the initial phase of evaluation. Stenosis length, location, distance between the vocal cords and proximal steno-sis, and distance from the distal aspect to the major carina must be documented. In patients with severe stenosis and | Surgery_Schwartz. A. A circumferential lesion at the cuff site after the use of an endotracheal tube. B. Potential lesions after the use of tracheostomy tubes. Anterolateral stenosis can be seen at the stomal level. Circumferential stenosis can be seen at the cuff level (lower than with an endotracheal tube). The segment in between is often inflamed and malacotic. C. Damage to the subglottic larynx. D. Tracheoesophageal fistula occurring at the level of the tracheostomy cuff; circumferential damage is usual at this level. E. Tracheoinnominate artery fistula. (Adapted with permission from Grillo H. Surgical treatment of postintubation tracheal injuries. J Thorac Cardiovasc Surg. 1979 Dec;78(6):860-875.)Acute Management. A comprehensive bronchoscopic evalua-tion is critical in the initial phase of evaluation. Stenosis length, location, distance between the vocal cords and proximal steno-sis, and distance from the distal aspect to the major carina must be documented. In patients with severe stenosis and |
Surgery_Schwartz_4508 | Surgery_Schwartz | Stenosis length, location, distance between the vocal cords and proximal steno-sis, and distance from the distal aspect to the major carina must be documented. In patients with severe stenosis and respiratory compromise, rigid bronchoscopy can be used to dilate the steno-sis; this provides immediate relief of the airway obstruction and facilitates thorough evaluation of the stenosis. Rarely, if ever, is tracheostomy necessary.Most intubation injuries are located in the upper third of the trachea and can be accessed for resection through a col-lar incision. Resection typically involves 2 to 4 cm of trachea for benign stenosis. It is critical to fully resect all inflamed and scarred tissue. However, a primary anastomosis can still be per-formed without undue tension, even if up to one half of the tra-chea requires resection.2 Ideally, the patient is extubated in the operating room or shortly thereafter. For patients in whom tra-cheal resection is not possible, such as patients with | Surgery_Schwartz. Stenosis length, location, distance between the vocal cords and proximal steno-sis, and distance from the distal aspect to the major carina must be documented. In patients with severe stenosis and respiratory compromise, rigid bronchoscopy can be used to dilate the steno-sis; this provides immediate relief of the airway obstruction and facilitates thorough evaluation of the stenosis. Rarely, if ever, is tracheostomy necessary.Most intubation injuries are located in the upper third of the trachea and can be accessed for resection through a col-lar incision. Resection typically involves 2 to 4 cm of trachea for benign stenosis. It is critical to fully resect all inflamed and scarred tissue. However, a primary anastomosis can still be per-formed without undue tension, even if up to one half of the tra-chea requires resection.2 Ideally, the patient is extubated in the operating room or shortly thereafter. For patients in whom tra-cheal resection is not possible, such as patients with |
Surgery_Schwartz_4509 | Surgery_Schwartz | of the tra-chea requires resection.2 Ideally, the patient is extubated in the operating room or shortly thereafter. For patients in whom tra-cheal resection is not possible, such as patients with significant comorbidities or with an excessively long stenosis, endotracheal stenting, typically silicone T-tubes, can provide palliation. Wire mesh stents should not be used, given their known propensity to erode through the wall of the airway. Balloon dilation, laser ablation, and tracheoplasty have also been described, although the efficacy is marginal.Tracheal replacement is evolving as an option for manage-ment of tracheal stenosis as bioengineering techniques for decel-lularizing donor trachea have been developed. This removes all antigens against which the recipient immune system might react and enables use of the donor trachea scaffolding without risk of rejection. Following decellularization, the donor tracheal scaf-folding is seeded with recipient chondrocytes, to restore tracheal | Surgery_Schwartz. of the tra-chea requires resection.2 Ideally, the patient is extubated in the operating room or shortly thereafter. For patients in whom tra-cheal resection is not possible, such as patients with significant comorbidities or with an excessively long stenosis, endotracheal stenting, typically silicone T-tubes, can provide palliation. Wire mesh stents should not be used, given their known propensity to erode through the wall of the airway. Balloon dilation, laser ablation, and tracheoplasty have also been described, although the efficacy is marginal.Tracheal replacement is evolving as an option for manage-ment of tracheal stenosis as bioengineering techniques for decel-lularizing donor trachea have been developed. This removes all antigens against which the recipient immune system might react and enables use of the donor trachea scaffolding without risk of rejection. Following decellularization, the donor tracheal scaf-folding is seeded with recipient chondrocytes, to restore tracheal |
Surgery_Schwartz_4510 | Surgery_Schwartz | and enables use of the donor trachea scaffolding without risk of rejection. Following decellularization, the donor tracheal scaf-folding is seeded with recipient chondrocytes, to restore tracheal rigidity, and with recipient epithelial cells, to recreate the inner epithelial lining. Several case reports of successful allogeneic tracheal transplantation have been published. The technique continues to be limited to a few highly specialized centers, due, in part, to the scarcity of donor trachea and the need for tissue bioengineering expertise as well as the lack of established effi-cacy for the approach. Current efforts are focused on creation of biosynthetic scaffolding that can be used instead of donor trachea. This would substantially increase the availability of the tracheal replacement material and enable widespread use of the technique, but early results have been contested, including three case reports called into question as containing multiple data fab-rications and | Surgery_Schwartz. and enables use of the donor trachea scaffolding without risk of rejection. Following decellularization, the donor tracheal scaf-folding is seeded with recipient chondrocytes, to restore tracheal rigidity, and with recipient epithelial cells, to recreate the inner epithelial lining. Several case reports of successful allogeneic tracheal transplantation have been published. The technique continues to be limited to a few highly specialized centers, due, in part, to the scarcity of donor trachea and the need for tissue bioengineering expertise as well as the lack of established effi-cacy for the approach. Current efforts are focused on creation of biosynthetic scaffolding that can be used instead of donor trachea. This would substantially increase the availability of the tracheal replacement material and enable widespread use of the technique, but early results have been contested, including three case reports called into question as containing multiple data fab-rications and |
Surgery_Schwartz_4511 | Surgery_Schwartz | replacement material and enable widespread use of the technique, but early results have been contested, including three case reports called into question as containing multiple data fab-rications and omissions.Tracheal FistulasTracheoinnominate Artery Fistula. Tracheoinnominate artery fistula has two main causes: low placement of a trache-ostomy and hyperinflation of the tracheal cuff. Tracheostomy placement should be through the second to fourth tracheal rings without reference to the location of the sternal notch. When placed below the fourth tracheal ring, the inner curve of the tracheostomy cannula will be positioned to exert pressure on the posterior aspect of the innominate artery, leading to arterial ero-sion. Similarly, the tracheal cuff, when hyperinflated, will cause ischemic injury to the anterior airway and subsequent erosion into the artery. Most cuff-induced fistulas will develop within 2 weeks after placement of the tracheostomy.Clinically, tracheoinnominate artery | Surgery_Schwartz. replacement material and enable widespread use of the technique, but early results have been contested, including three case reports called into question as containing multiple data fab-rications and omissions.Tracheal FistulasTracheoinnominate Artery Fistula. Tracheoinnominate artery fistula has two main causes: low placement of a trache-ostomy and hyperinflation of the tracheal cuff. Tracheostomy placement should be through the second to fourth tracheal rings without reference to the location of the sternal notch. When placed below the fourth tracheal ring, the inner curve of the tracheostomy cannula will be positioned to exert pressure on the posterior aspect of the innominate artery, leading to arterial ero-sion. Similarly, the tracheal cuff, when hyperinflated, will cause ischemic injury to the anterior airway and subsequent erosion into the artery. Most cuff-induced fistulas will develop within 2 weeks after placement of the tracheostomy.Clinically, tracheoinnominate artery |
Surgery_Schwartz_4512 | Surgery_Schwartz | injury to the anterior airway and subsequent erosion into the artery. Most cuff-induced fistulas will develop within 2 weeks after placement of the tracheostomy.Clinically, tracheoinnominate artery fistulas present with bleeding. A premonitory hemorrhage often occurs and, although it is usually not massive, must not be ignored or simply attrib-uted to general airway irritation or wound bleeding. With sig-nificant bleeding, the tracheostomy cuff can be hyperinflated to temporarily occlude the arterial injury. If such an effort is unsuccessful, the tracheostomy incision should be immediately opened widely and a finger inserted to compress the artery Brunicardi_Ch19_p0661-p0750.indd 66401/03/19 7:00 PM | Surgery_Schwartz. injury to the anterior airway and subsequent erosion into the artery. Most cuff-induced fistulas will develop within 2 weeks after placement of the tracheostomy.Clinically, tracheoinnominate artery fistulas present with bleeding. A premonitory hemorrhage often occurs and, although it is usually not massive, must not be ignored or simply attrib-uted to general airway irritation or wound bleeding. With sig-nificant bleeding, the tracheostomy cuff can be hyperinflated to temporarily occlude the arterial injury. If such an effort is unsuccessful, the tracheostomy incision should be immediately opened widely and a finger inserted to compress the artery Brunicardi_Ch19_p0661-p0750.indd 66401/03/19 7:00 PM |
Surgery_Schwartz_4513 | Surgery_Schwartz | CHAPTER 19665CHEST WALL, LUNG, MEDIASTINUM, AND PLEURA1Cuffhyperinflation2Digital control3 BronchoscopiccompressionOrotracheal tubeready in place if neededOrotrachealtube replacingtracheostomytubeForward pressureapplied withbronchoscopeFigure 19-4. Steps in the emergency management of a tracheoinnominate artery fistula.against the manubrium (Fig. 19-4). The patient can then be orally intubated, and the airway suctioned free of blood. Emer-gent surgical resection of the involved segment of artery is per-formed, usually without reconstruction.Tracheoesophageal Fistula. Tracheoesophageal fistu-las (TEFs) occur primarily in patients receiving prolonged mechanical ventilator support concomitant with an indwelling nasogastric tube.4 Cuff compression of the membranous trachea against the nasogastric tube leads to airway and esophageal injury and fistula development. Clinically, airway suctioning reveals saliva, gastric contents, or tube feedings. Gastric insuf-flation, secondary to positive | Surgery_Schwartz. CHAPTER 19665CHEST WALL, LUNG, MEDIASTINUM, AND PLEURA1Cuffhyperinflation2Digital control3 BronchoscopiccompressionOrotracheal tubeready in place if neededOrotrachealtube replacingtracheostomytubeForward pressureapplied withbronchoscopeFigure 19-4. Steps in the emergency management of a tracheoinnominate artery fistula.against the manubrium (Fig. 19-4). The patient can then be orally intubated, and the airway suctioned free of blood. Emer-gent surgical resection of the involved segment of artery is per-formed, usually without reconstruction.Tracheoesophageal Fistula. Tracheoesophageal fistu-las (TEFs) occur primarily in patients receiving prolonged mechanical ventilator support concomitant with an indwelling nasogastric tube.4 Cuff compression of the membranous trachea against the nasogastric tube leads to airway and esophageal injury and fistula development. Clinically, airway suctioning reveals saliva, gastric contents, or tube feedings. Gastric insuf-flation, secondary to positive |
Surgery_Schwartz_4514 | Surgery_Schwartz | tube leads to airway and esophageal injury and fistula development. Clinically, airway suctioning reveals saliva, gastric contents, or tube feedings. Gastric insuf-flation, secondary to positive pressure ventilation, can occur. Bronchoscopy is diagnostic; with the bronchoscope inserted, the endotracheal tube is withdrawn, and the fistula at the cuff site is exposed. Alternatively, esophagoscopy demonstrates the cuff of the endotracheal tube in the esophagus.Treatment, first and foremost, requires removing tubes from the esophagus and weaning the patient from the ventila-tor. The cuff of the endotracheal tube should be placed below the fistula, avoiding overinflation. To minimize aspiration, a gastrostomy tube should be placed for gastric decompression (to prevent reflux) and a jejunostomy tube for feeding. If aspira-tion persists, esophageal diversion with cervical esophagostomy can be performed. Once weaned from the ventilator, tracheal resection and primary anastomosis, repair of | Surgery_Schwartz. tube leads to airway and esophageal injury and fistula development. Clinically, airway suctioning reveals saliva, gastric contents, or tube feedings. Gastric insuf-flation, secondary to positive pressure ventilation, can occur. Bronchoscopy is diagnostic; with the bronchoscope inserted, the endotracheal tube is withdrawn, and the fistula at the cuff site is exposed. Alternatively, esophagoscopy demonstrates the cuff of the endotracheal tube in the esophagus.Treatment, first and foremost, requires removing tubes from the esophagus and weaning the patient from the ventila-tor. The cuff of the endotracheal tube should be placed below the fistula, avoiding overinflation. To minimize aspiration, a gastrostomy tube should be placed for gastric decompression (to prevent reflux) and a jejunostomy tube for feeding. If aspira-tion persists, esophageal diversion with cervical esophagostomy can be performed. Once weaned from the ventilator, tracheal resection and primary anastomosis, repair of |
Surgery_Schwartz_4515 | Surgery_Schwartz | tube for feeding. If aspira-tion persists, esophageal diversion with cervical esophagostomy can be performed. Once weaned from the ventilator, tracheal resection and primary anastomosis, repair of the esophageal defect, and interposition of a muscle flap between the trachea and esophagus can be performed (Fig. 19-5).5Tracheal NeoplasmsAlthough extremely rare, the most common primary tracheal neoplasms are squamous cell carcinomas (related to smoking) and adenoid cystic carcinomas. Clinically, tracheal tumors pres-ent with cough, dyspnea, hemoptysis, stridor, or symptoms of invasion of contiguous structures (such as the recurrent laryn-geal nerve or the esophagus). The most common radiologic finding of tracheal malignancy is tracheal stenosis, but it is found in only 50% of cases. With tumors other than squamous cell carcinomas, symptoms may persist for months because of slow tumor growth rates. Stage of presentation is advanced, with approximately 50% of patients presenting with stage | Surgery_Schwartz. tube for feeding. If aspira-tion persists, esophageal diversion with cervical esophagostomy can be performed. Once weaned from the ventilator, tracheal resection and primary anastomosis, repair of the esophageal defect, and interposition of a muscle flap between the trachea and esophagus can be performed (Fig. 19-5).5Tracheal NeoplasmsAlthough extremely rare, the most common primary tracheal neoplasms are squamous cell carcinomas (related to smoking) and adenoid cystic carcinomas. Clinically, tracheal tumors pres-ent with cough, dyspnea, hemoptysis, stridor, or symptoms of invasion of contiguous structures (such as the recurrent laryn-geal nerve or the esophagus). The most common radiologic finding of tracheal malignancy is tracheal stenosis, but it is found in only 50% of cases. With tumors other than squamous cell carcinomas, symptoms may persist for months because of slow tumor growth rates. Stage of presentation is advanced, with approximately 50% of patients presenting with stage |
Surgery_Schwartz_4516 | Surgery_Schwartz | other than squamous cell carcinomas, symptoms may persist for months because of slow tumor growth rates. Stage of presentation is advanced, with approximately 50% of patients presenting with stage IV disease. Five-year survival for all tracheal neoplasms is 40% but falls to 15% for those with stage IV disease.6Squamous cell carcinomas often present with regional lymph node metastases and are frequently unresectable at pre-sentation. Their biologic behavior is similar to that of squamous cell carcinoma of the lung. Adenoid cystic carcinomas, a type of Brunicardi_Ch19_p0661-p0750.indd 66501/03/19 7:00 PM 666SPECIFIC CONSIDERATIONSPART IIACBDCricoidSternohyoid m.EsophagusFigure 19-5. Single-stage operation for clo-sure of a tracheoesophageal fistula and tra-cheal resection. A. The fistula is divided, and the trachea is transected below the level of damage. B. The fistula is closed on the tra-cheal side in a single layer and the esopha-geal side in a double layer. The damaged trachea | Surgery_Schwartz. other than squamous cell carcinomas, symptoms may persist for months because of slow tumor growth rates. Stage of presentation is advanced, with approximately 50% of patients presenting with stage IV disease. Five-year survival for all tracheal neoplasms is 40% but falls to 15% for those with stage IV disease.6Squamous cell carcinomas often present with regional lymph node metastases and are frequently unresectable at pre-sentation. Their biologic behavior is similar to that of squamous cell carcinoma of the lung. Adenoid cystic carcinomas, a type of Brunicardi_Ch19_p0661-p0750.indd 66501/03/19 7:00 PM 666SPECIFIC CONSIDERATIONSPART IIACBDCricoidSternohyoid m.EsophagusFigure 19-5. Single-stage operation for clo-sure of a tracheoesophageal fistula and tra-cheal resection. A. The fistula is divided, and the trachea is transected below the level of damage. B. The fistula is closed on the tra-cheal side in a single layer and the esopha-geal side in a double layer. The damaged trachea |
Surgery_Schwartz_4517 | Surgery_Schwartz | is divided, and the trachea is transected below the level of damage. B. The fistula is closed on the tra-cheal side in a single layer and the esopha-geal side in a double layer. The damaged trachea segment is resected. C. A pedicled muscle flap, such as the sternohyoid muscle, is used to buttress the esophageal repair. D. View of completed tracheal anastomosis. m. = muscle.salivary gland tumor, are generally slow growing, spread sub-mucosally, and tend to infiltrate along nerve sheaths and within the tracheal wall. Although indolent in nature, adenoid cystic carcinomas are malignant and can spread to regional lymph nodes, lung, and bone. Squamous cell carcinoma and adenoid cystic carcinomas represent approximately 65% of all tracheal neoplasms. The remaining 35% is comprised of small cell car-cinomas, mucoepidermoid carcinomas, adenocarcinomas, lym-phomas, and others.7Therapy. Evaluation and treatment of patients with tracheal tumors should include neck and chest computed tomography | Surgery_Schwartz. is divided, and the trachea is transected below the level of damage. B. The fistula is closed on the tra-cheal side in a single layer and the esopha-geal side in a double layer. The damaged trachea segment is resected. C. A pedicled muscle flap, such as the sternohyoid muscle, is used to buttress the esophageal repair. D. View of completed tracheal anastomosis. m. = muscle.salivary gland tumor, are generally slow growing, spread sub-mucosally, and tend to infiltrate along nerve sheaths and within the tracheal wall. Although indolent in nature, adenoid cystic carcinomas are malignant and can spread to regional lymph nodes, lung, and bone. Squamous cell carcinoma and adenoid cystic carcinomas represent approximately 65% of all tracheal neoplasms. The remaining 35% is comprised of small cell car-cinomas, mucoepidermoid carcinomas, adenocarcinomas, lym-phomas, and others.7Therapy. Evaluation and treatment of patients with tracheal tumors should include neck and chest computed tomography |
Surgery_Schwartz_4518 | Surgery_Schwartz | car-cinomas, mucoepidermoid carcinomas, adenocarcinomas, lym-phomas, and others.7Therapy. Evaluation and treatment of patients with tracheal tumors should include neck and chest computed tomography (CT) and rigid bronchoscopy. Rigid bronchoscopy permits gen-eral assessment of the airway and tumor; it also allows debride-ment or laser ablation of the tumor to provide relief of dyspnea. If the tumor is judged to be completely resectable, primary resection and anastomosis is the treatment of choice for these tumors (Fig. 19-6). Up to 50% of the length of the trachea can be resected with primary anastomosis. In most tracheal resections, anterolateral tracheal mobilization and suturing of the chin to the sternum for 7 days are done routinely. Use of laryngeal and hilar release is determined at the time of surgery, based on the surgeon’s judgment of the degree of tension present. For longer resections, specialized maneuvers are necessary such as laryn-geal release and right hilar release to | Surgery_Schwartz. car-cinomas, mucoepidermoid carcinomas, adenocarcinomas, lym-phomas, and others.7Therapy. Evaluation and treatment of patients with tracheal tumors should include neck and chest computed tomography (CT) and rigid bronchoscopy. Rigid bronchoscopy permits gen-eral assessment of the airway and tumor; it also allows debride-ment or laser ablation of the tumor to provide relief of dyspnea. If the tumor is judged to be completely resectable, primary resection and anastomosis is the treatment of choice for these tumors (Fig. 19-6). Up to 50% of the length of the trachea can be resected with primary anastomosis. In most tracheal resections, anterolateral tracheal mobilization and suturing of the chin to the sternum for 7 days are done routinely. Use of laryngeal and hilar release is determined at the time of surgery, based on the surgeon’s judgment of the degree of tension present. For longer resections, specialized maneuvers are necessary such as laryn-geal release and right hilar release to |
Surgery_Schwartz_4519 | Surgery_Schwartz | the time of surgery, based on the surgeon’s judgment of the degree of tension present. For longer resections, specialized maneuvers are necessary such as laryn-geal release and right hilar release to minimize tension on the anastomosis.Postoperative mortality, which occurs in up to 10% of patients, is associated with the length of tracheal resection, use of laryngeal release, the type of resection, and the histologic type of the cancer. Factors associated with improved long-term survival include complete resection and use of radiation as adjuvant therapy in the setting of incomplete resection.8 Due to their radiosensitivity, radiotherapy is frequently given postop-eratively after resection of both adenoid cystic carcinomas and squamous cell carcinomas.9 A dose of 50 Gy or greater is usual. Nodal positivity does not seem to be associated with worse sur-vival. Survival at 5 and 10 years is much better for adenoid Brunicardi_Ch19_p0661-p0750.indd 66601/03/19 7:00 PM | Surgery_Schwartz. the time of surgery, based on the surgeon’s judgment of the degree of tension present. For longer resections, specialized maneuvers are necessary such as laryn-geal release and right hilar release to minimize tension on the anastomosis.Postoperative mortality, which occurs in up to 10% of patients, is associated with the length of tracheal resection, use of laryngeal release, the type of resection, and the histologic type of the cancer. Factors associated with improved long-term survival include complete resection and use of radiation as adjuvant therapy in the setting of incomplete resection.8 Due to their radiosensitivity, radiotherapy is frequently given postop-eratively after resection of both adenoid cystic carcinomas and squamous cell carcinomas.9 A dose of 50 Gy or greater is usual. Nodal positivity does not seem to be associated with worse sur-vival. Survival at 5 and 10 years is much better for adenoid Brunicardi_Ch19_p0661-p0750.indd 66601/03/19 7:00 PM |
Surgery_Schwartz_4520 | Surgery_Schwartz | CHAPTER 19667CHEST WALL, LUNG, MEDIASTINUM, AND PLEURAHigh-index of suspicion(cough, dyspnea, hemoptysis,stridor, and hoarseness)Complete staging: computedtomography/PETscan/mediastinoscopyFlexible/rigid bronchoscopyTumor resectablePerformance statusadequate for surgeryDebridement and/orlaser ablationPrinciples of tracheal resection• May resect up to 50% of tracheal length• Anterolateral mobilization only• Suture head in forward flexion for 7 days• Laryngeal and hilar release as needed for relief of tensionRadiotherapy 50 Gy (±chemotherapy)(primary treatment or postoperatively)Tumor unresectable1) Probable grossly positive tracheal resection margin2) Metastatic disease3) Length of resection precludes safe reconstruction4) Invasion of unresectable adjacent organsPoor performancestatuscystic (73% and 57%, respectively) than for tracheal cancers (47% and 36%, respectively; P <.05). For patients with unre-sectable tumors, radiation may be given as the primary therapy to improve local | Surgery_Schwartz. CHAPTER 19667CHEST WALL, LUNG, MEDIASTINUM, AND PLEURAHigh-index of suspicion(cough, dyspnea, hemoptysis,stridor, and hoarseness)Complete staging: computedtomography/PETscan/mediastinoscopyFlexible/rigid bronchoscopyTumor resectablePerformance statusadequate for surgeryDebridement and/orlaser ablationPrinciples of tracheal resection• May resect up to 50% of tracheal length• Anterolateral mobilization only• Suture head in forward flexion for 7 days• Laryngeal and hilar release as needed for relief of tensionRadiotherapy 50 Gy (±chemotherapy)(primary treatment or postoperatively)Tumor unresectable1) Probable grossly positive tracheal resection margin2) Metastatic disease3) Length of resection precludes safe reconstruction4) Invasion of unresectable adjacent organsPoor performancestatuscystic (73% and 57%, respectively) than for tracheal cancers (47% and 36%, respectively; P <.05). For patients with unre-sectable tumors, radiation may be given as the primary therapy to improve local |
Surgery_Schwartz_4521 | Surgery_Schwartz | (73% and 57%, respectively) than for tracheal cancers (47% and 36%, respectively; P <.05). For patients with unre-sectable tumors, radiation may be given as the primary therapy to improve local control, but it is rarely curative. For recurrent airway compromise, stenting or laser therapies should be con-sidered as part of the treatment algorithm.LUNGAnatomySegmental Anatomy. The segmental bronchial and vascular anatomy of the lungs allows subsegmental and segmental resec-tions, if the clinical situation requires or if lung tissue can be preserved10 (Fig. 19-7). Note the continuity of the pulmonary parenchyma between adjacent segments of each lobe.Lymphatic Drainage. Lymph nodes that drain the lungs are divided into two groups according to the tumor-node-metastasis (TNM) staging system for lung cancer: the pulmonary lymph nodes (N1) and the mediastinal nodes (N2) (Fig. 19-8).The N1 lymph nodes constitute the following: (a) intrapul-monary or segmental nodes that lie at points of | Surgery_Schwartz. (73% and 57%, respectively) than for tracheal cancers (47% and 36%, respectively; P <.05). For patients with unre-sectable tumors, radiation may be given as the primary therapy to improve local control, but it is rarely curative. For recurrent airway compromise, stenting or laser therapies should be con-sidered as part of the treatment algorithm.LUNGAnatomySegmental Anatomy. The segmental bronchial and vascular anatomy of the lungs allows subsegmental and segmental resec-tions, if the clinical situation requires or if lung tissue can be preserved10 (Fig. 19-7). Note the continuity of the pulmonary parenchyma between adjacent segments of each lobe.Lymphatic Drainage. Lymph nodes that drain the lungs are divided into two groups according to the tumor-node-metastasis (TNM) staging system for lung cancer: the pulmonary lymph nodes (N1) and the mediastinal nodes (N2) (Fig. 19-8).The N1 lymph nodes constitute the following: (a) intrapul-monary or segmental nodes that lie at points of |
Surgery_Schwartz_4522 | Surgery_Schwartz | for lung cancer: the pulmonary lymph nodes (N1) and the mediastinal nodes (N2) (Fig. 19-8).The N1 lymph nodes constitute the following: (a) intrapul-monary or segmental nodes that lie at points of division of seg-mental bronchi or in the bifurcations of the pulmonary artery; (b) lobar nodes that lie along the upper, middle, and lower lobe bronchi; (c) interlobar nodes located in the angles formed by the main bronchi bifurcating into the lobar bronchi; and (d) hilar nodes along the main bronchi. The interlobar lymph nodes lie in the depths of the interlobar fissure on each side and constitute a lymphatic sump for each lung, referred to as the lymphatic sump of Borrie; all of the pulmonary lobes of the corresponding lung drain into this group of nodes (Fig. 19-9). On the right, the nodes of the lymphatic sump lie around the bronchus inter-medius (bounded above by the right upper lobe bronchus and below by the middle lobe and superior segmental bronchi). On the left, the lymphatic sump | Surgery_Schwartz. for lung cancer: the pulmonary lymph nodes (N1) and the mediastinal nodes (N2) (Fig. 19-8).The N1 lymph nodes constitute the following: (a) intrapul-monary or segmental nodes that lie at points of division of seg-mental bronchi or in the bifurcations of the pulmonary artery; (b) lobar nodes that lie along the upper, middle, and lower lobe bronchi; (c) interlobar nodes located in the angles formed by the main bronchi bifurcating into the lobar bronchi; and (d) hilar nodes along the main bronchi. The interlobar lymph nodes lie in the depths of the interlobar fissure on each side and constitute a lymphatic sump for each lung, referred to as the lymphatic sump of Borrie; all of the pulmonary lobes of the corresponding lung drain into this group of nodes (Fig. 19-9). On the right, the nodes of the lymphatic sump lie around the bronchus inter-medius (bounded above by the right upper lobe bronchus and below by the middle lobe and superior segmental bronchi). On the left, the lymphatic sump |
Surgery_Schwartz_4523 | Surgery_Schwartz | the lymphatic sump lie around the bronchus inter-medius (bounded above by the right upper lobe bronchus and below by the middle lobe and superior segmental bronchi). On the left, the lymphatic sump is confined to the interlobar fis-sure, with the lymph nodes in the angle between the lingular and lower lobe bronchi. These nodes are always in close proximity to pulmonary arterial branches and typically must be carefully dissected to identify the pulmonary arterial segments for divi-sion during lung resection.The N2 lymph nodes consist of four main groups. (a) The anterior mediastinal nodes are located in association with the upper surface of the pericardium, the phrenic nerves, the liga-mentum arteriosum, and the left aspect of the innominate vein. (b) The posterior mediastinal group includes paraesophageal lymph nodes within the inferior pulmonary ligament and, more superiorly, between the esophagus and trachea near the arch of the azygos vein. (c) The tracheobronchial lymph nodes are | Surgery_Schwartz. the lymphatic sump lie around the bronchus inter-medius (bounded above by the right upper lobe bronchus and below by the middle lobe and superior segmental bronchi). On the left, the lymphatic sump is confined to the interlobar fis-sure, with the lymph nodes in the angle between the lingular and lower lobe bronchi. These nodes are always in close proximity to pulmonary arterial branches and typically must be carefully dissected to identify the pulmonary arterial segments for divi-sion during lung resection.The N2 lymph nodes consist of four main groups. (a) The anterior mediastinal nodes are located in association with the upper surface of the pericardium, the phrenic nerves, the liga-mentum arteriosum, and the left aspect of the innominate vein. (b) The posterior mediastinal group includes paraesophageal lymph nodes within the inferior pulmonary ligament and, more superiorly, between the esophagus and trachea near the arch of the azygos vein. (c) The tracheobronchial lymph nodes are |
Surgery_Schwartz_4524 | Surgery_Schwartz | paraesophageal lymph nodes within the inferior pulmonary ligament and, more superiorly, between the esophagus and trachea near the arch of the azygos vein. (c) The tracheobronchial lymph nodes are made up of three subgroups that are located near the bifurcation of the trachea. These include the subcarinal nodes, which lie in the obtuse angle between the trachea and each main stem bronchus, and the nodes that lay anterior to the lower end of the trachea. (d) Paratracheal lymph nodes are located in proximity to the trachea in the superior mediastinum. Those on the right side form a chain with the tracheobronchial nodes inferiorly and with some of the deep cervical nodes above (scalene lymph nodes).Lymphatic drainage to the mediastinal lymph nodes from the right lung is ipsilateral, except for occasional bilateral drain-age to the superior mediastinum. In contrast, in the left lung, particularly the left lower lobe, lymphatic drainage occurs with equal frequency to ipsilateral and | Surgery_Schwartz. paraesophageal lymph nodes within the inferior pulmonary ligament and, more superiorly, between the esophagus and trachea near the arch of the azygos vein. (c) The tracheobronchial lymph nodes are made up of three subgroups that are located near the bifurcation of the trachea. These include the subcarinal nodes, which lie in the obtuse angle between the trachea and each main stem bronchus, and the nodes that lay anterior to the lower end of the trachea. (d) Paratracheal lymph nodes are located in proximity to the trachea in the superior mediastinum. Those on the right side form a chain with the tracheobronchial nodes inferiorly and with some of the deep cervical nodes above (scalene lymph nodes).Lymphatic drainage to the mediastinal lymph nodes from the right lung is ipsilateral, except for occasional bilateral drain-age to the superior mediastinum. In contrast, in the left lung, particularly the left lower lobe, lymphatic drainage occurs with equal frequency to ipsilateral and |
Surgery_Schwartz_4525 | Surgery_Schwartz | for occasional bilateral drain-age to the superior mediastinum. In contrast, in the left lung, particularly the left lower lobe, lymphatic drainage occurs with equal frequency to ipsilateral and contralateral superior medi-astinal nodes.Figure 19-6. Algorithm for eval-uation and treatment of tracheal neoplasm. PET = positron emis-sion tomography.Brunicardi_Ch19_p0661-p0750.indd 66701/03/19 7:00 PM 668SPECIFIC CONSIDERATIONSPART IIRight lung and bronchiLeft lung and bronchi11112222333333444445555556666668888888999999101010101010107771+21+2Segments 1. Apical2. Posterior3. Anterior4. Lateral5. Medial6. Superior7. Medial Basal *8. Anterior Basal9. Lateral Basal10. Posterior Basal * Medial basal (7) not present in left lungFigure 19-7. Segmental anatomy of the lungs and bronchi.3p3a6AoPA512LBrachiocephalicartery2R4RAo4LAzygos vein10R711R12,13,14R8R9R9L8LPA11L10L12,13,14LFigure 19-8. The location of regional lymph node stations for lung cancer.Figure 19-9. The lymphatic sump of | Surgery_Schwartz. for occasional bilateral drain-age to the superior mediastinum. In contrast, in the left lung, particularly the left lower lobe, lymphatic drainage occurs with equal frequency to ipsilateral and contralateral superior medi-astinal nodes.Figure 19-6. Algorithm for eval-uation and treatment of tracheal neoplasm. PET = positron emis-sion tomography.Brunicardi_Ch19_p0661-p0750.indd 66701/03/19 7:00 PM 668SPECIFIC CONSIDERATIONSPART IIRight lung and bronchiLeft lung and bronchi11112222333333444445555556666668888888999999101010101010107771+21+2Segments 1. Apical2. Posterior3. Anterior4. Lateral5. Medial6. Superior7. Medial Basal *8. Anterior Basal9. Lateral Basal10. Posterior Basal * Medial basal (7) not present in left lungFigure 19-7. Segmental anatomy of the lungs and bronchi.3p3a6AoPA512LBrachiocephalicartery2R4RAo4LAzygos vein10R711R12,13,14R8R9R9L8LPA11L10L12,13,14LFigure 19-8. The location of regional lymph node stations for lung cancer.Figure 19-9. The lymphatic sump of |
Surgery_Schwartz_4526 | Surgery_Schwartz | vein10R711R12,13,14R8R9R9L8LPA11L10L12,13,14LFigure 19-8. The location of regional lymph node stations for lung cancer.Figure 19-9. The lymphatic sump of Borrie includes the groups of lymph nodes that receive lymphatic drainage from all pulmonary lobes of the corresponding lung.Normal Lung HistologyThe lung can be conveniently viewed as two linked compo-nents: the tracheobronchial tree (or conducting airways com-ponent) and the alveolar spaces (or gas exchange component). The tracheobronchial tree consists of approximately 23 airway divisions to the level of the alveoli. It includes the main bronchi, lobar bronchi, segmental bronchi (to designated bronchopulmo-nary segments), and terminal bronchioles (i.e., the smallest air-ways still lined by bronchial epithelium and without alveoli). The tracheobronchial tree is normally lined by pseudostratified ciliated columnar cells and mucous (or goblet) cells, which both derive from basal cells (Fig. 19-10). Ciliated cells predominate. Goblet | Surgery_Schwartz. vein10R711R12,13,14R8R9R9L8LPA11L10L12,13,14LFigure 19-8. The location of regional lymph node stations for lung cancer.Figure 19-9. The lymphatic sump of Borrie includes the groups of lymph nodes that receive lymphatic drainage from all pulmonary lobes of the corresponding lung.Normal Lung HistologyThe lung can be conveniently viewed as two linked compo-nents: the tracheobronchial tree (or conducting airways com-ponent) and the alveolar spaces (or gas exchange component). The tracheobronchial tree consists of approximately 23 airway divisions to the level of the alveoli. It includes the main bronchi, lobar bronchi, segmental bronchi (to designated bronchopulmo-nary segments), and terminal bronchioles (i.e., the smallest air-ways still lined by bronchial epithelium and without alveoli). The tracheobronchial tree is normally lined by pseudostratified ciliated columnar cells and mucous (or goblet) cells, which both derive from basal cells (Fig. 19-10). Ciliated cells predominate. Goblet |
Surgery_Schwartz_4527 | Surgery_Schwartz | tracheobronchial tree is normally lined by pseudostratified ciliated columnar cells and mucous (or goblet) cells, which both derive from basal cells (Fig. 19-10). Ciliated cells predominate. Goblet cells, which release mucus, can significantly increase in number in acute bronchial injury, such as exposure to cigarette smoke. The normal bronchial epithelium also contains bron-chial submucosal glands, which are mixed salivary-type glands Brunicardi_Ch19_p0661-p0750.indd 66801/03/19 7:00 PM | Surgery_Schwartz. tracheobronchial tree is normally lined by pseudostratified ciliated columnar cells and mucous (or goblet) cells, which both derive from basal cells (Fig. 19-10). Ciliated cells predominate. Goblet cells, which release mucus, can significantly increase in number in acute bronchial injury, such as exposure to cigarette smoke. The normal bronchial epithelium also contains bron-chial submucosal glands, which are mixed salivary-type glands Brunicardi_Ch19_p0661-p0750.indd 66801/03/19 7:00 PM |
Surgery_Schwartz_4528 | Surgery_Schwartz | CHAPTER 19669CHEST WALL, LUNG, MEDIASTINUM, AND PLEURABAFigure 19-10. Normal lung histology. A. Pseudostratified ciliated columnar cells and mucous cells normally line the tracheobronchial tree. B. A Kulchitsky cell is depicted (arrow).containing mucous cells, serous cells, and neuroendocrine cells called Kulchitsky cells, which are also found within the surface epithelium. The bronchial submucosal glands can give rise to salivary gland–type tumors, including mucoepidermoid carci-nomas and adenoid cystic carcinomas.Two cell types, called type I and type II pneumocytes, make up the alveolar epithelium. Type I pneumocytes com-prise 40% of the total number of alveolar epithelial cells, but cover 95% of the surface area of the alveolar wall. These cells are not capable of regeneration because they have no mitotic potential. Type II pneumocytes cover only 3% of the alveo-lar surface, but comprise 60% of the alveolar epithelial cells. In addition, clusters of neuroendocrine cells are seen | Surgery_Schwartz. CHAPTER 19669CHEST WALL, LUNG, MEDIASTINUM, AND PLEURABAFigure 19-10. Normal lung histology. A. Pseudostratified ciliated columnar cells and mucous cells normally line the tracheobronchial tree. B. A Kulchitsky cell is depicted (arrow).containing mucous cells, serous cells, and neuroendocrine cells called Kulchitsky cells, which are also found within the surface epithelium. The bronchial submucosal glands can give rise to salivary gland–type tumors, including mucoepidermoid carci-nomas and adenoid cystic carcinomas.Two cell types, called type I and type II pneumocytes, make up the alveolar epithelium. Type I pneumocytes com-prise 40% of the total number of alveolar epithelial cells, but cover 95% of the surface area of the alveolar wall. These cells are not capable of regeneration because they have no mitotic potential. Type II pneumocytes cover only 3% of the alveo-lar surface, but comprise 60% of the alveolar epithelial cells. In addition, clusters of neuroendocrine cells are seen |
Surgery_Schwartz_4529 | Surgery_Schwartz | they have no mitotic potential. Type II pneumocytes cover only 3% of the alveo-lar surface, but comprise 60% of the alveolar epithelial cells. In addition, clusters of neuroendocrine cells are seen in the alveolar spaces.Preinvasive LesionsThe term “precancerous” does not mean that an inevitable pro-gression to invasive carcinoma will occur, but such lesions, particularly those with high-grade dysplasia,11,12 do constitute a clear marker for potential development of invasive cancer. Three precancerous lesions of the respiratory tract are currently recognized.1. Squamous dysplasia and carcinoma in situ. Cigarette smoke can induce a transformation of the tracheobron-chial pseudostratified epithelium to metaplastic squamous mucosa, with subsequent evolution to dysplasia as cellu-lar abnormalities accumulate. Dysplastic changes include altered cellular polarity and increased cell size, number of cell layers, nuclear-to-cytoplasmic ratio, and number of mitoses. Gradations are considered | Surgery_Schwartz. they have no mitotic potential. Type II pneumocytes cover only 3% of the alveo-lar surface, but comprise 60% of the alveolar epithelial cells. In addition, clusters of neuroendocrine cells are seen in the alveolar spaces.Preinvasive LesionsThe term “precancerous” does not mean that an inevitable pro-gression to invasive carcinoma will occur, but such lesions, particularly those with high-grade dysplasia,11,12 do constitute a clear marker for potential development of invasive cancer. Three precancerous lesions of the respiratory tract are currently recognized.1. Squamous dysplasia and carcinoma in situ. Cigarette smoke can induce a transformation of the tracheobron-chial pseudostratified epithelium to metaplastic squamous mucosa, with subsequent evolution to dysplasia as cellu-lar abnormalities accumulate. Dysplastic changes include altered cellular polarity and increased cell size, number of cell layers, nuclear-to-cytoplasmic ratio, and number of mitoses. Gradations are considered |
Surgery_Schwartz_4530 | Surgery_Schwartz | accumulate. Dysplastic changes include altered cellular polarity and increased cell size, number of cell layers, nuclear-to-cytoplasmic ratio, and number of mitoses. Gradations are considered mild, moderate, or severe. Carcinoma in situ represents carcinoma still con-fined by the basement membrane.2. Atypical adenomatous hyperplasia (AAH). AAH is a lesion smaller than 5.0 mm, comprising epithelial cells lining the alveoli that are similar to type II pneumocytes. Histologically, AAH is similar to adenocarcinoma in situ; it represents the beginning stage of a stepwise evolution to adenocarcinoma in situ and then to adenocarcinoma. With the availability of thin-section CT, it is possible to detect Brunicardi_Ch19_p0661-p0750.indd 66901/03/19 7:00 PM 670SPECIFIC CONSIDERATIONSPART IIpreinvasive adenocarcinoma lesions as early as AAH. These lesions can be multiple, are typically small (5 mm or less), and have a ground-glass appearance.3. Diffuse idiopathic pulmonary neuroendocrine cell | Surgery_Schwartz. accumulate. Dysplastic changes include altered cellular polarity and increased cell size, number of cell layers, nuclear-to-cytoplasmic ratio, and number of mitoses. Gradations are considered mild, moderate, or severe. Carcinoma in situ represents carcinoma still con-fined by the basement membrane.2. Atypical adenomatous hyperplasia (AAH). AAH is a lesion smaller than 5.0 mm, comprising epithelial cells lining the alveoli that are similar to type II pneumocytes. Histologically, AAH is similar to adenocarcinoma in situ; it represents the beginning stage of a stepwise evolution to adenocarcinoma in situ and then to adenocarcinoma. With the availability of thin-section CT, it is possible to detect Brunicardi_Ch19_p0661-p0750.indd 66901/03/19 7:00 PM 670SPECIFIC CONSIDERATIONSPART IIpreinvasive adenocarcinoma lesions as early as AAH. These lesions can be multiple, are typically small (5 mm or less), and have a ground-glass appearance.3. Diffuse idiopathic pulmonary neuroendocrine cell |
Surgery_Schwartz_4531 | Surgery_Schwartz | adenocarcinoma lesions as early as AAH. These lesions can be multiple, are typically small (5 mm or less), and have a ground-glass appearance.3. Diffuse idiopathic pulmonary neuroendocrine cell hyper-plasia. This rare lesion represents a diffuse proliferation of neuroendocrine cells, but without invasion of the basement membrane. It can exist as a diffuse increase in the number of single neuroendocrine cells, or as small lesions less than 5.0 mm in diameter. Lesions over 5.0 mm in size or that breach the basement membrane are carcinoid tumors.Invasive or Malignant LesionsThe pathologic diagnosis of lung cancer is currently based on light microscopic criteria and is broadly divided into two main groups: non–small cell lung carcinoma and neuroendocrine tumors.13 Immunohistochemical staining and electron micros-copy are used as adjuncts in diagnosis, particularly in the assess-ment of potential neuroendocrine tumors.Non–Small Cell Lung Carcinoma. The term non–small cell lung carcinoma | Surgery_Schwartz. adenocarcinoma lesions as early as AAH. These lesions can be multiple, are typically small (5 mm or less), and have a ground-glass appearance.3. Diffuse idiopathic pulmonary neuroendocrine cell hyper-plasia. This rare lesion represents a diffuse proliferation of neuroendocrine cells, but without invasion of the basement membrane. It can exist as a diffuse increase in the number of single neuroendocrine cells, or as small lesions less than 5.0 mm in diameter. Lesions over 5.0 mm in size or that breach the basement membrane are carcinoid tumors.Invasive or Malignant LesionsThe pathologic diagnosis of lung cancer is currently based on light microscopic criteria and is broadly divided into two main groups: non–small cell lung carcinoma and neuroendocrine tumors.13 Immunohistochemical staining and electron micros-copy are used as adjuncts in diagnosis, particularly in the assess-ment of potential neuroendocrine tumors.Non–Small Cell Lung Carcinoma. The term non–small cell lung carcinoma |
Surgery_Schwartz_4532 | Surgery_Schwartz | and electron micros-copy are used as adjuncts in diagnosis, particularly in the assess-ment of potential neuroendocrine tumors.Non–Small Cell Lung Carcinoma. The term non–small cell lung carcinoma (NSCLC) includes many tumor cell types, including large cell, squamous cell, and adenocarcinoma. His-torically, these subtypes were considered to be a uniform group based on limited understanding of the distinct clinical behaviors of the subtypes as well as the fact that there were few treat-ment options available. With increasing understanding of the molecular biology underlying these tumor subtypes, however, the approach to diagnosis and management and the terminology used in describing these tumors are evolving rapidly.Adenocarcinoma The incidence of adenocarcinoma has increased over the last several decades, and it is now the most common lung cancer, accounting for 30% of lung cancers in Table 19-1Difference between invasive mucinous adenocarcinoma and nonmucinous adenocarcinoma in | Surgery_Schwartz. and electron micros-copy are used as adjuncts in diagnosis, particularly in the assess-ment of potential neuroendocrine tumors.Non–Small Cell Lung Carcinoma. The term non–small cell lung carcinoma (NSCLC) includes many tumor cell types, including large cell, squamous cell, and adenocarcinoma. His-torically, these subtypes were considered to be a uniform group based on limited understanding of the distinct clinical behaviors of the subtypes as well as the fact that there were few treat-ment options available. With increasing understanding of the molecular biology underlying these tumor subtypes, however, the approach to diagnosis and management and the terminology used in describing these tumors are evolving rapidly.Adenocarcinoma The incidence of adenocarcinoma has increased over the last several decades, and it is now the most common lung cancer, accounting for 30% of lung cancers in Table 19-1Difference between invasive mucinous adenocarcinoma and nonmucinous adenocarcinoma in |
Surgery_Schwartz_4533 | Surgery_Schwartz | last several decades, and it is now the most common lung cancer, accounting for 30% of lung cancers in Table 19-1Difference between invasive mucinous adenocarcinoma and nonmucinous adenocarcinoma in situ/minimally invasive adenocarcinoma/lepidic predominant adenocarcinoma INVASIVE MUCINOUS ADENOCARCINOMA (FORMERLY MUCINOUS BAC)NONMUCINOUS AIS/MIA/LPA (FORMERLY NONMUCINOUS BAC)Female49/84 (58%)52,120-123101/140 (72%)52,120-123Smoker39/87 (45%)52,120-122,12475/164 (46%)52,120-122,124Radiographic appearanceMajority consolidation; air bronchogram125Majority ground-glass attenuation23,56,58,103,129-134 Frequent multifocal and multilobar presentation56,125-128 Cell typeMucin-filled, columnar, and/or goblet50-52,125,135Type II pneumocyte and/or Clara cell50-52,125,135Phenotype CK7Mostly positive (∼88%)a54,55,136-139Positive (∼98%)a54,55,136-139 CK20Positive (∼54%)a54,55,136-139Negative (∼5%)a54,55,136-139 TTF-1Mostly negative (∼17%)a54,55,120,137-139Positive | Surgery_Schwartz. last several decades, and it is now the most common lung cancer, accounting for 30% of lung cancers in Table 19-1Difference between invasive mucinous adenocarcinoma and nonmucinous adenocarcinoma in situ/minimally invasive adenocarcinoma/lepidic predominant adenocarcinoma INVASIVE MUCINOUS ADENOCARCINOMA (FORMERLY MUCINOUS BAC)NONMUCINOUS AIS/MIA/LPA (FORMERLY NONMUCINOUS BAC)Female49/84 (58%)52,120-123101/140 (72%)52,120-123Smoker39/87 (45%)52,120-122,12475/164 (46%)52,120-122,124Radiographic appearanceMajority consolidation; air bronchogram125Majority ground-glass attenuation23,56,58,103,129-134 Frequent multifocal and multilobar presentation56,125-128 Cell typeMucin-filled, columnar, and/or goblet50-52,125,135Type II pneumocyte and/or Clara cell50-52,125,135Phenotype CK7Mostly positive (∼88%)a54,55,136-139Positive (∼98%)a54,55,136-139 CK20Positive (∼54%)a54,55,136-139Negative (∼5%)a54,55,136-139 TTF-1Mostly negative (∼17%)a54,55,120,137-139Positive |
Surgery_Schwartz_4534 | Surgery_Schwartz | positive (∼88%)a54,55,136-139Positive (∼98%)a54,55,136-139 CK20Positive (∼54%)a54,55,136-139Negative (∼5%)a54,55,136-139 TTF-1Mostly negative (∼17%)a54,55,120,137-139Positive (∼67%)a54,55,120,137-139Genotype KRAS mutationFrequent (∼76%)a55,94,121,127,140-144Some (∼13%)a55,121,127,140-144 EGFR mutationAlmost none (∼3)a55,121,127,140-142Frequent (∼45%)a55,121,127,140-142Note: aNumbers represent the percentage of cases that are reported to be positive.Abbreviations: BAC = bronchioloalveolar carcinoma; AIS = adenocarcinoma in situ; MIA = minimally invasive adenocarcinoma; LPA = lepidic predominant adenocarcinoma; EGFR = epidermal growth factor receptor; TTF = thyroid transcription factor.Reproduced with permission from Travis WD, Brambilla E, Noguchi M, et al: International association for the study of lung cancer/american thoracic society/european respiratory society international multidisciplinary classification of lung adenocarcinoma, J Thorac Oncol. 2011 Feb;6(2):244-285.male | Surgery_Schwartz. positive (∼88%)a54,55,136-139Positive (∼98%)a54,55,136-139 CK20Positive (∼54%)a54,55,136-139Negative (∼5%)a54,55,136-139 TTF-1Mostly negative (∼17%)a54,55,120,137-139Positive (∼67%)a54,55,120,137-139Genotype KRAS mutationFrequent (∼76%)a55,94,121,127,140-144Some (∼13%)a55,121,127,140-144 EGFR mutationAlmost none (∼3)a55,121,127,140-142Frequent (∼45%)a55,121,127,140-142Note: aNumbers represent the percentage of cases that are reported to be positive.Abbreviations: BAC = bronchioloalveolar carcinoma; AIS = adenocarcinoma in situ; MIA = minimally invasive adenocarcinoma; LPA = lepidic predominant adenocarcinoma; EGFR = epidermal growth factor receptor; TTF = thyroid transcription factor.Reproduced with permission from Travis WD, Brambilla E, Noguchi M, et al: International association for the study of lung cancer/american thoracic society/european respiratory society international multidisciplinary classification of lung adenocarcinoma, J Thorac Oncol. 2011 Feb;6(2):244-285.male |
Surgery_Schwartz_4535 | Surgery_Schwartz | for the study of lung cancer/american thoracic society/european respiratory society international multidisciplinary classification of lung adenocarcinoma, J Thorac Oncol. 2011 Feb;6(2):244-285.male smokers and 40% of lung cancers in female smokers. Adenocarcinoma is the histologic subtype for 80% and 60% of lung cancers in nonsmoking females and males, respectively. It occurs more frequently in females than in males. It is the most frequent histologic subtype in women, patients who are under 45 years of age, and Asian populations.14Histologic Subtyping of Adenocarcinoma. Increasing under-standing of lung adenocarcinoma, such as important clinical, radiologic, pathologic, and genetic differences between mucinous and nonmucinous adenocarcinomas, prompted multiple changes in the classification system in 2011.15 Based on consensus, the international working group proposed a multidisciplinary approach, with standardized criteria and terminology for diagno-sis in cytologic and small biopsy | Surgery_Schwartz. for the study of lung cancer/american thoracic society/european respiratory society international multidisciplinary classification of lung adenocarcinoma, J Thorac Oncol. 2011 Feb;6(2):244-285.male smokers and 40% of lung cancers in female smokers. Adenocarcinoma is the histologic subtype for 80% and 60% of lung cancers in nonsmoking females and males, respectively. It occurs more frequently in females than in males. It is the most frequent histologic subtype in women, patients who are under 45 years of age, and Asian populations.14Histologic Subtyping of Adenocarcinoma. Increasing under-standing of lung adenocarcinoma, such as important clinical, radiologic, pathologic, and genetic differences between mucinous and nonmucinous adenocarcinomas, prompted multiple changes in the classification system in 2011.15 Based on consensus, the international working group proposed a multidisciplinary approach, with standardized criteria and terminology for diagno-sis in cytologic and small biopsy |
Surgery_Schwartz_4536 | Surgery_Schwartz | system in 2011.15 Based on consensus, the international working group proposed a multidisciplinary approach, with standardized criteria and terminology for diagno-sis in cytologic and small biopsy specimens, and routine molecu-lar testing for known mutations, such as EGFR and KRAS mutations (Table 19-1). The new classification system delineated a stepwise pathologic progression, from AAH to invasive adenocarcinoma based on the predominant histologic growth patterns; the terms bronchioloalveolar carcinoma and mixed subtype adenocarcinoma were eliminated in favor of more biologically driven classification (Table 19-2).1. Adenocarcinoma in situ (AIS). AISs are small (≤3 cm) sol-itary adenocarcinomas that have pure lepidic growth; lepidic growth is characterized by tumor growth within the alveolar spaces. These lesions are not invasive into the stroma, vas-cular system, or pleura and do not have papillary or micro-papillary patterns or intra-alveolar tumor cells. They are very rarely | Surgery_Schwartz. system in 2011.15 Based on consensus, the international working group proposed a multidisciplinary approach, with standardized criteria and terminology for diagno-sis in cytologic and small biopsy specimens, and routine molecu-lar testing for known mutations, such as EGFR and KRAS mutations (Table 19-1). The new classification system delineated a stepwise pathologic progression, from AAH to invasive adenocarcinoma based on the predominant histologic growth patterns; the terms bronchioloalveolar carcinoma and mixed subtype adenocarcinoma were eliminated in favor of more biologically driven classification (Table 19-2).1. Adenocarcinoma in situ (AIS). AISs are small (≤3 cm) sol-itary adenocarcinomas that have pure lepidic growth; lepidic growth is characterized by tumor growth within the alveolar spaces. These lesions are not invasive into the stroma, vas-cular system, or pleura and do not have papillary or micro-papillary patterns or intra-alveolar tumor cells. They are very rarely |
Surgery_Schwartz_4537 | Surgery_Schwartz | alveolar spaces. These lesions are not invasive into the stroma, vas-cular system, or pleura and do not have papillary or micro-papillary patterns or intra-alveolar tumor cells. They are very rarely mucinous, consisting of type II pneumocytes or Clara cells. These patients are expected to have 100% dis-ease-specific survival with complete surgical resection. On CT scan, AIS can appear as a pure ground-glass neoplasm, 123Brunicardi_Ch19_p0661-p0750.indd 67001/03/19 7:00 PM | Surgery_Schwartz. alveolar spaces. These lesions are not invasive into the stroma, vas-cular system, or pleura and do not have papillary or micro-papillary patterns or intra-alveolar tumor cells. They are very rarely mucinous, consisting of type II pneumocytes or Clara cells. These patients are expected to have 100% dis-ease-specific survival with complete surgical resection. On CT scan, AIS can appear as a pure ground-glass neoplasm, 123Brunicardi_Ch19_p0661-p0750.indd 67001/03/19 7:00 PM |
Surgery_Schwartz_4538 | Surgery_Schwartz | CHAPTER 19671CHEST WALL, LUNG, MEDIASTINUM, AND PLEURATable 19-2New classification system for lung adenocarcinomaPreinvasive lesions Atypical adenomatous hyperplasia Adenocarcinoma in situ (≤3 cm formerly BAC) Nonmucinous Mucinous Mixed mucinous/nonmucinousMinimally invasive adenocarcinoma (≤3 cm lepidic predominant tumor with ≤5 mm invasion) Nonmucinous Mucinous Mixed mucinous/nonmucinousInvasive adenocarcinoma Lepidic predominant (formerly nonmucinous BAC pattern, with >5 mm invasion) Acinar predominant Papillary predominant Micropapillary predominant Solid predominant with mucin productionVariants of invasive adenocarcinoma Invasive mucinous adenocarcinoma (formerly mucinous BAC) Colloid Fetal (low and high grade) EntericAbbreviations: BAC = bronchioloalveolar carcinoma; IASLC = International Association for the Study of Lung Cancer; ATS = American Thoracic Society; ERS = European Respiratory Society.Reproduced with permission from Travis WD, Brambilla E, Noguchi M, et al: | Surgery_Schwartz. CHAPTER 19671CHEST WALL, LUNG, MEDIASTINUM, AND PLEURATable 19-2New classification system for lung adenocarcinomaPreinvasive lesions Atypical adenomatous hyperplasia Adenocarcinoma in situ (≤3 cm formerly BAC) Nonmucinous Mucinous Mixed mucinous/nonmucinousMinimally invasive adenocarcinoma (≤3 cm lepidic predominant tumor with ≤5 mm invasion) Nonmucinous Mucinous Mixed mucinous/nonmucinousInvasive adenocarcinoma Lepidic predominant (formerly nonmucinous BAC pattern, with >5 mm invasion) Acinar predominant Papillary predominant Micropapillary predominant Solid predominant with mucin productionVariants of invasive adenocarcinoma Invasive mucinous adenocarcinoma (formerly mucinous BAC) Colloid Fetal (low and high grade) EntericAbbreviations: BAC = bronchioloalveolar carcinoma; IASLC = International Association for the Study of Lung Cancer; ATS = American Thoracic Society; ERS = European Respiratory Society.Reproduced with permission from Travis WD, Brambilla E, Noguchi M, et al: |
Surgery_Schwartz_4539 | Surgery_Schwartz | International Association for the Study of Lung Cancer; ATS = American Thoracic Society; ERS = European Respiratory Society.Reproduced with permission from Travis WD, Brambilla E, Noguchi M, et al: International association for the study of lung cancer/american thoracic society/european respiratory society international multidisciplinary classification of lung adenocarcinoma, J Thorac Oncol. 2011 Feb;6(2):244-285.but occasionally it will present as part of a solid or part-solid nodule. Mucinous AIS is more likely to appear solid or to have the appearance of consolidation. As with AAH, the lesions can be single or multiple; the ground-glass changes in AIS, however, tend to have a higher attenuation com-pared to AAH. The 8th edition American Joint Committee on Cancer (AJCC) staging manual t-stage for AIS is tumor in situ (Tis).2. Minimally invasive adenocarcinoma (MIA). In the same size solitary lesion, if less than 5 mm of invasion are noted within a predominantly lepidic growth | Surgery_Schwartz. International Association for the Study of Lung Cancer; ATS = American Thoracic Society; ERS = European Respiratory Society.Reproduced with permission from Travis WD, Brambilla E, Noguchi M, et al: International association for the study of lung cancer/american thoracic society/european respiratory society international multidisciplinary classification of lung adenocarcinoma, J Thorac Oncol. 2011 Feb;6(2):244-285.but occasionally it will present as part of a solid or part-solid nodule. Mucinous AIS is more likely to appear solid or to have the appearance of consolidation. As with AAH, the lesions can be single or multiple; the ground-glass changes in AIS, however, tend to have a higher attenuation com-pared to AAH. The 8th edition American Joint Committee on Cancer (AJCC) staging manual t-stage for AIS is tumor in situ (Tis).2. Minimally invasive adenocarcinoma (MIA). In the same size solitary lesion, if less than 5 mm of invasion are noted within a predominantly lepidic growth |
Surgery_Schwartz_4540 | Surgery_Schwartz | t-stage for AIS is tumor in situ (Tis).2. Minimally invasive adenocarcinoma (MIA). In the same size solitary lesion, if less than 5 mm of invasion are noted within a predominantly lepidic growth pattern, the lesion is termed minimally invasive adenocarcinoma (MIA) to indicate a patient group with near 100% survival when the lesion is completely resected. This differentiates patients with AIS, but recognizes the fact that the presence of invasion becomes prognostically significant when the size of the invasive com-ponent reaches 5 mm or greater in size.16 If multiple areas of microscopic invasion are found within the lepidic growth, the size of the largest invasive area, measured in the larg-est dimension, is used; this area must be ≤5 mm to be con-sidered MIA. As with AIS, MIA is very rarely mucinous. The invasive component histologically is acinar, papillary, micropapillary, and/or solid and shows tumor cells infil-trating into the surrounding myofibroblastic stroma. On CT scan, the | Surgery_Schwartz. t-stage for AIS is tumor in situ (Tis).2. Minimally invasive adenocarcinoma (MIA). In the same size solitary lesion, if less than 5 mm of invasion are noted within a predominantly lepidic growth pattern, the lesion is termed minimally invasive adenocarcinoma (MIA) to indicate a patient group with near 100% survival when the lesion is completely resected. This differentiates patients with AIS, but recognizes the fact that the presence of invasion becomes prognostically significant when the size of the invasive com-ponent reaches 5 mm or greater in size.16 If multiple areas of microscopic invasion are found within the lepidic growth, the size of the largest invasive area, measured in the larg-est dimension, is used; this area must be ≤5 mm to be con-sidered MIA. As with AIS, MIA is very rarely mucinous. The invasive component histologically is acinar, papillary, micropapillary, and/or solid and shows tumor cells infil-trating into the surrounding myofibroblastic stroma. On CT scan, the |
Surgery_Schwartz_4541 | Surgery_Schwartz | mucinous. The invasive component histologically is acinar, papillary, micropapillary, and/or solid and shows tumor cells infil-trating into the surrounding myofibroblastic stroma. On CT scan, the appearance of MIA is often a part-solid nodule (≤5 mm) with a predominant ground-glass component, but can be highly variable. The 8th edition American Joint Committee on Cancer (AJCC) staging manual t-stage for MIA is T1mi.3. Lepidic predominant adenocarcinoma (LPA). If lympho-vascular invasion, pleural invasion, tumor necrosis, or more than 5 mm of invasion are noted in a lesion that has lepidic growth as its predominant component, MIA is excluded, the lesion is called lepidic predominant adenocarcinoma (LPA), and the size of the invasive component is recorded for the T stage.4. Invasive adenocarcinoma. The new classification system now recommends classifying invasive adenocarcinoma by the most predominant subtype after histologic evaluation of the resection specimen. To determine the | Surgery_Schwartz. mucinous. The invasive component histologically is acinar, papillary, micropapillary, and/or solid and shows tumor cells infil-trating into the surrounding myofibroblastic stroma. On CT scan, the appearance of MIA is often a part-solid nodule (≤5 mm) with a predominant ground-glass component, but can be highly variable. The 8th edition American Joint Committee on Cancer (AJCC) staging manual t-stage for MIA is T1mi.3. Lepidic predominant adenocarcinoma (LPA). If lympho-vascular invasion, pleural invasion, tumor necrosis, or more than 5 mm of invasion are noted in a lesion that has lepidic growth as its predominant component, MIA is excluded, the lesion is called lepidic predominant adenocarcinoma (LPA), and the size of the invasive component is recorded for the T stage.4. Invasive adenocarcinoma. The new classification system now recommends classifying invasive adenocarcinoma by the most predominant subtype after histologic evaluation of the resection specimen. To determine the |
Surgery_Schwartz_4542 | Surgery_Schwartz | The new classification system now recommends classifying invasive adenocarcinoma by the most predominant subtype after histologic evaluation of the resection specimen. To determine the predominant subtype, histologic sections are evaluated, and the patterns are determined, in 5% increments, throughout the speci-men. This semiquantitative method encourages the viewer to identify and quantify all patterns present, rather than focus-ing on a single pattern. In the pathology report, the tumor is classified by the predominant pattern, with percentages of the subtypes also reported (Fig. 19-11).Subtypes include:a. Lepidic predominantb. Acinar predominantc. Papillary predominantd. Micropapillary predominante. Solid predominantAdenocarcinoma is often peripherally located and frequently discovered incidentally on routine chest radiographs, unlike squamous cell cancers. When symptoms occur, they are due to pleural or chest wall invasion (pleuritic or chest wall pain) or pleural seeding with | Surgery_Schwartz. The new classification system now recommends classifying invasive adenocarcinoma by the most predominant subtype after histologic evaluation of the resection specimen. To determine the predominant subtype, histologic sections are evaluated, and the patterns are determined, in 5% increments, throughout the speci-men. This semiquantitative method encourages the viewer to identify and quantify all patterns present, rather than focus-ing on a single pattern. In the pathology report, the tumor is classified by the predominant pattern, with percentages of the subtypes also reported (Fig. 19-11).Subtypes include:a. Lepidic predominantb. Acinar predominantc. Papillary predominantd. Micropapillary predominante. Solid predominantAdenocarcinoma is often peripherally located and frequently discovered incidentally on routine chest radiographs, unlike squamous cell cancers. When symptoms occur, they are due to pleural or chest wall invasion (pleuritic or chest wall pain) or pleural seeding with |
Surgery_Schwartz_4543 | Surgery_Schwartz | incidentally on routine chest radiographs, unlike squamous cell cancers. When symptoms occur, they are due to pleural or chest wall invasion (pleuritic or chest wall pain) or pleural seeding with malignant pleural effusion. Invasive adenocarcinoma is usually solid by CT scan, but can also be part-solid and even a ground-glass nodule. Occasionally, a lobar ground-glass opacification may be present, which is often associated with significant respiratory compromise and can be mistaken for lobar pneumonia. Bubble-like or cystic lucency on CT scan in small (≤2 cm) adenocarcinomas or extensive associated ground-glass components correlate with slow growth and well-differentiated tumors and a more favor-able prognosis. Intratumoral air bronchograms are usually indicative of well-differentiated tumor, whereas spiculations that are coarse and thick (≥2 mm) portend vascular invasion and nodal metastasis and are associated with decreased sur-vival following complete surgical resection. Pleural | Surgery_Schwartz. incidentally on routine chest radiographs, unlike squamous cell cancers. When symptoms occur, they are due to pleural or chest wall invasion (pleuritic or chest wall pain) or pleural seeding with malignant pleural effusion. Invasive adenocarcinoma is usually solid by CT scan, but can also be part-solid and even a ground-glass nodule. Occasionally, a lobar ground-glass opacification may be present, which is often associated with significant respiratory compromise and can be mistaken for lobar pneumonia. Bubble-like or cystic lucency on CT scan in small (≤2 cm) adenocarcinomas or extensive associated ground-glass components correlate with slow growth and well-differentiated tumors and a more favor-able prognosis. Intratumoral air bronchograms are usually indicative of well-differentiated tumor, whereas spiculations that are coarse and thick (≥2 mm) portend vascular invasion and nodal metastasis and are associated with decreased sur-vival following complete surgical resection. Pleural |
Surgery_Schwartz_4544 | Surgery_Schwartz | tumor, whereas spiculations that are coarse and thick (≥2 mm) portend vascular invasion and nodal metastasis and are associated with decreased sur-vival following complete surgical resection. Pleural retraction is also a poor prognostic indicator.5. Additional histologic variants include colloid adenocarci-noma (formerly mucinous cystadenocarcinoma), fetal ade-nocarcinoma, and enteric adenocarcinoma. Clear cell and signet ring cell types are no longer considered to be distinct subtypes as they are found in association with most of the five dominant histologic patterns (lepidic, acinar, papillary, micropapillary, and solid). However, they are still notable, as they can signal clinically relevant molecular changes, such as the presence of the EML4-ALK fusion gene in solid tumors with signet ring features.Squamous Cell Carcinoma Representing 30% to 40% of lung cancers, squamous cell carcinoma is the most frequent cancer in men and highly correlated with cigarette smoking. They arise | Surgery_Schwartz. tumor, whereas spiculations that are coarse and thick (≥2 mm) portend vascular invasion and nodal metastasis and are associated with decreased sur-vival following complete surgical resection. Pleural retraction is also a poor prognostic indicator.5. Additional histologic variants include colloid adenocarci-noma (formerly mucinous cystadenocarcinoma), fetal ade-nocarcinoma, and enteric adenocarcinoma. Clear cell and signet ring cell types are no longer considered to be distinct subtypes as they are found in association with most of the five dominant histologic patterns (lepidic, acinar, papillary, micropapillary, and solid). However, they are still notable, as they can signal clinically relevant molecular changes, such as the presence of the EML4-ALK fusion gene in solid tumors with signet ring features.Squamous Cell Carcinoma Representing 30% to 40% of lung cancers, squamous cell carcinoma is the most frequent cancer in men and highly correlated with cigarette smoking. They arise |
Surgery_Schwartz_4545 | Surgery_Schwartz | ring features.Squamous Cell Carcinoma Representing 30% to 40% of lung cancers, squamous cell carcinoma is the most frequent cancer in men and highly correlated with cigarette smoking. They arise primarily in the main, lobar, or first segmental bronchi, which are collectively referred to as the central airways. Symptoms of airway irritation or obstruction are common, and include cough, Brunicardi_Ch19_p0661-p0750.indd 67101/03/19 7:00 PM 672SPECIFIC CONSIDERATIONSPART IIFigure 19-11. Major histologic patterns of invasive adenocarcinoma. A. Lepidic predominant pattern with mostly lepidic growth (right) and a smaller area of invasive acinar adenocarcinoma (left). B. Lepidic pattern consists of a proliferation type II pneumo-cytes and Clara cells along the surface alveolar walls. C. Area of invasive acinar adenocarcinoma (same tumor as in A and B). D. Acinar adenocarcinoma con-sists of round to oval-shaped malignant glands invad-ing a fibrous stroma. E. Papillary adenocarcinoma | Surgery_Schwartz. ring features.Squamous Cell Carcinoma Representing 30% to 40% of lung cancers, squamous cell carcinoma is the most frequent cancer in men and highly correlated with cigarette smoking. They arise primarily in the main, lobar, or first segmental bronchi, which are collectively referred to as the central airways. Symptoms of airway irritation or obstruction are common, and include cough, Brunicardi_Ch19_p0661-p0750.indd 67101/03/19 7:00 PM 672SPECIFIC CONSIDERATIONSPART IIFigure 19-11. Major histologic patterns of invasive adenocarcinoma. A. Lepidic predominant pattern with mostly lepidic growth (right) and a smaller area of invasive acinar adenocarcinoma (left). B. Lepidic pattern consists of a proliferation type II pneumo-cytes and Clara cells along the surface alveolar walls. C. Area of invasive acinar adenocarcinoma (same tumor as in A and B). D. Acinar adenocarcinoma con-sists of round to oval-shaped malignant glands invad-ing a fibrous stroma. E. Papillary adenocarcinoma |
Surgery_Schwartz_4546 | Surgery_Schwartz | Area of invasive acinar adenocarcinoma (same tumor as in A and B). D. Acinar adenocarcinoma con-sists of round to oval-shaped malignant glands invad-ing a fibrous stroma. E. Papillary adenocarcinoma consists of malignant cuboidal to columnar tumor cells growing on the surface of fibrovascular cores. F. Micropapillary adenocarcinoma consists of small papillary clusters of glandular cells growing within this airspace, most of which do not show fibrovascular cores. G. Solid adenocarcinoma with mucin consist-ing of sheets of tumor cells with abundant cytoplasm and mostly vesicular nuclei with several conspicuous nucleoli. No acinar, papillary, or lepidic patterns are seen, but multiple cells have intracytoplasmic baso-philic globules that suggest intracytoplasmic mucin. H. Solid adenocarcinoma with mucin. Numerous intracytoplasmic droplets of mucin are highlighted with this diastase-periodic acid Schiff stain. (Repro-duced with permission from Travis WD, Brambilla E, Noguchi M, et al: | Surgery_Schwartz. Area of invasive acinar adenocarcinoma (same tumor as in A and B). D. Acinar adenocarcinoma con-sists of round to oval-shaped malignant glands invad-ing a fibrous stroma. E. Papillary adenocarcinoma consists of malignant cuboidal to columnar tumor cells growing on the surface of fibrovascular cores. F. Micropapillary adenocarcinoma consists of small papillary clusters of glandular cells growing within this airspace, most of which do not show fibrovascular cores. G. Solid adenocarcinoma with mucin consist-ing of sheets of tumor cells with abundant cytoplasm and mostly vesicular nuclei with several conspicuous nucleoli. No acinar, papillary, or lepidic patterns are seen, but multiple cells have intracytoplasmic baso-philic globules that suggest intracytoplasmic mucin. H. Solid adenocarcinoma with mucin. Numerous intracytoplasmic droplets of mucin are highlighted with this diastase-periodic acid Schiff stain. (Repro-duced with permission from Travis WD, Brambilla E, Noguchi M, et al: |
Surgery_Schwartz_4547 | Surgery_Schwartz | with mucin. Numerous intracytoplasmic droplets of mucin are highlighted with this diastase-periodic acid Schiff stain. (Repro-duced with permission from Travis WD, Brambilla E, Noguchi M, et al: International association for the study of lung cancer/american thoracic society/european respiratory society international multidisci-plinary classification of lung adenocarcinoma, J Thorac Oncol. 2011 Feb;6(2):244-285.)hemoptysis, wheezing (due to high-grade airway obstruction), dyspnea (due to bronchial obstruction with or without postob-structive atelectasis), and pneumonia (caused by airway obstruc-tion with secretion retention and atelectasis).Occasionally a more peripherally based squamous cell carcinoma will develop in a tuberculosis scar or in the wall of a bronchiectatic cavity. Histologically, cells develop a pattern of clusters with intracellular bridges and keratin pearls. Central necrosis is frequent and may lead to the radiographic findings of a cavity (possibly with an | Surgery_Schwartz. with mucin. Numerous intracytoplasmic droplets of mucin are highlighted with this diastase-periodic acid Schiff stain. (Repro-duced with permission from Travis WD, Brambilla E, Noguchi M, et al: International association for the study of lung cancer/american thoracic society/european respiratory society international multidisci-plinary classification of lung adenocarcinoma, J Thorac Oncol. 2011 Feb;6(2):244-285.)hemoptysis, wheezing (due to high-grade airway obstruction), dyspnea (due to bronchial obstruction with or without postob-structive atelectasis), and pneumonia (caused by airway obstruc-tion with secretion retention and atelectasis).Occasionally a more peripherally based squamous cell carcinoma will develop in a tuberculosis scar or in the wall of a bronchiectatic cavity. Histologically, cells develop a pattern of clusters with intracellular bridges and keratin pearls. Central necrosis is frequent and may lead to the radiographic findings of a cavity (possibly with an |
Surgery_Schwartz_4548 | Surgery_Schwartz | Histologically, cells develop a pattern of clusters with intracellular bridges and keratin pearls. Central necrosis is frequent and may lead to the radiographic findings of a cavity (possibly with an air-fluid level). Such cavities may become infected, with resultant abscess formation.Large Cell Carcinoma Large cell carcinoma accounts for 10% to 20% of lung cancers and may be located centrally or periph-erally. These tumors have cell diameters of 30 to 50 µm, which are often admixed with various other malignant cell types. Large cell carcinoma can be confused with a large cell variant of neu-roendocrine carcinoma, but can be differentiated by special immunohistochemical stains.Salivary Gland–Type Neoplasms. Salivary-type submucosal bronchial glands throughout the tracheobronchial tree can give rise to tumors that are histologically identical to those seen in the salivary glands. The two most common are adenoid cystic carcinoma and mucoepidermoid carcinoma. Both occur cen-trally due to | Surgery_Schwartz. Histologically, cells develop a pattern of clusters with intracellular bridges and keratin pearls. Central necrosis is frequent and may lead to the radiographic findings of a cavity (possibly with an air-fluid level). Such cavities may become infected, with resultant abscess formation.Large Cell Carcinoma Large cell carcinoma accounts for 10% to 20% of lung cancers and may be located centrally or periph-erally. These tumors have cell diameters of 30 to 50 µm, which are often admixed with various other malignant cell types. Large cell carcinoma can be confused with a large cell variant of neu-roendocrine carcinoma, but can be differentiated by special immunohistochemical stains.Salivary Gland–Type Neoplasms. Salivary-type submucosal bronchial glands throughout the tracheobronchial tree can give rise to tumors that are histologically identical to those seen in the salivary glands. The two most common are adenoid cystic carcinoma and mucoepidermoid carcinoma. Both occur cen-trally due to |
Surgery_Schwartz_4549 | Surgery_Schwartz | give rise to tumors that are histologically identical to those seen in the salivary glands. The two most common are adenoid cystic carcinoma and mucoepidermoid carcinoma. Both occur cen-trally due to their site of origin. Adenoid cystic carcinoma is a slow-growing tumor that is locally and systemically invasive, growing submucosally and infiltrating along perineural sheaths. Mucoepidermoid carcinoma consists of squamous and mucous cells and is graded as low or high grade, depending on mitotic rate and degree of necrosis.Neuroendocrine Neoplasms. Neuroendocrine lung tumors are classified into neuroendocrine hyperplasia and three grades of neuroendocrine carcinoma (NEC). Immunohistochemical staining for neuroendocrine markers (including chromogranins, synaptophysin, CD57, and neuron-specific enolase) is essential to accurate diagnosis.17Grade I NEC (classic or typical carcinoid) is a low-grade NEC; 80% arise in the central airway epithelium and occur primarily in younger patients. | Surgery_Schwartz. give rise to tumors that are histologically identical to those seen in the salivary glands. The two most common are adenoid cystic carcinoma and mucoepidermoid carcinoma. Both occur cen-trally due to their site of origin. Adenoid cystic carcinoma is a slow-growing tumor that is locally and systemically invasive, growing submucosally and infiltrating along perineural sheaths. Mucoepidermoid carcinoma consists of squamous and mucous cells and is graded as low or high grade, depending on mitotic rate and degree of necrosis.Neuroendocrine Neoplasms. Neuroendocrine lung tumors are classified into neuroendocrine hyperplasia and three grades of neuroendocrine carcinoma (NEC). Immunohistochemical staining for neuroendocrine markers (including chromogranins, synaptophysin, CD57, and neuron-specific enolase) is essential to accurate diagnosis.17Grade I NEC (classic or typical carcinoid) is a low-grade NEC; 80% arise in the central airway epithelium and occur primarily in younger patients. |
Surgery_Schwartz_4550 | Surgery_Schwartz | enolase) is essential to accurate diagnosis.17Grade I NEC (classic or typical carcinoid) is a low-grade NEC; 80% arise in the central airway epithelium and occur primarily in younger patients. Because it is a central lesion, hemoptysis, with or without airway obstruction and pneumonia is the most common presentation. Histologically, tumor cells Brunicardi_Ch19_p0661-p0750.indd 67201/03/19 7:00 PM | Surgery_Schwartz. enolase) is essential to accurate diagnosis.17Grade I NEC (classic or typical carcinoid) is a low-grade NEC; 80% arise in the central airway epithelium and occur primarily in younger patients. Because it is a central lesion, hemoptysis, with or without airway obstruction and pneumonia is the most common presentation. Histologically, tumor cells Brunicardi_Ch19_p0661-p0750.indd 67201/03/19 7:00 PM |
Surgery_Schwartz_4551 | Surgery_Schwartz | CHAPTER 19673CHEST WALL, LUNG, MEDIASTINUM, AND PLEURAare arranged in cords and clusters with a rich vascular stroma, which can lead to life-threatening hemorrhage with even simple bronchoscopic biopsy maneuvers. Regional lymph node metas-tases are seen in 15% of patients, but systemic spread and death from Grade I NEC is rare.Grade II NECs (atypical carcinoid) have a much higher malignant potential and, unlike grade I NEC, are etiologically linked to cigarette smoking and more likely to be peripherally located. Histologic findings may include areas of necrosis, nuclear pleomorphism, and higher mitotic rates. Lymph node metastases are found in 30% to 50% of patients. At diagnosis, 25% of patients already have remote metastases.Grade III NEC large cell–type tumors occur primarily in heavy smokers and in the mid to peripheral lung fields. Often large with central necrosis and a high mitotic rate, their neuro-endocrine nature is revealed by positive immunohistochemical staining for at | Surgery_Schwartz. CHAPTER 19673CHEST WALL, LUNG, MEDIASTINUM, AND PLEURAare arranged in cords and clusters with a rich vascular stroma, which can lead to life-threatening hemorrhage with even simple bronchoscopic biopsy maneuvers. Regional lymph node metas-tases are seen in 15% of patients, but systemic spread and death from Grade I NEC is rare.Grade II NECs (atypical carcinoid) have a much higher malignant potential and, unlike grade I NEC, are etiologically linked to cigarette smoking and more likely to be peripherally located. Histologic findings may include areas of necrosis, nuclear pleomorphism, and higher mitotic rates. Lymph node metastases are found in 30% to 50% of patients. At diagnosis, 25% of patients already have remote metastases.Grade III NEC large cell–type tumors occur primarily in heavy smokers and in the mid to peripheral lung fields. Often large with central necrosis and a high mitotic rate, their neuro-endocrine nature is revealed by positive immunohistochemical staining for at |
Surgery_Schwartz_4552 | Surgery_Schwartz | smokers and in the mid to peripheral lung fields. Often large with central necrosis and a high mitotic rate, their neuro-endocrine nature is revealed by positive immunohistochemical staining for at least one neuroendocrine marker.Grade IV NEC (small cell lung carcinoma [SCLC]) is the most malignant NEC and accounts for 25% of all lung cancers; these NECs often have early, widespread metastases. These cancers also arise primarily in the central airways. As with squamous cell cancers, symptoms include cough, hemoptysis, wheezing (due to high-grade airway obstruction), dyspnea (due to bronchial obstruction with or without postobstructive atel-ectasis), and pneumonia (caused by airway obstruction with secretion retention and atelectasis). Evaluation includes expert pathology review and comprehensive evaluation for metastatic disease. Three groups of grade IV NEC are recognized: pure small cell carcinoma (previously referred to as oat cell carci-noma), small cell carcinoma with a large | Surgery_Schwartz. smokers and in the mid to peripheral lung fields. Often large with central necrosis and a high mitotic rate, their neuro-endocrine nature is revealed by positive immunohistochemical staining for at least one neuroendocrine marker.Grade IV NEC (small cell lung carcinoma [SCLC]) is the most malignant NEC and accounts for 25% of all lung cancers; these NECs often have early, widespread metastases. These cancers also arise primarily in the central airways. As with squamous cell cancers, symptoms include cough, hemoptysis, wheezing (due to high-grade airway obstruction), dyspnea (due to bronchial obstruction with or without postobstructive atel-ectasis), and pneumonia (caused by airway obstruction with secretion retention and atelectasis). Evaluation includes expert pathology review and comprehensive evaluation for metastatic disease. Three groups of grade IV NEC are recognized: pure small cell carcinoma (previously referred to as oat cell carci-noma), small cell carcinoma with a large |
Surgery_Schwartz_4553 | Surgery_Schwartz | evaluation for metastatic disease. Three groups of grade IV NEC are recognized: pure small cell carcinoma (previously referred to as oat cell carci-noma), small cell carcinoma with a large cell component, and combined (mixed) tumors.Grade IV NECs consist of smaller cells (diameter 10 to 20 µm) with little cytoplasm and very dark nuclei; they can be difficult to distinguish from lymphoproliferative lesions and atypical carcinoid tumors. Histologically, a high mitotic rate with easily visualized multiple mitoses and areas of extensive necrosis are characteristic. Importantly, very small bronchoscopic biopsies can distinguish NSCLC from SCLC, but crush artifact may make NSCLC appear similar to SCLC. If uncertainty exists, special immunohistochemical stains or rebiopsy (or both) will be necessary. These tumors are the leading producer of paraneoplastic syndromes.Lung Cancer EpidemiologyLung cancer is the leading cancer killer and second most frequently diagnosed cancer in the United | Surgery_Schwartz. evaluation for metastatic disease. Three groups of grade IV NEC are recognized: pure small cell carcinoma (previously referred to as oat cell carci-noma), small cell carcinoma with a large cell component, and combined (mixed) tumors.Grade IV NECs consist of smaller cells (diameter 10 to 20 µm) with little cytoplasm and very dark nuclei; they can be difficult to distinguish from lymphoproliferative lesions and atypical carcinoid tumors. Histologically, a high mitotic rate with easily visualized multiple mitoses and areas of extensive necrosis are characteristic. Importantly, very small bronchoscopic biopsies can distinguish NSCLC from SCLC, but crush artifact may make NSCLC appear similar to SCLC. If uncertainty exists, special immunohistochemical stains or rebiopsy (or both) will be necessary. These tumors are the leading producer of paraneoplastic syndromes.Lung Cancer EpidemiologyLung cancer is the leading cancer killer and second most frequently diagnosed cancer in the United |
Surgery_Schwartz_4554 | Surgery_Schwartz | necessary. These tumors are the leading producer of paraneoplastic syndromes.Lung Cancer EpidemiologyLung cancer is the leading cancer killer and second most frequently diagnosed cancer in the United States, account-ing for 26% of all cancer deaths in 2017—more than cancers of the breast, prostate, ovary, and colon and rectum com-bined (Fig. 19-12).18 Lung cancer incidence continues to decline, though at twice the rate for men compared to women (Fig. 19-13A, B). It is encouraging, however, that the average annual death rate declined by 3.5% per year for men and 2% per year for women from 2010 to 2014, representing a 43% decline in mortality for men and a 17% decline for women from 1990 MalesFemalesBreastLung & bronchusColon & rectumUterine corpusNon-Hodgkin lymphomaThyroidMelanoma of the skinPancreasLeukemiaKidney & renal pelvisAll Sites252,710105,51064,01061,38042,47034,94032,16025,84025,70023,380852,63030%12%8%7%5%4%4%3%3%3%100%MalesFemalesLung & bronchusProstateColon & | Surgery_Schwartz. necessary. These tumors are the leading producer of paraneoplastic syndromes.Lung Cancer EpidemiologyLung cancer is the leading cancer killer and second most frequently diagnosed cancer in the United States, account-ing for 26% of all cancer deaths in 2017—more than cancers of the breast, prostate, ovary, and colon and rectum com-bined (Fig. 19-12).18 Lung cancer incidence continues to decline, though at twice the rate for men compared to women (Fig. 19-13A, B). It is encouraging, however, that the average annual death rate declined by 3.5% per year for men and 2% per year for women from 2010 to 2014, representing a 43% decline in mortality for men and a 17% decline for women from 1990 MalesFemalesBreastLung & bronchusColon & rectumUterine corpusNon-Hodgkin lymphomaThyroidMelanoma of the skinPancreasLeukemiaKidney & renal pelvisAll Sites252,710105,51064,01061,38042,47034,94032,16025,84025,70023,380852,63030%12%8%7%5%4%4%3%3%3%100%MalesFemalesLung & bronchusProstateColon & |
Surgery_Schwartz_4555 | Surgery_Schwartz | of the skinPancreasLeukemiaKidney & renal pelvisAll Sites252,710105,51064,01061,38042,47034,94032,16025,84025,70023,380852,63030%12%8%7%5%4%4%3%3%3%100%MalesFemalesLung & bronchusProstateColon & rectumPancreasLiver & intrahepatic bile ductLeukemiaEsophagusUrinary bladderNon-Hodgkin lymphomaBrain & other nervous systemAll SitesLung & bronchusBreastColon & rectumPancreasOvaryLeukemiaNon-Hodgkin lymphomaUterine corpusLiver & intrahepatic bile ductBrain & other nervous systemAll Sites71,28040,61023,11020,79014,08010,92010,2009,3108,6907,080282,50025%14%8%7%5%4%4%3%3%3%100%84,59027,15026,73022,30019,61014,30012,72012,24011,4509,620318,42027%9%8%7%6%4%4%4%4%3%100%ProstateLung & bronchusColon & rectumUrinary bladderMelanoma of the skinNon-Hodgkin lymphomaKidney & renal pelvisOral cavity & pharynxLeukemiaLiver & intrahepatic bile ductAll Sites161,360116,99071,42060,49052,17040,61040,08036,29035,72029,200836,15019%14%9%7%6%5%5%4%4%3%100%Estimated new casesEstimated deathsFigure 19-12. Leading | Surgery_Schwartz. of the skinPancreasLeukemiaKidney & renal pelvisAll Sites252,710105,51064,01061,38042,47034,94032,16025,84025,70023,380852,63030%12%8%7%5%4%4%3%3%3%100%MalesFemalesLung & bronchusProstateColon & rectumPancreasLiver & intrahepatic bile ductLeukemiaEsophagusUrinary bladderNon-Hodgkin lymphomaBrain & other nervous systemAll SitesLung & bronchusBreastColon & rectumPancreasOvaryLeukemiaNon-Hodgkin lymphomaUterine corpusLiver & intrahepatic bile ductBrain & other nervous systemAll Sites71,28040,61023,11020,79014,08010,92010,2009,3108,6907,080282,50025%14%8%7%5%4%4%3%3%3%100%84,59027,15026,73022,30019,61014,30012,72012,24011,4509,620318,42027%9%8%7%6%4%4%4%4%3%100%ProstateLung & bronchusColon & rectumUrinary bladderMelanoma of the skinNon-Hodgkin lymphomaKidney & renal pelvisOral cavity & pharynxLeukemiaLiver & intrahepatic bile ductAll Sites161,360116,99071,42060,49052,17040,61040,08036,29035,72029,200836,15019%14%9%7%6%5%5%4%4%3%100%Estimated new casesEstimated deathsFigure 19-12. Leading |
Surgery_Schwartz_4556 | Surgery_Schwartz | & intrahepatic bile ductAll Sites161,360116,99071,42060,49052,17040,61040,08036,29035,72029,200836,15019%14%9%7%6%5%5%4%4%3%100%Estimated new casesEstimated deathsFigure 19-12. Leading new cancer cases and deaths: 2017 estimates. *Excludes basal and squamous cell skin cancers and in situ carcinomas except urinary bladder. (Reproduced with permission from Siegel RL, Miller KD, Jemal A: Cancer Statistics, 2017, CA Cancer J Clin. 2017 Jan;67(1):7-30.)Brunicardi_Ch19_p0661-p0750.indd 67301/03/19 7:00 PM 674SPECIFIC CONSIDERATIONSPART IIFigure 19-13. Trends in death rates by sex for select cancers, United States, 1930 to 2014. A. Males. B. Female rates are age-adjusted to the 2000 U.S. standard population. Due to improvements in International Classification of Diseases (ICD) coding over time, numerator data for cancers of the lung and bronchus, colon and rectum, liver, and uterus differ from the contemporary time period. For example, rates for lung and bronchus include pleura, trachea, | Surgery_Schwartz. & intrahepatic bile ductAll Sites161,360116,99071,42060,49052,17040,61040,08036,29035,72029,200836,15019%14%9%7%6%5%5%4%4%3%100%Estimated new casesEstimated deathsFigure 19-12. Leading new cancer cases and deaths: 2017 estimates. *Excludes basal and squamous cell skin cancers and in situ carcinomas except urinary bladder. (Reproduced with permission from Siegel RL, Miller KD, Jemal A: Cancer Statistics, 2017, CA Cancer J Clin. 2017 Jan;67(1):7-30.)Brunicardi_Ch19_p0661-p0750.indd 67301/03/19 7:00 PM 674SPECIFIC CONSIDERATIONSPART IIFigure 19-13. Trends in death rates by sex for select cancers, United States, 1930 to 2014. A. Males. B. Female rates are age-adjusted to the 2000 U.S. standard population. Due to improvements in International Classification of Diseases (ICD) coding over time, numerator data for cancers of the lung and bronchus, colon and rectum, liver, and uterus differ from the contemporary time period. For example, rates for lung and bronchus include pleura, trachea, |
Surgery_Schwartz_4557 | Surgery_Schwartz | numerator data for cancers of the lung and bronchus, colon and rectum, liver, and uterus differ from the contemporary time period. For example, rates for lung and bronchus include pleura, trachea, mediastinum, and other respiratory organs. (Adapted with permission from Siegel RL, Miller KD, Jemal A: Cancer Statistics, 2017, CA Cancer J Clin. 2017 Jan;67(1):7-30.)0102030405060708090100Pancreas†StomachLung and BronchusColon and RectumProstateLiver†LeukemiaTrends in Age-Adjusted Cancer Death Rates* by Site, Males, US, 1930-2014*Per 100,000, age adjusted to the 2000 US standard population.†Mortality rates for pancreatic and liver cancers are increasing.1930193419381942194619501954195819621966197019741978198219861990199419982002200620102014Trends in Age-Adjusted Cancer Death Rates* by Site, Females, US, 1930-2014*Per 100,000, age adjusted to the 2000 US standard population.†Uterus refers to uterine cervix and uterine corpus combined.‡Mortality rates for liver cancer are | Surgery_Schwartz. numerator data for cancers of the lung and bronchus, colon and rectum, liver, and uterus differ from the contemporary time period. For example, rates for lung and bronchus include pleura, trachea, mediastinum, and other respiratory organs. (Adapted with permission from Siegel RL, Miller KD, Jemal A: Cancer Statistics, 2017, CA Cancer J Clin. 2017 Jan;67(1):7-30.)0102030405060708090100Pancreas†StomachLung and BronchusColon and RectumProstateLiver†LeukemiaTrends in Age-Adjusted Cancer Death Rates* by Site, Males, US, 1930-2014*Per 100,000, age adjusted to the 2000 US standard population.†Mortality rates for pancreatic and liver cancers are increasing.1930193419381942194619501954195819621966197019741978198219861990199419982002200620102014Trends in Age-Adjusted Cancer Death Rates* by Site, Females, US, 1930-2014*Per 100,000, age adjusted to the 2000 US standard population.†Uterus refers to uterine cervix and uterine corpus combined.‡Mortality rates for liver cancer are |
Surgery_Schwartz_4558 | Surgery_Schwartz | Rates* by Site, Females, US, 1930-2014*Per 100,000, age adjusted to the 2000 US standard population.†Uterus refers to uterine cervix and uterine corpus combined.‡Mortality rates for liver cancer are increasing.010203040505152535451930193419381942194619501954195819621966197019741978198219861990199419982002200620102014StomachColon and RectumPancreas‡Lung and BronchusBreastUterus†Liver‡Brunicardi_Ch19_p0661-p0750.indd 67401/03/19 7:00 PM | Surgery_Schwartz. Rates* by Site, Females, US, 1930-2014*Per 100,000, age adjusted to the 2000 US standard population.†Uterus refers to uterine cervix and uterine corpus combined.‡Mortality rates for liver cancer are increasing.010203040505152535451930193419381942194619501954195819621966197019741978198219861990199419982002200620102014StomachColon and RectumPancreas‡Lung and BronchusBreastUterus†Liver‡Brunicardi_Ch19_p0661-p0750.indd 67401/03/19 7:00 PM |
Surgery_Schwartz_4559 | Surgery_Schwartz | CHAPTER 19675CHEST WALL, LUNG, MEDIASTINUM, AND PLEURATable 19-3Relative risk of lung cancer in smokersSMOKING CATEGORYRELATIVE RISKNever smoked1.0Currently smoke15.8–16.3Formerly smoked Years of abstinence 1–95.9–19.5 10–192.0–6.1 >201.9–3.7Data from Samet JM. Health benefits of smoking cessation, Clin Chest Med. 1991;12(4):669-679.to 2014.18 Unfortunately, most patients are still diagnosed at an advanced stage of disease (22% with regional metastasis and 57% with distant metastasis), so therapy is rarely curative.18Prognostic markers for lung cancer survival include female sex (5-year survival of 18.3% for women vs. 13.8% for men), younger age (5-year survival of 22.8% for those <45 years vs. 13.7% for those >65 years), and white race (5-year survival of 16.1% for whites vs. 12.2% for blacks). When access to advanced medical care is unrestricted, as for the military pop-ulation, the racial difference in survival disappears, suggesting that, at least in part, differences in | Surgery_Schwartz. CHAPTER 19675CHEST WALL, LUNG, MEDIASTINUM, AND PLEURATable 19-3Relative risk of lung cancer in smokersSMOKING CATEGORYRELATIVE RISKNever smoked1.0Currently smoke15.8–16.3Formerly smoked Years of abstinence 1–95.9–19.5 10–192.0–6.1 >201.9–3.7Data from Samet JM. Health benefits of smoking cessation, Clin Chest Med. 1991;12(4):669-679.to 2014.18 Unfortunately, most patients are still diagnosed at an advanced stage of disease (22% with regional metastasis and 57% with distant metastasis), so therapy is rarely curative.18Prognostic markers for lung cancer survival include female sex (5-year survival of 18.3% for women vs. 13.8% for men), younger age (5-year survival of 22.8% for those <45 years vs. 13.7% for those >65 years), and white race (5-year survival of 16.1% for whites vs. 12.2% for blacks). When access to advanced medical care is unrestricted, as for the military pop-ulation, the racial difference in survival disappears, suggesting that, at least in part, differences in |
Surgery_Schwartz_4560 | Surgery_Schwartz | for blacks). When access to advanced medical care is unrestricted, as for the military pop-ulation, the racial difference in survival disappears, suggesting that, at least in part, differences in survival may be explained by less access to advanced medical care and later diagnosis.19Risk Factors for Lung Cancer. Cigarette smoking is the leading preventable cause of cancer death, accounting for 29% of the popu-lation attributable fraction in 2010, and is implicated as a causal factor in approximately 90% of lung cancers in men and nearly 80% in women. Two lung cancer types—squamous cell and small cell carcinoma—are extraordinarily rare in the absence of cigarette smoking. The risk of developing lung cancer escalates with the number of cigarettes smoked, the number of years of smoking, and the use of unfiltered cigarettes. Conversely, the risk of lung cancer declines with smoking cessation, but never drops to that of never smokers, regardless of the length of abstinence (Table 19-3).20 | Surgery_Schwartz. for blacks). When access to advanced medical care is unrestricted, as for the military pop-ulation, the racial difference in survival disappears, suggesting that, at least in part, differences in survival may be explained by less access to advanced medical care and later diagnosis.19Risk Factors for Lung Cancer. Cigarette smoking is the leading preventable cause of cancer death, accounting for 29% of the popu-lation attributable fraction in 2010, and is implicated as a causal factor in approximately 90% of lung cancers in men and nearly 80% in women. Two lung cancer types—squamous cell and small cell carcinoma—are extraordinarily rare in the absence of cigarette smoking. The risk of developing lung cancer escalates with the number of cigarettes smoked, the number of years of smoking, and the use of unfiltered cigarettes. Conversely, the risk of lung cancer declines with smoking cessation, but never drops to that of never smokers, regardless of the length of abstinence (Table 19-3).20 |
Surgery_Schwartz_4561 | Surgery_Schwartz | the use of unfiltered cigarettes. Conversely, the risk of lung cancer declines with smoking cessation, but never drops to that of never smokers, regardless of the length of abstinence (Table 19-3).20 Radon exposure accounts for the vast majority of the remaining cancers. Approximately 25% of all lung cancers worldwide and 53% of cancers in women are not related to smoking, and most of them (62%) are adenocarcinomas. Table 19-4 summarizes the existing data regarding the etiology of lung cancer in nonsmokers.21Nearly 3500 deaths from lung cancer each year are attrib-utable to secondhand (environmental) smoke exposure, which confers an excess risk for lung cancer of 24% when a non-smoker lives with a smoker.22 Risk is conferred by exposure to any burning tobacco, including cigars. The amount of second-hand exposure from one large cigar is equivalent to the exposure from 21 cigarettes. As with active smoking, risk of developing lung cancer increases with longer duration and higher level | Surgery_Schwartz. the use of unfiltered cigarettes. Conversely, the risk of lung cancer declines with smoking cessation, but never drops to that of never smokers, regardless of the length of abstinence (Table 19-3).20 Radon exposure accounts for the vast majority of the remaining cancers. Approximately 25% of all lung cancers worldwide and 53% of cancers in women are not related to smoking, and most of them (62%) are adenocarcinomas. Table 19-4 summarizes the existing data regarding the etiology of lung cancer in nonsmokers.21Nearly 3500 deaths from lung cancer each year are attrib-utable to secondhand (environmental) smoke exposure, which confers an excess risk for lung cancer of 24% when a non-smoker lives with a smoker.22 Risk is conferred by exposure to any burning tobacco, including cigars. The amount of second-hand exposure from one large cigar is equivalent to the exposure from 21 cigarettes. As with active smoking, risk of developing lung cancer increases with longer duration and higher level |
Surgery_Schwartz_4562 | Surgery_Schwartz | of second-hand exposure from one large cigar is equivalent to the exposure from 21 cigarettes. As with active smoking, risk of developing lung cancer increases with longer duration and higher level of exposure to environmental tobacco.Over 7000 chemicals have been identified in tobacco smoke, and more than 70 of the compounds are known to be carcinogens. The main chemical carcinogens are polycyclic aromatic hydrocarbons, which are actively or passively inhaled in the tobacco smoke and absorbed; these compounds are acti-vated by specific enzymes and become mutagenic, bind to mac-romolecules such as deoxyribonucleic acid (DNA), and induce genetic mutations. In treating any patient with a previous smok-ing history, it is important to remember that there has been field cancerization of the entire aerodigestive tract. The patient’s risk is increased for cancers of the oral cavity, pharynx, larynx, tra-cheobronchial tree and lung, and esophagus. In examining such patients, a detailed | Surgery_Schwartz. of second-hand exposure from one large cigar is equivalent to the exposure from 21 cigarettes. As with active smoking, risk of developing lung cancer increases with longer duration and higher level of exposure to environmental tobacco.Over 7000 chemicals have been identified in tobacco smoke, and more than 70 of the compounds are known to be carcinogens. The main chemical carcinogens are polycyclic aromatic hydrocarbons, which are actively or passively inhaled in the tobacco smoke and absorbed; these compounds are acti-vated by specific enzymes and become mutagenic, bind to mac-romolecules such as deoxyribonucleic acid (DNA), and induce genetic mutations. In treating any patient with a previous smok-ing history, it is important to remember that there has been field cancerization of the entire aerodigestive tract. The patient’s risk is increased for cancers of the oral cavity, pharynx, larynx, tra-cheobronchial tree and lung, and esophagus. In examining such patients, a detailed |
Surgery_Schwartz_4563 | Surgery_Schwartz | the entire aerodigestive tract. The patient’s risk is increased for cancers of the oral cavity, pharynx, larynx, tra-cheobronchial tree and lung, and esophagus. In examining such patients, a detailed history and physical examination of these organ systems must be performed.Other causes of lung cancer include exposure to a num-ber of industrial compounds, including asbestos, arsenic, and chromium compounds. In fact, the combination of asbestos and cigarette smoke exposure has a multiplicative effect on risk. Pre-existing lung disease confers an increased risk of lung cancer—up to 13%—for individuals who have never smoked. Patients with chronic obstructive pulmonary disease are at higher risk for lung cancer than would be predicted based on smoking risk alone. Patients with secondary scar formation related to a his-tory of tuberculosis or other lung infections also have a higher risk of primary lung carcinoma. This increase is thought to be related to poor clearance of inhaled | Surgery_Schwartz. the entire aerodigestive tract. The patient’s risk is increased for cancers of the oral cavity, pharynx, larynx, tra-cheobronchial tree and lung, and esophagus. In examining such patients, a detailed history and physical examination of these organ systems must be performed.Other causes of lung cancer include exposure to a num-ber of industrial compounds, including asbestos, arsenic, and chromium compounds. In fact, the combination of asbestos and cigarette smoke exposure has a multiplicative effect on risk. Pre-existing lung disease confers an increased risk of lung cancer—up to 13%—for individuals who have never smoked. Patients with chronic obstructive pulmonary disease are at higher risk for lung cancer than would be predicted based on smoking risk alone. Patients with secondary scar formation related to a his-tory of tuberculosis or other lung infections also have a higher risk of primary lung carcinoma. This increase is thought to be related to poor clearance of inhaled |
Surgery_Schwartz_4564 | Surgery_Schwartz | scar formation related to a his-tory of tuberculosis or other lung infections also have a higher risk of primary lung carcinoma. This increase is thought to be related to poor clearance of inhaled carcinogens and/or to the effects of chronic inflammation.Screening for Lung Cancer in High-Risk PopulationsIn 2002, the National Lung Screening Trial (NLST) was launched to determine whether screening with CT in high-risk populations would reduce mortality from lung cancer. The study randomized 53,353 eligible patients age 55 to 74 years to either three annual low-dose helical CT scans (LDCT; aka spiral CT) or posteroante-rior view chest radiograph. Patients were eligible for the trial if they had a greater than 30 pack-year history of cigarette smoking; had smoked within the past 15 years if a former smoker; had no prior history of lung cancer; had no history of other life-threatening cancers in the prior 5 years; did not have symptoms suggestive of an undiagnosed lung cancer (such as | Surgery_Schwartz. scar formation related to a his-tory of tuberculosis or other lung infections also have a higher risk of primary lung carcinoma. This increase is thought to be related to poor clearance of inhaled carcinogens and/or to the effects of chronic inflammation.Screening for Lung Cancer in High-Risk PopulationsIn 2002, the National Lung Screening Trial (NLST) was launched to determine whether screening with CT in high-risk populations would reduce mortality from lung cancer. The study randomized 53,353 eligible patients age 55 to 74 years to either three annual low-dose helical CT scans (LDCT; aka spiral CT) or posteroante-rior view chest radiograph. Patients were eligible for the trial if they had a greater than 30 pack-year history of cigarette smoking; had smoked within the past 15 years if a former smoker; had no prior history of lung cancer; had no history of other life-threatening cancers in the prior 5 years; did not have symptoms suggestive of an undiagnosed lung cancer (such as |
Surgery_Schwartz_4565 | Surgery_Schwartz | if a former smoker; had no prior history of lung cancer; had no history of other life-threatening cancers in the prior 5 years; did not have symptoms suggestive of an undiagnosed lung cancer (such as hemoptysis or weight loss); and had not had a chest CT scan in the prior 18 months. Accrual to the study was excellent, and the primary endpoint of a 20% rela-tive reduction in mortality was achieved in 2010. An absolute risk reduction of lung cancer death of four per 1000 individuals screened by LDCT was realized. Interestingly, all-cause mortality was also reduced by nearly 7% in the LDCT group, further empha-sizing the impact of lung cancer on the mortality of smokers and former smokers.23 The U.S. Preventive Services Task Force (USPSTF) now recommends annual screening for lung cancer with low-dose computed tomography screening in high risk patients. Annual screening averted 14% of lung cancer deaths when applied to a population of asymptomatic adults age 55 to 80 years who have a 30 | Surgery_Schwartz. if a former smoker; had no prior history of lung cancer; had no history of other life-threatening cancers in the prior 5 years; did not have symptoms suggestive of an undiagnosed lung cancer (such as hemoptysis or weight loss); and had not had a chest CT scan in the prior 18 months. Accrual to the study was excellent, and the primary endpoint of a 20% rela-tive reduction in mortality was achieved in 2010. An absolute risk reduction of lung cancer death of four per 1000 individuals screened by LDCT was realized. Interestingly, all-cause mortality was also reduced by nearly 7% in the LDCT group, further empha-sizing the impact of lung cancer on the mortality of smokers and former smokers.23 The U.S. Preventive Services Task Force (USPSTF) now recommends annual screening for lung cancer with low-dose computed tomography screening in high risk patients. Annual screening averted 14% of lung cancer deaths when applied to a population of asymptomatic adults age 55 to 80 years who have a 30 |
Surgery_Schwartz_4566 | Surgery_Schwartz | low-dose computed tomography screening in high risk patients. Annual screening averted 14% of lung cancer deaths when applied to a population of asymptomatic adults age 55 to 80 years who have a 30 pack-year smoking history and are either currently smoking or have quit within the past 15 years. Patients should be healthy enough to tolerate curative treatment, specifically surgery per guidelines, and screening should be dis-continued once the patient has not smoked for 15 years or develops a life-limiting health condition, becomes unable to tolerate lung surgery or is unwilling to undergo curative lung resection. Require-ments for coverage differ between Medicare and private insurers, with private insurers following the USPSTF guidelines, while Medicare uses age 55 to 77 years with the same smoking history but does not define comorbid conditions. Use of standardized reporting with criteria for lung nodule identification and classifica-tion is required by the Center for Medicaid & | Surgery_Schwartz. low-dose computed tomography screening in high risk patients. Annual screening averted 14% of lung cancer deaths when applied to a population of asymptomatic adults age 55 to 80 years who have a 30 pack-year smoking history and are either currently smoking or have quit within the past 15 years. Patients should be healthy enough to tolerate curative treatment, specifically surgery per guidelines, and screening should be dis-continued once the patient has not smoked for 15 years or develops a life-limiting health condition, becomes unable to tolerate lung surgery or is unwilling to undergo curative lung resection. Require-ments for coverage differ between Medicare and private insurers, with private insurers following the USPSTF guidelines, while Medicare uses age 55 to 77 years with the same smoking history but does not define comorbid conditions. Use of standardized reporting with criteria for lung nodule identification and classifica-tion is required by the Center for Medicaid & |
Surgery_Schwartz_4567 | Surgery_Schwartz | same smoking history but does not define comorbid conditions. Use of standardized reporting with criteria for lung nodule identification and classifica-tion is required by the Center for Medicaid & Medicare Services (CMS) but is only recommended by private insurers. Shared deci-sion-making is also required by Medicare, but it is only recom-mended by private insurers. Medicare also differs from private 4Brunicardi_Ch19_p0661-p0750.indd 67501/03/19 7:00 PM 676SPECIFIC CONSIDERATIONSPART IITable 19-4Summary of selected studies of risk factors for lung cancer in individuals who never smokedRISK FACTORRISK ESTIMATE (95% CI)COMMENTSREFERENCEEnvironmental tobacco smoke1.19 (90% CI: 1.04–1.35)Meta-analysis of 11 U.S. studies of spousal exposure (females only)2251.21 (1.13–1.30)Meta-analysis of 44 case-control studies worldwide of spousal exposure2261.22 (1.13–1.33)Meta-analysis of 25 studies worldwide of workplace exposure2261.24 (1.18–1.29)Meta-analysis of 22 studies worldwide of | Surgery_Schwartz. same smoking history but does not define comorbid conditions. Use of standardized reporting with criteria for lung nodule identification and classifica-tion is required by the Center for Medicaid & Medicare Services (CMS) but is only recommended by private insurers. Shared deci-sion-making is also required by Medicare, but it is only recom-mended by private insurers. Medicare also differs from private 4Brunicardi_Ch19_p0661-p0750.indd 67501/03/19 7:00 PM 676SPECIFIC CONSIDERATIONSPART IITable 19-4Summary of selected studies of risk factors for lung cancer in individuals who never smokedRISK FACTORRISK ESTIMATE (95% CI)COMMENTSREFERENCEEnvironmental tobacco smoke1.19 (90% CI: 1.04–1.35)Meta-analysis of 11 U.S. studies of spousal exposure (females only)2251.21 (1.13–1.30)Meta-analysis of 44 case-control studies worldwide of spousal exposure2261.22 (1.13–1.33)Meta-analysis of 25 studies worldwide of workplace exposure2261.24 (1.18–1.29)Meta-analysis of 22 studies worldwide of |
Surgery_Schwartz_4568 | Surgery_Schwartz | of 44 case-control studies worldwide of spousal exposure2261.22 (1.13–1.33)Meta-analysis of 25 studies worldwide of workplace exposure2261.24 (1.18–1.29)Meta-analysis of 22 studies worldwide of workplace exposure227Residential radon8.4% (3.0%–15.8%) per 100 Bq m3 increase in measured radonMeta-analysis of 13 European studies22811% (0%–28%) per 100 Bq m3Meta-analysis of 7 North American studies229Cooking oil vapors2.12 (1.81–2.47)Meta-analysis of 7 studies from China and Taiwan (females who never smoked)230Indoor coal and wood burning2.66 (1.39–5.07)Meta-analysis of 7 studies from China and Taiwan (both sexes)2301.22 (1.04–1.44)Large case-control study (2861 cases and 3118 controls) from Eastern and Central Europe (both sexes)2312.5 (1.5–3.6)Large case-control study (1205 cases and 1541 controls) from Canada (significant for women only)232Genetic factors: family history, CYP1A1 Ile462Val polymorphism, XRCC1 variants1.51 (1.11–2.06)Meta-analysis of 28 case-control, 17 cohort, and 7 twin | Surgery_Schwartz. of 44 case-control studies worldwide of spousal exposure2261.22 (1.13–1.33)Meta-analysis of 25 studies worldwide of workplace exposure2261.24 (1.18–1.29)Meta-analysis of 22 studies worldwide of workplace exposure227Residential radon8.4% (3.0%–15.8%) per 100 Bq m3 increase in measured radonMeta-analysis of 13 European studies22811% (0%–28%) per 100 Bq m3Meta-analysis of 7 North American studies229Cooking oil vapors2.12 (1.81–2.47)Meta-analysis of 7 studies from China and Taiwan (females who never smoked)230Indoor coal and wood burning2.66 (1.39–5.07)Meta-analysis of 7 studies from China and Taiwan (both sexes)2301.22 (1.04–1.44)Large case-control study (2861 cases and 3118 controls) from Eastern and Central Europe (both sexes)2312.5 (1.5–3.6)Large case-control study (1205 cases and 1541 controls) from Canada (significant for women only)232Genetic factors: family history, CYP1A1 Ile462Val polymorphism, XRCC1 variants1.51 (1.11–2.06)Meta-analysis of 28 case-control, 17 cohort, and 7 twin |
Surgery_Schwartz_4569 | Surgery_Schwartz | from Canada (significant for women only)232Genetic factors: family history, CYP1A1 Ile462Val polymorphism, XRCC1 variants1.51 (1.11–2.06)Meta-analysis of 28 case-control, 17 cohort, and 7 twin studies2332.99 (1.51–5.91)Meta-analysis of 14 case-control studies of Caucasian never smokers2342.04 (1.17–3.54)Meta-analysis of 21 case-control studies of Caucasian and Asian never smokers (significant for Caucasians only)235No associationMeta-analysis of 13 case-control studies236No association overall; reduced risk 0.65 (0.46–0.83) with Arg194Trp polymorphism and 0.56 (0.36–0.86) with Arg280His for heavy smokersLarge case-control study from Europe (2188 cases and 2198 controls)237Increased risk for never smokers 1.3 (1.0–1.8) and decreased risk for heavy smokers 0.5 (0.3–1.0) with Arg299GlnLarge case-control study from the United States (1091 cases and 1240 controls)238Viral factors: HPV 16 and 1810.12 (3.88–26.4) for never smoking women >60 yCase-control study (141 cases, 60 controls) from | Surgery_Schwartz. from Canada (significant for women only)232Genetic factors: family history, CYP1A1 Ile462Val polymorphism, XRCC1 variants1.51 (1.11–2.06)Meta-analysis of 28 case-control, 17 cohort, and 7 twin studies2332.99 (1.51–5.91)Meta-analysis of 14 case-control studies of Caucasian never smokers2342.04 (1.17–3.54)Meta-analysis of 21 case-control studies of Caucasian and Asian never smokers (significant for Caucasians only)235No associationMeta-analysis of 13 case-control studies236No association overall; reduced risk 0.65 (0.46–0.83) with Arg194Trp polymorphism and 0.56 (0.36–0.86) with Arg280His for heavy smokersLarge case-control study from Europe (2188 cases and 2198 controls)237Increased risk for never smokers 1.3 (1.0–1.8) and decreased risk for heavy smokers 0.5 (0.3–1.0) with Arg299GlnLarge case-control study from the United States (1091 cases and 1240 controls)238Viral factors: HPV 16 and 1810.12 (3.88–26.4) for never smoking women >60 yCase-control study (141 cases, 60 controls) from |
Surgery_Schwartz_4570 | Surgery_Schwartz | study from the United States (1091 cases and 1240 controls)238Viral factors: HPV 16 and 1810.12 (3.88–26.4) for never smoking women >60 yCase-control study (141 cases, 60 controls) from Taiwan of never smoking women239Abbreviations: Bq = becquerels; CI = confidence interval; CYP1A1 = cytochrome P450 enzyme 1A1; HPV = human papilloma virus.Reproduced with permission from Sun S, Schiller JH, Gazdar AF: Lung cancer in never smokers—a different disease, Nat Rev Cancer. 2007 Oct; 7(10):778-790.insurers in that it requires accreditation of the imaging center and submission of all low-dose CT data to a CMS-approved national registry, among other specifications. With this approach, it is expected that 50% of diagnosed cancers will be early stage. Screening of patients age 50 years or older with a 20 pack-year or greater history and additional risk factors (as determined by the Tammemagi lung cancer risk calculator or other validated risk scores) that increase the risk of lung cancer to 1.3% | Surgery_Schwartz. study from the United States (1091 cases and 1240 controls)238Viral factors: HPV 16 and 1810.12 (3.88–26.4) for never smoking women >60 yCase-control study (141 cases, 60 controls) from Taiwan of never smoking women239Abbreviations: Bq = becquerels; CI = confidence interval; CYP1A1 = cytochrome P450 enzyme 1A1; HPV = human papilloma virus.Reproduced with permission from Sun S, Schiller JH, Gazdar AF: Lung cancer in never smokers—a different disease, Nat Rev Cancer. 2007 Oct; 7(10):778-790.insurers in that it requires accreditation of the imaging center and submission of all low-dose CT data to a CMS-approved national registry, among other specifications. With this approach, it is expected that 50% of diagnosed cancers will be early stage. Screening of patients age 50 years or older with a 20 pack-year or greater history and additional risk factors (as determined by the Tammemagi lung cancer risk calculator or other validated risk scores) that increase the risk of lung cancer to 1.3% |
Surgery_Schwartz_4571 | Surgery_Schwartz | a 20 pack-year or greater history and additional risk factors (as determined by the Tammemagi lung cancer risk calculator or other validated risk scores) that increase the risk of lung cancer to 1.3% or greater should also be considered as part of lung cancer screening pro-grams. In all cases, patient–physician shared decision-making should be undertaken, with a discussion of the risks and benefits of screening. It is important to note that there was a 7% false-positive rate in NLST trial, which can lead to patient anxiety, invasive testing, and potentially morbid procedures to further evaluate the finding. The impact of these issues on patient quality of life and cost-effectiveness requires further study, particularly as screening programs are implemented outside of the controlled set-ting of a clinical trial. It is also critical that regulatory guidelines for patient eligibility, frequency of screening, interpretation of the scans, processes for further evaluation and management of | Surgery_Schwartz. a 20 pack-year or greater history and additional risk factors (as determined by the Tammemagi lung cancer risk calculator or other validated risk scores) that increase the risk of lung cancer to 1.3% or greater should also be considered as part of lung cancer screening pro-grams. In all cases, patient–physician shared decision-making should be undertaken, with a discussion of the risks and benefits of screening. It is important to note that there was a 7% false-positive rate in NLST trial, which can lead to patient anxiety, invasive testing, and potentially morbid procedures to further evaluate the finding. The impact of these issues on patient quality of life and cost-effectiveness requires further study, particularly as screening programs are implemented outside of the controlled set-ting of a clinical trial. It is also critical that regulatory guidelines for patient eligibility, frequency of screening, interpretation of the scans, processes for further evaluation and management of |
Surgery_Schwartz_4572 | Surgery_Schwartz | of a clinical trial. It is also critical that regulatory guidelines for patient eligibility, frequency of screening, interpretation of the scans, processes for further evaluation and management of posi-tive findings, and dose of radiation are well established and well accepted to ensure the generalizability of the results for patients who will be screened in the general medical community rather than in the specialized centers that performed the trial.Brunicardi_Ch19_p0661-p0750.indd 67601/03/19 7:00 PM | Surgery_Schwartz. of a clinical trial. It is also critical that regulatory guidelines for patient eligibility, frequency of screening, interpretation of the scans, processes for further evaluation and management of posi-tive findings, and dose of radiation are well established and well accepted to ensure the generalizability of the results for patients who will be screened in the general medical community rather than in the specialized centers that performed the trial.Brunicardi_Ch19_p0661-p0750.indd 67601/03/19 7:00 PM |
Surgery_Schwartz_4573 | Surgery_Schwartz | CHAPTER 19677CHEST WALL, LUNG, MEDIASTINUM, AND PLEURAABCDFigure 19-14. Spiral computed tomography scan showing normal transverse chest anatomy at four levels. A. At the level of the tracheal bifurcation, the aorticopulmonary window can be seen. B. The origin of the left pulmonary artery can be seen at a level 1 cm inferior to A. C. The origin and course of the right pulmonary artery can be seen at this next most cephalad level. The left upper lobe bronchus can be seen at its origin from the left main bronchus. D. Cardiac chambers and pulmonary veins are seen in the lower thorax. AA = ascending aorta; APW = aorticopulmonary window; DA = descending aorta; LA = left ventricle; LMB = left main bronchus; LPA = left pulmonary artery; MPA = main pulmonary artery; RA = right atrium; RPA = right pulmonary artery; RV = right ventricle; SVC = superior vena cava; T = trachea.Solitary Pulmonary NoduleA solitary pulmonary nodule is typically described as a single, well-circumscribed, spherical | Surgery_Schwartz. CHAPTER 19677CHEST WALL, LUNG, MEDIASTINUM, AND PLEURAABCDFigure 19-14. Spiral computed tomography scan showing normal transverse chest anatomy at four levels. A. At the level of the tracheal bifurcation, the aorticopulmonary window can be seen. B. The origin of the left pulmonary artery can be seen at a level 1 cm inferior to A. C. The origin and course of the right pulmonary artery can be seen at this next most cephalad level. The left upper lobe bronchus can be seen at its origin from the left main bronchus. D. Cardiac chambers and pulmonary veins are seen in the lower thorax. AA = ascending aorta; APW = aorticopulmonary window; DA = descending aorta; LA = left ventricle; LMB = left main bronchus; LPA = left pulmonary artery; MPA = main pulmonary artery; RA = right atrium; RPA = right pulmonary artery; RV = right ventricle; SVC = superior vena cava; T = trachea.Solitary Pulmonary NoduleA solitary pulmonary nodule is typically described as a single, well-circumscribed, spherical |
Surgery_Schwartz_4574 | Surgery_Schwartz | pulmonary artery; RV = right ventricle; SVC = superior vena cava; T = trachea.Solitary Pulmonary NoduleA solitary pulmonary nodule is typically described as a single, well-circumscribed, spherical lesion that is 3 cm or less cm in diameter and completely surrounded by normal aerated lung parenchyma.24 Lung atelectasis, hilar enlargement, and pleural effusion are absent. The majority are detected incidentally on chest radiographs (CXRs) or CT scans obtained for some other purpose. About 150,000 solitary nodules are found inciden-tally each year, with increasing numbers as low-dose computed tomography screening in high-risk populations is adopted. The clinical significance of such a lesion depends on whether or not it represents a malignancy.The differential diagnosis of a solitary pulmonary nodule should include a broad variety of congenital, neoplastic, inflam-matory, vascular, and traumatic disorders. The probability of cancer in a solitary pulmonary nodule increases if the patient | Surgery_Schwartz. pulmonary artery; RV = right ventricle; SVC = superior vena cava; T = trachea.Solitary Pulmonary NoduleA solitary pulmonary nodule is typically described as a single, well-circumscribed, spherical lesion that is 3 cm or less cm in diameter and completely surrounded by normal aerated lung parenchyma.24 Lung atelectasis, hilar enlargement, and pleural effusion are absent. The majority are detected incidentally on chest radiographs (CXRs) or CT scans obtained for some other purpose. About 150,000 solitary nodules are found inciden-tally each year, with increasing numbers as low-dose computed tomography screening in high-risk populations is adopted. The clinical significance of such a lesion depends on whether or not it represents a malignancy.The differential diagnosis of a solitary pulmonary nodule should include a broad variety of congenital, neoplastic, inflam-matory, vascular, and traumatic disorders. The probability of cancer in a solitary pulmonary nodule increases if the patient |
Surgery_Schwartz_4575 | Surgery_Schwartz | nodule should include a broad variety of congenital, neoplastic, inflam-matory, vascular, and traumatic disorders. The probability of cancer in a solitary pulmonary nodule increases if the patient has a history of smoking (50% or higher for smokers compared to 20% to 40% in never smokers). It is also more likely to be malignant if it is symptomatic or the patient is older, male, or has had occupational exposures.Solitary pulmonary nodules were defined by findings on CXR, but with the increased sensitivity of low-dose screening CT, up to 50% of solitary lesions are found to be associated with multiple (one to six) other, usually subcentimeter, nodules. In the Early Lung Cancer Action project, almost 7% of healthy volunteers were found to have between one and three nodules, and 25% had up to six nodules. CT scanning is necessary to characterize nodule number, location, size, margin morphol-ogy, calcification pattern, and growth rate.25 Spiral (helical) CT allows continuous scanning as | Surgery_Schwartz. nodule should include a broad variety of congenital, neoplastic, inflam-matory, vascular, and traumatic disorders. The probability of cancer in a solitary pulmonary nodule increases if the patient has a history of smoking (50% or higher for smokers compared to 20% to 40% in never smokers). It is also more likely to be malignant if it is symptomatic or the patient is older, male, or has had occupational exposures.Solitary pulmonary nodules were defined by findings on CXR, but with the increased sensitivity of low-dose screening CT, up to 50% of solitary lesions are found to be associated with multiple (one to six) other, usually subcentimeter, nodules. In the Early Lung Cancer Action project, almost 7% of healthy volunteers were found to have between one and three nodules, and 25% had up to six nodules. CT scanning is necessary to characterize nodule number, location, size, margin morphol-ogy, calcification pattern, and growth rate.25 Spiral (helical) CT allows continuous scanning as |
Surgery_Schwartz_4576 | Surgery_Schwartz | to six nodules. CT scanning is necessary to characterize nodule number, location, size, margin morphol-ogy, calcification pattern, and growth rate.25 Spiral (helical) CT allows continuous scanning as the patient is moved through a scanning gantry, allowing the entire thorax to be imaged during a single breath hold (Fig. 19-14). Compared to conventional CT, this provides a superior image quality, because motion artifacts are eliminated, and improves detection of pulmonary nodules and central airway abnormalities.26 The shorter acquisition time of spiral CT also allows for consistent contrast filling of the great vessels, resulting in markedly improved visualization of pathologic states and anatomic variation contiguous to vascular structures. In addition, three-dimensional spiral CT images can be reconstructed for enhanced visualization of spatial anatomic relationships.27 Thin sections (1 to 2 mm collimation) at 1-cm intervals should be used to evaluate pulmonary parenchyma and | Surgery_Schwartz. to six nodules. CT scanning is necessary to characterize nodule number, location, size, margin morphol-ogy, calcification pattern, and growth rate.25 Spiral (helical) CT allows continuous scanning as the patient is moved through a scanning gantry, allowing the entire thorax to be imaged during a single breath hold (Fig. 19-14). Compared to conventional CT, this provides a superior image quality, because motion artifacts are eliminated, and improves detection of pulmonary nodules and central airway abnormalities.26 The shorter acquisition time of spiral CT also allows for consistent contrast filling of the great vessels, resulting in markedly improved visualization of pathologic states and anatomic variation contiguous to vascular structures. In addition, three-dimensional spiral CT images can be reconstructed for enhanced visualization of spatial anatomic relationships.27 Thin sections (1 to 2 mm collimation) at 1-cm intervals should be used to evaluate pulmonary parenchyma and |
Surgery_Schwartz_4577 | Surgery_Schwartz | images can be reconstructed for enhanced visualization of spatial anatomic relationships.27 Thin sections (1 to 2 mm collimation) at 1-cm intervals should be used to evaluate pulmonary parenchyma and peripheral bronchi. If the goal is to find any pulmonary metas-tases, thin sections at intervals of 5 to 7 mm collimation are recommended. For assessing the trachea and central bronchi, collimation of 3 to 5 mm is recommended. Providing accurate clinical history and data is of paramount importance to obtaining appropriate imaging.CT findings characteristic of benign lesions include small size, calcification within the nodule, and stability over time. Brunicardi_Ch19_p0661-p0750.indd 67701/03/19 7:00 PM 678SPECIFIC CONSIDERATIONSPART IIABCFigure 19-15. Computed tomography scan images of solitary pulmonary nodules. A. The corona radiata sign demonstrated by a solitary nodule. Multiple fine striations extend perpendicularly from the surface of the nodule like the spokes of a wheel. B. A | Surgery_Schwartz. images can be reconstructed for enhanced visualization of spatial anatomic relationships.27 Thin sections (1 to 2 mm collimation) at 1-cm intervals should be used to evaluate pulmonary parenchyma and peripheral bronchi. If the goal is to find any pulmonary metas-tases, thin sections at intervals of 5 to 7 mm collimation are recommended. For assessing the trachea and central bronchi, collimation of 3 to 5 mm is recommended. Providing accurate clinical history and data is of paramount importance to obtaining appropriate imaging.CT findings characteristic of benign lesions include small size, calcification within the nodule, and stability over time. Brunicardi_Ch19_p0661-p0750.indd 67701/03/19 7:00 PM 678SPECIFIC CONSIDERATIONSPART IIABCFigure 19-15. Computed tomography scan images of solitary pulmonary nodules. A. The corona radiata sign demonstrated by a solitary nodule. Multiple fine striations extend perpendicularly from the surface of the nodule like the spokes of a wheel. B. A |
Surgery_Schwartz_4578 | Surgery_Schwartz | pulmonary nodules. A. The corona radiata sign demonstrated by a solitary nodule. Multiple fine striations extend perpendicularly from the surface of the nodule like the spokes of a wheel. B. A biopsy-proven adenocarcinoma demonstrating spiculation. C. A lesion with a scalloped border, an indeterminate finding suggesting an intermediate probability for malignancy.Table 19-5Actuarial survival data from the International Registry of Lung MetastasesSURVIVALCOMPLETE RESECTION (%)INCOMPLETE RESECTION (%)5 years361310 years26715 years22—Four patterns of benign calcification are common: diffuse, solid, central, and laminated or “popcorn.” Granulomatous infections such as tuberculosis can demonstrate the first three patterns, whereas the popcorn pattern is most common in hamartomas. In areas of endemic granulomatous disease, differentiating benign versus malignant can be challenging. Infectious granulomas arising from a variety of organisms account for 70% to 80% of this type of benign | Surgery_Schwartz. pulmonary nodules. A. The corona radiata sign demonstrated by a solitary nodule. Multiple fine striations extend perpendicularly from the surface of the nodule like the spokes of a wheel. B. A biopsy-proven adenocarcinoma demonstrating spiculation. C. A lesion with a scalloped border, an indeterminate finding suggesting an intermediate probability for malignancy.Table 19-5Actuarial survival data from the International Registry of Lung MetastasesSURVIVALCOMPLETE RESECTION (%)INCOMPLETE RESECTION (%)5 years361310 years26715 years22—Four patterns of benign calcification are common: diffuse, solid, central, and laminated or “popcorn.” Granulomatous infections such as tuberculosis can demonstrate the first three patterns, whereas the popcorn pattern is most common in hamartomas. In areas of endemic granulomatous disease, differentiating benign versus malignant can be challenging. Infectious granulomas arising from a variety of organisms account for 70% to 80% of this type of benign |
Surgery_Schwartz_4579 | Surgery_Schwartz | of endemic granulomatous disease, differentiating benign versus malignant can be challenging. Infectious granulomas arising from a variety of organisms account for 70% to 80% of this type of benign solitary nodules; hamartomas are the next most common single cause, accounting for about 10%.CT findings characteristic of malignancy include growth over time; increasing density on CT scan (40% to 50% of partial solid lesions are malignant compared to only 15% of subcenti-meter solid or nonsolid nodules); size >3 cm; irregular, lobu-lated, or spiculated edges; and the finding of the corona radiata sign (consisting of fine linear strands extending 4 to 5 mm out-ward and appearing spiculated on radiographs) (Fig. 19-15). Calcification that is stippled, amorphous, or eccentric is usually associated with cancer.Growth over time is an important characteristic for differentiating benign and malignant lesions. Lung cancers have volume-doubling times from 20 to 400 days; lesions with shorter | Surgery_Schwartz. of endemic granulomatous disease, differentiating benign versus malignant can be challenging. Infectious granulomas arising from a variety of organisms account for 70% to 80% of this type of benign solitary nodules; hamartomas are the next most common single cause, accounting for about 10%.CT findings characteristic of malignancy include growth over time; increasing density on CT scan (40% to 50% of partial solid lesions are malignant compared to only 15% of subcenti-meter solid or nonsolid nodules); size >3 cm; irregular, lobu-lated, or spiculated edges; and the finding of the corona radiata sign (consisting of fine linear strands extending 4 to 5 mm out-ward and appearing spiculated on radiographs) (Fig. 19-15). Calcification that is stippled, amorphous, or eccentric is usually associated with cancer.Growth over time is an important characteristic for differentiating benign and malignant lesions. Lung cancers have volume-doubling times from 20 to 400 days; lesions with shorter |
Surgery_Schwartz_4580 | Surgery_Schwartz | with cancer.Growth over time is an important characteristic for differentiating benign and malignant lesions. Lung cancers have volume-doubling times from 20 to 400 days; lesions with shorter doubling times are likely due to infection, and longer doubling times suggest benign tumors, but can represent slower-growing lung cancer. Positron emission tomography (PET) scan-ning can differentiate benign from malignant nodules28; most lung tumors have increased signatures of glucose uptake, as compared with healthy tissues, and thus glucose metabolism can be measured using radio-labeled 18F-fluorodeoxyglucose (FDG). Meta-analysis estimates 97% sensitivity and 78% spec-ificity for predicting malignancy in a nodule. False-negative results can occur (especially in patients who have AIS, MIA, or LPA, carcinoids, and tumors <1 cm in diameter), as well as false-positive results (because of confusion with other infectious or inflammatory processes).Metastatic Lesions to the LungThe cause of a new | Surgery_Schwartz. with cancer.Growth over time is an important characteristic for differentiating benign and malignant lesions. Lung cancers have volume-doubling times from 20 to 400 days; lesions with shorter doubling times are likely due to infection, and longer doubling times suggest benign tumors, but can represent slower-growing lung cancer. Positron emission tomography (PET) scan-ning can differentiate benign from malignant nodules28; most lung tumors have increased signatures of glucose uptake, as compared with healthy tissues, and thus glucose metabolism can be measured using radio-labeled 18F-fluorodeoxyglucose (FDG). Meta-analysis estimates 97% sensitivity and 78% spec-ificity for predicting malignancy in a nodule. False-negative results can occur (especially in patients who have AIS, MIA, or LPA, carcinoids, and tumors <1 cm in diameter), as well as false-positive results (because of confusion with other infectious or inflammatory processes).Metastatic Lesions to the LungThe cause of a new |
Surgery_Schwartz_4581 | Surgery_Schwartz | carcinoids, and tumors <1 cm in diameter), as well as false-positive results (because of confusion with other infectious or inflammatory processes).Metastatic Lesions to the LungThe cause of a new pulmonary nodule(s) in a patient with a previous malignancy can be difficult to discern.29 Features sug-gestive of metastatic disease are multiplicity; smooth, round borders on CT scan; and temporal proximity to the original pri-mary lesion. One must always entertain the possibility that a single new lesion is a primary lung cancer. The probability of a new primary cancer vs. metastasis in patients presenting with solitary lesions depends on the type of initial neoplasm. The highest likelihood of a new primary lung cancer is in patients with a history of uterine (74%), bladder (89%), lung (92%), and head and neck (94%) carcinomas.Surgical resection of pulmonary metastases has a role in properly selected patients.30 The best data regarding outcomes of resection of pulmonary metastases come | Surgery_Schwartz. carcinoids, and tumors <1 cm in diameter), as well as false-positive results (because of confusion with other infectious or inflammatory processes).Metastatic Lesions to the LungThe cause of a new pulmonary nodule(s) in a patient with a previous malignancy can be difficult to discern.29 Features sug-gestive of metastatic disease are multiplicity; smooth, round borders on CT scan; and temporal proximity to the original pri-mary lesion. One must always entertain the possibility that a single new lesion is a primary lung cancer. The probability of a new primary cancer vs. metastasis in patients presenting with solitary lesions depends on the type of initial neoplasm. The highest likelihood of a new primary lung cancer is in patients with a history of uterine (74%), bladder (89%), lung (92%), and head and neck (94%) carcinomas.Surgical resection of pulmonary metastases has a role in properly selected patients.30 The best data regarding outcomes of resection of pulmonary metastases come |
Surgery_Schwartz_4582 | Surgery_Schwartz | and head and neck (94%) carcinomas.Surgical resection of pulmonary metastases has a role in properly selected patients.30 The best data regarding outcomes of resection of pulmonary metastases come from the Interna-tional Registry of Lung Metastases (IRLM). The registry was established in 1991 by 18 thoracic surgery departments in Europe, the United States, and Canada and included data on 5206 patients. About 88% of patients underwent complete resection. Survival analysis at 5, 10, and 15 years (grouping all primary tumor types) was performed (Table 19-5). Multivariate analysis showed a better prognosis for patients with germ cell tumors, osteosarcomas, a disease-free interval over 36 months, and a single metastasis.31 Depicted in Fig. 19-16, survival after metastasectomy in a variety of cancers is optimal when meta-static disease is resectable, solitary, and identified 36 or more months after initial treatment. When any or all of these optimal characteristics are absent, survival | Surgery_Schwartz. and head and neck (94%) carcinomas.Surgical resection of pulmonary metastases has a role in properly selected patients.30 The best data regarding outcomes of resection of pulmonary metastases come from the Interna-tional Registry of Lung Metastases (IRLM). The registry was established in 1991 by 18 thoracic surgery departments in Europe, the United States, and Canada and included data on 5206 patients. About 88% of patients underwent complete resection. Survival analysis at 5, 10, and 15 years (grouping all primary tumor types) was performed (Table 19-5). Multivariate analysis showed a better prognosis for patients with germ cell tumors, osteosarcomas, a disease-free interval over 36 months, and a single metastasis.31 Depicted in Fig. 19-16, survival after metastasectomy in a variety of cancers is optimal when meta-static disease is resectable, solitary, and identified 36 or more months after initial treatment. When any or all of these optimal characteristics are absent, survival |
Surgery_Schwartz_4583 | Surgery_Schwartz | of cancers is optimal when meta-static disease is resectable, solitary, and identified 36 or more months after initial treatment. When any or all of these optimal characteristics are absent, survival progressively declines.Brunicardi_Ch19_p0661-p0750.indd 67801/03/19 7:00 PM | Surgery_Schwartz. of cancers is optimal when meta-static disease is resectable, solitary, and identified 36 or more months after initial treatment. When any or all of these optimal characteristics are absent, survival progressively declines.Brunicardi_Ch19_p0661-p0750.indd 67801/03/19 7:00 PM |
Surgery_Schwartz_4584 | Surgery_Schwartz | CHAPTER 19679CHEST WALL, LUNG, MEDIASTINUM, AND PLEURA10080604020002448All Sites7296120Soft Tissue Sarcomas100806040200024487296120Breast Cancer100806040200024487296120Osteosarcoma1001234806040200024487296120Colon Cancer100806040200024487296120Melanoma100806040200024487296120ABCDEFFigure 19-16. The actuarial survival after metastasectomy is depicted for patients with various tumor types (A-F) further categorized into four groups according to resectabil-ity, solitary or multiple, the inter-val between primary resection and metastesectomy, and a combination of factors known in our work and in others, as follows: (1) resectable, soli-tary, and disease-free interval (DFI) greater than or equal to 36 months; (2) resectable, solitary, and DFI 36+ months; (3) resectable, multiple metastases, and DFI <36 months; and (4) unresectable. (Reproduced with permission from Pastorino U: The development of an international registry, J Thorac Oncol. 2010 Jun; 5(6 Suppl 2):S196-S197.)The general | Surgery_Schwartz. CHAPTER 19679CHEST WALL, LUNG, MEDIASTINUM, AND PLEURA10080604020002448All Sites7296120Soft Tissue Sarcomas100806040200024487296120Breast Cancer100806040200024487296120Osteosarcoma1001234806040200024487296120Colon Cancer100806040200024487296120Melanoma100806040200024487296120ABCDEFFigure 19-16. The actuarial survival after metastasectomy is depicted for patients with various tumor types (A-F) further categorized into four groups according to resectabil-ity, solitary or multiple, the inter-val between primary resection and metastesectomy, and a combination of factors known in our work and in others, as follows: (1) resectable, soli-tary, and disease-free interval (DFI) greater than or equal to 36 months; (2) resectable, solitary, and DFI 36+ months; (3) resectable, multiple metastases, and DFI <36 months; and (4) unresectable. (Reproduced with permission from Pastorino U: The development of an international registry, J Thorac Oncol. 2010 Jun; 5(6 Suppl 2):S196-S197.)The general |
Surgery_Schwartz_4585 | Surgery_Schwartz | and DFI <36 months; and (4) unresectable. (Reproduced with permission from Pastorino U: The development of an international registry, J Thorac Oncol. 2010 Jun; 5(6 Suppl 2):S196-S197.)The general principles of patient selection for metasta-sectomy are listed in Table 19-6. The technical aim of pulmo-nary metastasectomy is complete resection of all macroscopic tumors. In addition, any involved adjacent structures should be resected en bloc (i.e., chest wall, diaphragm, and pericardium). Multiple lesions and/or hilar lesions may require lobectomy. Pneumonectomy is rarely justified or employed.Pulmonary metastasectomy can be approached through a thoracotomy or via video-assisted thoracic surgery (VATS) techniques. McCormack and colleagues reported their expe-rience at Memorial Sloan-Kettering in a prospective study of 18 patients who presented with no more than two pulmonary metastatic lesions and underwent VATS resection.32 A thora-cotomy was performed during the same operation; if | Surgery_Schwartz. and DFI <36 months; and (4) unresectable. (Reproduced with permission from Pastorino U: The development of an international registry, J Thorac Oncol. 2010 Jun; 5(6 Suppl 2):S196-S197.)The general principles of patient selection for metasta-sectomy are listed in Table 19-6. The technical aim of pulmo-nary metastasectomy is complete resection of all macroscopic tumors. In addition, any involved adjacent structures should be resected en bloc (i.e., chest wall, diaphragm, and pericardium). Multiple lesions and/or hilar lesions may require lobectomy. Pneumonectomy is rarely justified or employed.Pulmonary metastasectomy can be approached through a thoracotomy or via video-assisted thoracic surgery (VATS) techniques. McCormack and colleagues reported their expe-rience at Memorial Sloan-Kettering in a prospective study of 18 patients who presented with no more than two pulmonary metastatic lesions and underwent VATS resection.32 A thora-cotomy was performed during the same operation; if |
Surgery_Schwartz_4586 | Surgery_Schwartz | in a prospective study of 18 patients who presented with no more than two pulmonary metastatic lesions and underwent VATS resection.32 A thora-cotomy was performed during the same operation; if palpation Brunicardi_Ch19_p0661-p0750.indd 67901/03/19 7:00 PM 680SPECIFIC CONSIDERATIONSPART IITable 19-7Clinical presentation of lung cancerCATEGORYSYMPTOMCAUSEPulmonary symptomsCoughBronchus irritation or compressionDyspneaAirway obstruction or compressionWheezing>50% airway obstructionHemoptysisTumor erosion or irritationPneumoniaAirway obstructionNonpulmonary thoracic symptoms Pleuritic painParietal pleural irritation or invasionLocal chest wall painRib and/or muscle involvementRadicular chest painIntercostal nerve involvementPancoast’s syndromeStellate ganglion, chest wall, brachial plexus involvementHoarsenessRecurrent laryngeal nerve involvementSwelling of head and armsBulky involved mediastinal lymph nodes Medially based right upper lobe tumorTable 19-6General principles governing | Surgery_Schwartz. in a prospective study of 18 patients who presented with no more than two pulmonary metastatic lesions and underwent VATS resection.32 A thora-cotomy was performed during the same operation; if palpation Brunicardi_Ch19_p0661-p0750.indd 67901/03/19 7:00 PM 680SPECIFIC CONSIDERATIONSPART IITable 19-7Clinical presentation of lung cancerCATEGORYSYMPTOMCAUSEPulmonary symptomsCoughBronchus irritation or compressionDyspneaAirway obstruction or compressionWheezing>50% airway obstructionHemoptysisTumor erosion or irritationPneumoniaAirway obstructionNonpulmonary thoracic symptoms Pleuritic painParietal pleural irritation or invasionLocal chest wall painRib and/or muscle involvementRadicular chest painIntercostal nerve involvementPancoast’s syndromeStellate ganglion, chest wall, brachial plexus involvementHoarsenessRecurrent laryngeal nerve involvementSwelling of head and armsBulky involved mediastinal lymph nodes Medially based right upper lobe tumorTable 19-6General principles governing |
Surgery_Schwartz_4587 | Surgery_Schwartz | involvementHoarsenessRecurrent laryngeal nerve involvementSwelling of head and armsBulky involved mediastinal lymph nodes Medially based right upper lobe tumorTable 19-6General principles governing appropriate selection of patients for pulmonary metastasectomy1. Primary tumor must already be controlled.2. Patient must be able to tolerate general anesthesia, potential single-lung ventilation, and the planned pulmonary resection.3. Metastases must be completely resectable based on computed tomographic imaging.4. There is no evidence of extrapulmonary tumor burden.5. Alternative superior therapy must not be available.identified any additional lesions, they were resected. The study concluded that the probability that a metastatic lesion will be missed by VATS excision is 56%. Patients in the Memorial study were evaluated before the advent of spiral CT scanning, however, and it remains controversial whether metastasis resec-tion should be performed via VATS. Proponents of VATS argue that | Surgery_Schwartz. involvementHoarsenessRecurrent laryngeal nerve involvementSwelling of head and armsBulky involved mediastinal lymph nodes Medially based right upper lobe tumorTable 19-6General principles governing appropriate selection of patients for pulmonary metastasectomy1. Primary tumor must already be controlled.2. Patient must be able to tolerate general anesthesia, potential single-lung ventilation, and the planned pulmonary resection.3. Metastases must be completely resectable based on computed tomographic imaging.4. There is no evidence of extrapulmonary tumor burden.5. Alternative superior therapy must not be available.identified any additional lesions, they were resected. The study concluded that the probability that a metastatic lesion will be missed by VATS excision is 56%. Patients in the Memorial study were evaluated before the advent of spiral CT scanning, however, and it remains controversial whether metastasis resec-tion should be performed via VATS. Proponents of VATS argue that |
Surgery_Schwartz_4588 | Surgery_Schwartz | Memorial study were evaluated before the advent of spiral CT scanning, however, and it remains controversial whether metastasis resec-tion should be performed via VATS. Proponents of VATS argue that the resolution of spiral CT scanning is so superior that prior studies using standard CT scanners are no longer relevant. Indeed, a recent study suggested that only 18% of malignant nodules would be missed using a VATS approach in the current era while another study from the United Kingdom found equiv-alent outcomes with regard to missed lesions and pulmonary progression comparing open and VATS approaches. To date, no prospective study using spiral CT scan has been performed to resolve this clinical dilemma.Primary Lung Cancer-Associated Signs and SymptomsLung cancer displays one of the most diverse presentation pat-terns of all human maladies (Table 19-7). The wide range of symptoms and signs is related to (a) histologic features, which often help determine the anatomic site of origin in | Surgery_Schwartz. Memorial study were evaluated before the advent of spiral CT scanning, however, and it remains controversial whether metastasis resec-tion should be performed via VATS. Proponents of VATS argue that the resolution of spiral CT scanning is so superior that prior studies using standard CT scanners are no longer relevant. Indeed, a recent study suggested that only 18% of malignant nodules would be missed using a VATS approach in the current era while another study from the United Kingdom found equiv-alent outcomes with regard to missed lesions and pulmonary progression comparing open and VATS approaches. To date, no prospective study using spiral CT scan has been performed to resolve this clinical dilemma.Primary Lung Cancer-Associated Signs and SymptomsLung cancer displays one of the most diverse presentation pat-terns of all human maladies (Table 19-7). The wide range of symptoms and signs is related to (a) histologic features, which often help determine the anatomic site of origin in |
Surgery_Schwartz_4589 | Surgery_Schwartz | presentation pat-terns of all human maladies (Table 19-7). The wide range of symptoms and signs is related to (a) histologic features, which often help determine the anatomic site of origin in the lung; (b) the specific tumor location in the lung and its relationship to surrounding structures; (c) biologic features and the pro-duction of a variety of paraneoplastic syndromes; and (d) the presence or absence of metastatic disease. Symptoms related to the local intrathoracic effect of the primary tumor can be conveniently divided into two groups: pulmonary and nonpul-monary thoracic.Pulmonary Symptoms. Pulmonary symptoms result from the direct effect of the tumor on the bronchus or lung tissue. Symptoms (in order of frequency) include cough (secondary to irritation or compression of a bronchus), dyspnea (usually due to central airway obstruction or compression, with or without atelectasis), wheezing (with narrowing of a central airway of >50%), hemoptysis (typically, blood streaking of | Surgery_Schwartz. presentation pat-terns of all human maladies (Table 19-7). The wide range of symptoms and signs is related to (a) histologic features, which often help determine the anatomic site of origin in the lung; (b) the specific tumor location in the lung and its relationship to surrounding structures; (c) biologic features and the pro-duction of a variety of paraneoplastic syndromes; and (d) the presence or absence of metastatic disease. Symptoms related to the local intrathoracic effect of the primary tumor can be conveniently divided into two groups: pulmonary and nonpul-monary thoracic.Pulmonary Symptoms. Pulmonary symptoms result from the direct effect of the tumor on the bronchus or lung tissue. Symptoms (in order of frequency) include cough (secondary to irritation or compression of a bronchus), dyspnea (usually due to central airway obstruction or compression, with or without atelectasis), wheezing (with narrowing of a central airway of >50%), hemoptysis (typically, blood streaking of |
Surgery_Schwartz_4590 | Surgery_Schwartz | dyspnea (usually due to central airway obstruction or compression, with or without atelectasis), wheezing (with narrowing of a central airway of >50%), hemoptysis (typically, blood streaking of mucus that is rarely massive; indicates a central airway location), pneu-monia (usually due to airway obstruction by the tumor), and lung abscess (due to necrosis and cavitation, with subsequent infection).Nonpulmonary Thoracic Symptoms. Nonpulmonary tho-racic symptoms result from invasion of the primary tumor directly into a contiguous structure (e.g., chest wall, diaphragm, pericardium, phrenic nerve, recurrent laryngeal nerve, superior vena cava, and esophagus), or from mechanical compression of a structure (e.g., esophagus or superior vena cava) by enlarged tumor-bearing lymph nodes.Peripherally located tumors (often adenocarcinomas) extending through the visceral pleura lead to irritation or growth into the parietal pleura and potentially to continued growth into the chest wall structures. | Surgery_Schwartz. dyspnea (usually due to central airway obstruction or compression, with or without atelectasis), wheezing (with narrowing of a central airway of >50%), hemoptysis (typically, blood streaking of mucus that is rarely massive; indicates a central airway location), pneu-monia (usually due to airway obstruction by the tumor), and lung abscess (due to necrosis and cavitation, with subsequent infection).Nonpulmonary Thoracic Symptoms. Nonpulmonary tho-racic symptoms result from invasion of the primary tumor directly into a contiguous structure (e.g., chest wall, diaphragm, pericardium, phrenic nerve, recurrent laryngeal nerve, superior vena cava, and esophagus), or from mechanical compression of a structure (e.g., esophagus or superior vena cava) by enlarged tumor-bearing lymph nodes.Peripherally located tumors (often adenocarcinomas) extending through the visceral pleura lead to irritation or growth into the parietal pleura and potentially to continued growth into the chest wall structures. |
Surgery_Schwartz_4591 | Surgery_Schwartz | located tumors (often adenocarcinomas) extending through the visceral pleura lead to irritation or growth into the parietal pleura and potentially to continued growth into the chest wall structures. Three types of symptoms, depend-ing on the extent of chest wall involvement, are possible: (a) pleuritic pain, from noninvasive contact of the parietal pleura with inflammatory irritation or direct parietal pleural invasion; (b) localized chest wall pain, from deeper invasion and involvement of the rib and/or intercostal muscles; and (c) radicular pain, from involvement of the intercostal nerve(s). Radicular pain may be mistaken for renal colic in the case of tumors invading the inferoposterior chest wall.Other specific nonpulmonary thoracic symptoms include:1. Pancoast’s syndrome. Tumors originating in the supe-rior sulcus (posterior apex) elicit: apical chest wall and/or shoulder pain (from involvement of the first rib and chest wall); Horner’s syndrome (unilateral enophthal-mos, | Surgery_Schwartz. located tumors (often adenocarcinomas) extending through the visceral pleura lead to irritation or growth into the parietal pleura and potentially to continued growth into the chest wall structures. Three types of symptoms, depend-ing on the extent of chest wall involvement, are possible: (a) pleuritic pain, from noninvasive contact of the parietal pleura with inflammatory irritation or direct parietal pleural invasion; (b) localized chest wall pain, from deeper invasion and involvement of the rib and/or intercostal muscles; and (c) radicular pain, from involvement of the intercostal nerve(s). Radicular pain may be mistaken for renal colic in the case of tumors invading the inferoposterior chest wall.Other specific nonpulmonary thoracic symptoms include:1. Pancoast’s syndrome. Tumors originating in the supe-rior sulcus (posterior apex) elicit: apical chest wall and/or shoulder pain (from involvement of the first rib and chest wall); Horner’s syndrome (unilateral enophthal-mos, |
Surgery_Schwartz_4592 | Surgery_Schwartz | originating in the supe-rior sulcus (posterior apex) elicit: apical chest wall and/or shoulder pain (from involvement of the first rib and chest wall); Horner’s syndrome (unilateral enophthal-mos, ptosis, miosis, and facial anhidrosis from invasion of the stellate sympathetic ganglion); and radicular arm pain (from invasion of T1, and occasionally C8, brachial plexus nerve roots).2. Phrenic nerve palsy. The phrenic nerve traverses the hemi-thorax along the mediastinum, parallel and posterior to the superior vena cava and anterior to the pulmonary hilum. Tumors at the medial lung surface or anterior hilum can directly invade the nerve; symptoms include shoulder pain (referred), hiccups, and dyspnea with exertion because of Brunicardi_Ch19_p0661-p0750.indd 68001/03/19 7:00 PM | Surgery_Schwartz. originating in the supe-rior sulcus (posterior apex) elicit: apical chest wall and/or shoulder pain (from involvement of the first rib and chest wall); Horner’s syndrome (unilateral enophthal-mos, ptosis, miosis, and facial anhidrosis from invasion of the stellate sympathetic ganglion); and radicular arm pain (from invasion of T1, and occasionally C8, brachial plexus nerve roots).2. Phrenic nerve palsy. The phrenic nerve traverses the hemi-thorax along the mediastinum, parallel and posterior to the superior vena cava and anterior to the pulmonary hilum. Tumors at the medial lung surface or anterior hilum can directly invade the nerve; symptoms include shoulder pain (referred), hiccups, and dyspnea with exertion because of Brunicardi_Ch19_p0661-p0750.indd 68001/03/19 7:00 PM |
Surgery_Schwartz_4593 | Surgery_Schwartz | CHAPTER 19681CHEST WALL, LUNG, MEDIASTINUM, AND PLEURAdiaphragm paralysis. Radiographically, unilateral diaphragm elevation on chest radiograph is present; the diagnosis is confirmed by fluoroscopic examination of the diaphragm with paradoxical motion with breathing and sniffing (the “sniff” test).3. Recurrent laryngeal nerve palsy. Recurrent laryngeal nerve (RLN) involvement most commonly occurs on the left side, given the hilar location of the left RLN as it passes under the aortic arch. Paralysis results from: (a) invasion of the vagus nerve above the aortic arch by a medially based left upper lobe tumor; or (b) direct invasion of the RLN by hilar tumor and/or hilar or aortopulmonary lymph node metastases. Symptoms include voice change, often referred to as hoarseness, but more typically a loss of tone associ-ated with a breathy quality, and coughing, particularly when drinking liquids.4. Superior vena cava (SVC) syndrome. As a result of bulky enlargement of involved mediastinal | Surgery_Schwartz. CHAPTER 19681CHEST WALL, LUNG, MEDIASTINUM, AND PLEURAdiaphragm paralysis. Radiographically, unilateral diaphragm elevation on chest radiograph is present; the diagnosis is confirmed by fluoroscopic examination of the diaphragm with paradoxical motion with breathing and sniffing (the “sniff” test).3. Recurrent laryngeal nerve palsy. Recurrent laryngeal nerve (RLN) involvement most commonly occurs on the left side, given the hilar location of the left RLN as it passes under the aortic arch. Paralysis results from: (a) invasion of the vagus nerve above the aortic arch by a medially based left upper lobe tumor; or (b) direct invasion of the RLN by hilar tumor and/or hilar or aortopulmonary lymph node metastases. Symptoms include voice change, often referred to as hoarseness, but more typically a loss of tone associ-ated with a breathy quality, and coughing, particularly when drinking liquids.4. Superior vena cava (SVC) syndrome. As a result of bulky enlargement of involved mediastinal |
Surgery_Schwartz_4594 | Surgery_Schwartz | a loss of tone associ-ated with a breathy quality, and coughing, particularly when drinking liquids.4. Superior vena cava (SVC) syndrome. As a result of bulky enlargement of involved mediastinal lymph nodes com-pressing or a medially based right upper lobe tumor invad-ing the SVC, SVC syndrome symptoms include variable degrees of swelling of the head, neck, and arms; headache; and conjunctival edema. It is seen most commonly with NEC grade IV (small cell) lung cancer.5. Pericardial tamponade. Pericardial effusions (benign or malignant), associated with increasing levels of dyspnea and/or arrhythmias, and pericardial tamponade occur with direct pericardial invasion. Diagnosis requires a high index of suspicion in the setting of a medially based tumor with symptoms of dyspnea and is confirmed by CT scan or echocardiography.6. Back pain. Results from direct invasion of a vertebral body and is often localized and severe. If the neural foramina are involved, radicular pain may also be | Surgery_Schwartz. a loss of tone associ-ated with a breathy quality, and coughing, particularly when drinking liquids.4. Superior vena cava (SVC) syndrome. As a result of bulky enlargement of involved mediastinal lymph nodes com-pressing or a medially based right upper lobe tumor invad-ing the SVC, SVC syndrome symptoms include variable degrees of swelling of the head, neck, and arms; headache; and conjunctival edema. It is seen most commonly with NEC grade IV (small cell) lung cancer.5. Pericardial tamponade. Pericardial effusions (benign or malignant), associated with increasing levels of dyspnea and/or arrhythmias, and pericardial tamponade occur with direct pericardial invasion. Diagnosis requires a high index of suspicion in the setting of a medially based tumor with symptoms of dyspnea and is confirmed by CT scan or echocardiography.6. Back pain. Results from direct invasion of a vertebral body and is often localized and severe. If the neural foramina are involved, radicular pain may also be |
Surgery_Schwartz_4595 | Surgery_Schwartz | by CT scan or echocardiography.6. Back pain. Results from direct invasion of a vertebral body and is often localized and severe. If the neural foramina are involved, radicular pain may also be present.7. Other local symptoms. Dysphagia is usually secondary to external esophageal compression by enlarged lymph nodes involved with metastatic disease, usually with lower lobe tumors. Finally, dyspnea, pleural effusion, or referred shoulder pain can result from invasion of the diaphragm by a tumor at the base of a lower lobe.Associated Paraneoplastic Syndromes. All lung cancer his-tologies are capable of producing a variety of paraneoplastic syndromes, most often from systemic release of tumor-derived biologically active materials (Table 19-8). Paraneoplastic syn-dromes may produce symptoms even before any local symp-toms are produced by the primary tumor, thereby aiding in early diagnosis. Their presence does not influence resectabil-ity or treatment options. Symptoms often abate with | Surgery_Schwartz. by CT scan or echocardiography.6. Back pain. Results from direct invasion of a vertebral body and is often localized and severe. If the neural foramina are involved, radicular pain may also be present.7. Other local symptoms. Dysphagia is usually secondary to external esophageal compression by enlarged lymph nodes involved with metastatic disease, usually with lower lobe tumors. Finally, dyspnea, pleural effusion, or referred shoulder pain can result from invasion of the diaphragm by a tumor at the base of a lower lobe.Associated Paraneoplastic Syndromes. All lung cancer his-tologies are capable of producing a variety of paraneoplastic syndromes, most often from systemic release of tumor-derived biologically active materials (Table 19-8). Paraneoplastic syn-dromes may produce symptoms even before any local symp-toms are produced by the primary tumor, thereby aiding in early diagnosis. Their presence does not influence resectabil-ity or treatment options. Symptoms often abate with |
Surgery_Schwartz_4596 | Surgery_Schwartz | even before any local symp-toms are produced by the primary tumor, thereby aiding in early diagnosis. Their presence does not influence resectabil-ity or treatment options. Symptoms often abate with success-ful treatment; paraneoplastic symptom recurrence may herald tumor recurrence. The majority of such syndromes are associ-ated with grade IV NEC (small cell carcinoma), including many endocrinopathies.1. Hypertrophic pulmonary osteoarthropathy (HPO). Often severely debilitating, symptoms of HPO may antedate the diagnosis of cancer by months. Clinically, ankle, feet, fore-arm, and hand tenderness and swelling are characteristic, resulting from periostitis of the fibula, tibia, radius, meta-carpals, and metatarsals. Clubbing of the digits may occur in up to 30% of patients with grade IV NEC (Fig. 19-17). Plain radiographs show periosteal inflammation and elevation, while bone scans demonstrate intense but Table 19-8Paraneoplastic syndromes in patients with lung | Surgery_Schwartz. even before any local symp-toms are produced by the primary tumor, thereby aiding in early diagnosis. Their presence does not influence resectabil-ity or treatment options. Symptoms often abate with success-ful treatment; paraneoplastic symptom recurrence may herald tumor recurrence. The majority of such syndromes are associ-ated with grade IV NEC (small cell carcinoma), including many endocrinopathies.1. Hypertrophic pulmonary osteoarthropathy (HPO). Often severely debilitating, symptoms of HPO may antedate the diagnosis of cancer by months. Clinically, ankle, feet, fore-arm, and hand tenderness and swelling are characteristic, resulting from periostitis of the fibula, tibia, radius, meta-carpals, and metatarsals. Clubbing of the digits may occur in up to 30% of patients with grade IV NEC (Fig. 19-17). Plain radiographs show periosteal inflammation and elevation, while bone scans demonstrate intense but Table 19-8Paraneoplastic syndromes in patients with lung |
Surgery_Schwartz_4597 | Surgery_Schwartz | with grade IV NEC (Fig. 19-17). Plain radiographs show periosteal inflammation and elevation, while bone scans demonstrate intense but Table 19-8Paraneoplastic syndromes in patients with lung cancerEndocrineHypercalcemia (ectopic parathyroid hormone)Cushing’s syndromeSyndrome of inappropriate secretion of antidiuretic hormoneCarcinoid syndromeGynecomastiaHypercalcitoninemiaElevated growth hormone levelElevated levels of prolactin, follicle-stimulating hormone, luteinizing hormoneHypoglycemiaHyperthyroidismNeurologicEncephalopathySubacute cerebellar degenerationProgressive multifocal leukoencephalopathyPeripheral neuropathyPolymyositisAutonomic neuropathyEaton-Lambert syndromeOptic neuritisSkeletalClubbingPulmonary hypertrophic osteoarthropathyHematologicAnemiaLeukemoid reactionsThrombocytosisThrombocytopeniaEosinophiliaPure red cell aplasiaLeukoerythroblastosisDisseminated intravascular coagulationCutaneousHyperkeratosisDermatomyositisAcanthosis nigricansHyperpigmentationErythema | Surgery_Schwartz. with grade IV NEC (Fig. 19-17). Plain radiographs show periosteal inflammation and elevation, while bone scans demonstrate intense but Table 19-8Paraneoplastic syndromes in patients with lung cancerEndocrineHypercalcemia (ectopic parathyroid hormone)Cushing’s syndromeSyndrome of inappropriate secretion of antidiuretic hormoneCarcinoid syndromeGynecomastiaHypercalcitoninemiaElevated growth hormone levelElevated levels of prolactin, follicle-stimulating hormone, luteinizing hormoneHypoglycemiaHyperthyroidismNeurologicEncephalopathySubacute cerebellar degenerationProgressive multifocal leukoencephalopathyPeripheral neuropathyPolymyositisAutonomic neuropathyEaton-Lambert syndromeOptic neuritisSkeletalClubbingPulmonary hypertrophic osteoarthropathyHematologicAnemiaLeukemoid reactionsThrombocytosisThrombocytopeniaEosinophiliaPure red cell aplasiaLeukoerythroblastosisDisseminated intravascular coagulationCutaneousHyperkeratosisDermatomyositisAcanthosis nigricansHyperpigmentationErythema |
Surgery_Schwartz_4598 | Surgery_Schwartz | red cell aplasiaLeukoerythroblastosisDisseminated intravascular coagulationCutaneousHyperkeratosisDermatomyositisAcanthosis nigricansHyperpigmentationErythema gyratum repensHypertrichosis lanuginosa acquistaOtherNephrotic syndromeHypouricemiaSecretion of vasoactive intestinal peptide with diarrheaHyperamylasemiaAnorexia or cachexiasymmetric uptake in the long bones. Aspirin or nonsteroidal anti-inflammatory agents provide temporary relief; treat-ment requires successful tumor eradication.2. Hypercalcemia. Up to 10% of patients with lung cancer will have hypercalcemia, most often due to metastatic disease. Ectopic parathyroid hormone secretion by the tumor, most often squamous cell carcinoma, is causative in up to 15%, however, and should be suspected if metastatic bone disease is not present. Symptoms of hypercalcemia include leth-argy, depressed level of consciousness, nausea, vomiting, Brunicardi_Ch19_p0661-p0750.indd 68101/03/19 7:00 PM 682SPECIFIC | Surgery_Schwartz. red cell aplasiaLeukoerythroblastosisDisseminated intravascular coagulationCutaneousHyperkeratosisDermatomyositisAcanthosis nigricansHyperpigmentationErythema gyratum repensHypertrichosis lanuginosa acquistaOtherNephrotic syndromeHypouricemiaSecretion of vasoactive intestinal peptide with diarrheaHyperamylasemiaAnorexia or cachexiasymmetric uptake in the long bones. Aspirin or nonsteroidal anti-inflammatory agents provide temporary relief; treat-ment requires successful tumor eradication.2. Hypercalcemia. Up to 10% of patients with lung cancer will have hypercalcemia, most often due to metastatic disease. Ectopic parathyroid hormone secretion by the tumor, most often squamous cell carcinoma, is causative in up to 15%, however, and should be suspected if metastatic bone disease is not present. Symptoms of hypercalcemia include leth-argy, depressed level of consciousness, nausea, vomiting, Brunicardi_Ch19_p0661-p0750.indd 68101/03/19 7:00 PM 682SPECIFIC |
Surgery_Schwartz_4599 | Surgery_Schwartz | bone disease is not present. Symptoms of hypercalcemia include leth-argy, depressed level of consciousness, nausea, vomiting, Brunicardi_Ch19_p0661-p0750.indd 68101/03/19 7:00 PM 682SPECIFIC CONSIDERATIONSPART IIABCFigure 19-17. Hypertrophic pulmonary osteoarthropathy associated with small cell carcinoma. A. Painful clubbing of the fingers. B. Painful clubbing of the toes (close-up). C. The arrows point to new bone formation on the femur.and dehydration. Following complete tumor eradication, the calcium level will normalize. Unfortunately, tumor recur-rence is extremely common and may manifest as recurrent hypercalcemia.3. Hyponatremia. Characterized by confusion, lethargy, and possible seizures, hyponatremia can result from the inappro-priate secretion of antidiuretic hormone from the tumor into the systemic circulation (syndrome of inappropriate secretion of antidiuretic hormone [SIADH]) in 10% to 45% of patients with grade IV NEC (small cell). It is diagnosed by the pres-ence | Surgery_Schwartz. bone disease is not present. Symptoms of hypercalcemia include leth-argy, depressed level of consciousness, nausea, vomiting, Brunicardi_Ch19_p0661-p0750.indd 68101/03/19 7:00 PM 682SPECIFIC CONSIDERATIONSPART IIABCFigure 19-17. Hypertrophic pulmonary osteoarthropathy associated with small cell carcinoma. A. Painful clubbing of the fingers. B. Painful clubbing of the toes (close-up). C. The arrows point to new bone formation on the femur.and dehydration. Following complete tumor eradication, the calcium level will normalize. Unfortunately, tumor recur-rence is extremely common and may manifest as recurrent hypercalcemia.3. Hyponatremia. Characterized by confusion, lethargy, and possible seizures, hyponatremia can result from the inappro-priate secretion of antidiuretic hormone from the tumor into the systemic circulation (syndrome of inappropriate secretion of antidiuretic hormone [SIADH]) in 10% to 45% of patients with grade IV NEC (small cell). It is diagnosed by the pres-ence |
Surgery_Schwartz_4600 | Surgery_Schwartz | tumor into the systemic circulation (syndrome of inappropriate secretion of antidiuretic hormone [SIADH]) in 10% to 45% of patients with grade IV NEC (small cell). It is diagnosed by the pres-ence of hyponatremia, low serum osmolality, and high urinary sodium and osmolality. Another cause of hyponatremia can be the ectopic secretion of atrial natriuretic peptide (ANP).4. Cushing’s syndrome. Autonomous tumor production of an adrenocorticotropic hormone (ACTH)-like molecule leads to rapid serum elevation of ACTH and subsequent severe hypokalemia, metabolic alkalosis, and hyperglycemia. Symptoms are primarily related to the metabolic changes while the physical signs of Cushing’s syndrome (e.g., trun-cal obesity, buffalo hump, striae) are unusual due to the rapidity of ACTH elevation. Diagnosis is made by dem-onstrating hypokalemia (<3.0 mmol/L); nonsuppressible elevated plasma cortisol levels that lack the normal diurnal variation; elevated blood ACTH levels; or elevated urinary | Surgery_Schwartz. tumor into the systemic circulation (syndrome of inappropriate secretion of antidiuretic hormone [SIADH]) in 10% to 45% of patients with grade IV NEC (small cell). It is diagnosed by the pres-ence of hyponatremia, low serum osmolality, and high urinary sodium and osmolality. Another cause of hyponatremia can be the ectopic secretion of atrial natriuretic peptide (ANP).4. Cushing’s syndrome. Autonomous tumor production of an adrenocorticotropic hormone (ACTH)-like molecule leads to rapid serum elevation of ACTH and subsequent severe hypokalemia, metabolic alkalosis, and hyperglycemia. Symptoms are primarily related to the metabolic changes while the physical signs of Cushing’s syndrome (e.g., trun-cal obesity, buffalo hump, striae) are unusual due to the rapidity of ACTH elevation. Diagnosis is made by dem-onstrating hypokalemia (<3.0 mmol/L); nonsuppressible elevated plasma cortisol levels that lack the normal diurnal variation; elevated blood ACTH levels; or elevated urinary |
Surgery_Schwartz_4601 | Surgery_Schwartz | Diagnosis is made by dem-onstrating hypokalemia (<3.0 mmol/L); nonsuppressible elevated plasma cortisol levels that lack the normal diurnal variation; elevated blood ACTH levels; or elevated urinary 17-hydroxycorticosteroids, all of which are not suppressible by administration of exogenous dexamethasone. Immuno-reactive ACTH is present in nearly all extracts of SCLC, and a high percentage of patients with SCLC have elevated ACTH levels by radioimmunoassay, yet fewer than 5% have symptoms of Cushing’s syndrome.5. Peripheral and central neuropathies. Unlike other para-neoplastic syndromes, which are usually due to ectopic secretion of an active substance, these syndromes are felt to be immune mediated. Cancer cells are thought to secrete antigens normally expressed only by the nervous system, generating antibodies leading either to interference with neurologic function or to immune neurologic destruction. Up to 16% of lung cancer patients have neuromuscular dis-ability, and, of these, | Surgery_Schwartz. Diagnosis is made by dem-onstrating hypokalemia (<3.0 mmol/L); nonsuppressible elevated plasma cortisol levels that lack the normal diurnal variation; elevated blood ACTH levels; or elevated urinary 17-hydroxycorticosteroids, all of which are not suppressible by administration of exogenous dexamethasone. Immuno-reactive ACTH is present in nearly all extracts of SCLC, and a high percentage of patients with SCLC have elevated ACTH levels by radioimmunoassay, yet fewer than 5% have symptoms of Cushing’s syndrome.5. Peripheral and central neuropathies. Unlike other para-neoplastic syndromes, which are usually due to ectopic secretion of an active substance, these syndromes are felt to be immune mediated. Cancer cells are thought to secrete antigens normally expressed only by the nervous system, generating antibodies leading either to interference with neurologic function or to immune neurologic destruction. Up to 16% of lung cancer patients have neuromuscular dis-ability, and, of these, |
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