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Surgery_Schwartz. and debridement and drainage of the spreading infectious process within the mediastinum, neck, pleura, and other tissue planes. Antibiotics, fluid resusci-tation, and other supportive measures are also important. Brunicardi_Ch19_p0661-p0750.indd 73501/03/19 7:01 PM 736SPECIFIC CONSIDERATIONSPART IITable 19-32Etiologic factors in acute mediastinitisEsophageal perforation Iatrogenic Balloon dilatation (for achalasia) Bougienage (for peptic stricture) Esophagoscopy Sclerotherapy (for variceal bleeding) Spontaneous Postemetic (Boerhaave’s syndrome) Straining during: Elimination Weight lifting Seizure Pregnancy Childbirth Ingestion of foreign bodies Trauma Blunt Penetrating Postsurgical Infection Anastomotic leak Erosion by cancerDeep sternotomy wound infectionOropharynx and neck infectionsLudwig’s anginaQuinsyRetropharyngeal abscessCellulitis and suppurative lymphadenitis of the neckInfections of the lung and pleuraSubphrenic abscessRib or vertebral


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Surgery_Schwartz. and neck infectionsLudwig’s anginaQuinsyRetropharyngeal abscessCellulitis and suppurative lymphadenitis of the neckInfections of the lung and pleuraSubphrenic abscessRib or vertebral osteomyelitisHematogenous or metastatic abscessReproduced with permission from Pearson FG, Cooper JD, Deslauriers J, et al: Thoracic Surgery, 2nd ed. New York, NY: Elsevier/Churchill Livingstone; 2002.Debridement may need to be repeated and other planes and cavities explored depending on the patient’s clinical status. Blood cell counts and serial CT scans may also be required. Persistent sepsis or collections on CT scan may require further radical surgical debridement.Chronic Mediastinitis. Sclerosing or fibrosing mediastinitis results from chronic mediastinal inflammation that originates in the lymph nodes, most frequently from granulomatous infec-tions such as histoplasmosis or tuberculosis. Chronic, low-grade inflammation leads to fibrosis and scarring, which can, in some patients, result in entrapment


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Surgery_Schwartz. frequently from granulomatous infec-tions such as histoplasmosis or tuberculosis. Chronic, low-grade inflammation leads to fibrosis and scarring, which can, in some patients, result in entrapment and compression of the low-pressure veins (including the SVC and innominate and azy-gos veins), the esophagus, and pulmonary arteries. There is no definitive treatment. Surgery is indicated only for diagnosis or in specific patients to relieve airway or esophageal obstruction or to achieve vascular reconstruction. Reports of palliative suc-cess with less invasive procedures (such as dilation and stenting of airways, the esophagus, or the SVC) are promising. In one series of 22 patients, ketoconazole was effective in controlling progression. In another series of 71 patients, 30% died from disease-associated complications during long-term follow-up. Chronic mediastinitis is similar to retroperitoneal fibrosis, scle-rosing cholangitis, and Riedel’s thyroiditis.PLEURA AND PLEURAL SPACEAnatomyEach


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Surgery_Schwartz. complications during long-term follow-up. Chronic mediastinitis is similar to retroperitoneal fibrosis, scle-rosing cholangitis, and Riedel’s thyroiditis.PLEURA AND PLEURAL SPACEAnatomyEach hemithorax has a mesothelial lining that invaginates at the hilum of each lung and continues on to cover each lung. The portion lining the bony rib cage, mediastinum, and dia-phragm is called the parietal pleura, whereas the portion encas-ing the lung is known as the visceral pleura. Between these two surfaces is the potential pleural space, which is normally occupied by a thin layer of lubricating pleural fluid. A network of somatic, sympathetic, and parasympathetic fibers innervates the parietal pleura. Irritation of the parietal surface by inflam-mation, tumor invasion, trauma, and other processes can lead to a sensation of chest wall pain. The visceral pleura have no somatic innervation.171,172Pleural EffusionPleural effusion refers to any significant collection of fluid within the pleural


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Surgery_Schwartz. can lead to a sensation of chest wall pain. The visceral pleura have no somatic innervation.171,172Pleural EffusionPleural effusion refers to any significant collection of fluid within the pleural space. Normally, between 5 and 10 L of fluid enters the pleural space each day by filtration through microves-sels supplying the parietal pleura (located mainly in the less dependent regions of the cavity). The net balance of pressures in these capillaries leads to fluid flow from the parietal pleural surface into the pleural space, and the net balance of forces in the pulmonary circulation leads to absorption through the vis-ceral pleura. Normally, 15 to 20 mL of pleural fluid is present at any given time. Any disturbance in these forces can lead to imbalance and accumulation of pleural fluid. Common patho-logic conditions in North America that lead to pleural effusion include congestive heart failure, bacterial pneumonia, malig-nancy, and pulmonary emboli (Table 19-33).173Access and


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Surgery_Schwartz. Common patho-logic conditions in North America that lead to pleural effusion include congestive heart failure, bacterial pneumonia, malig-nancy, and pulmonary emboli (Table 19-33).173Access and Drainage of Pleural Fluid CollectionsMost patients with pleural effusions of unknown cause should undergo thoracentesis with the following exceptions: effusions in the setting of congestive heart failure, hepatic failure or renal fail-ure, or small effusions associated with an improving pneumonia. If the clinical history suggests congestive heart failure as a cause, particularly in the setting of bilateral effusions, a trial of diuresis may be indicated (rather than thoracentesis). Up to 75% of effu-sions due to congestive heart failure resolve within 48 hours with diuresis alone. Similarly, thoracentesis can be avoided in patients with small effusions associated with resolving pneumonia. These patients typically present with cough, fever, leukocytosis, and uni-lateral infiltrate, and the


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Surgery_Schwartz. can be avoided in patients with small effusions associated with resolving pneumonia. These patients typically present with cough, fever, leukocytosis, and uni-lateral infiltrate, and the effusion is usually a result of a reactive, parapneumonic process. If the effusion is small and the patient responds to antibiotics, a diagnostic thoracentesis may be unneces-sary. If the effusion is large and compromising respiratory efforts, or if the patient has a persistent white blood cell count despite improving signs of pneumonia, an empyema of the pleural space must be considered. In these patients, early and aggressive drainage with chest tubes is required, possibly with surgical intervention.Once the decision is made to access a pleural effusion, the next step is to determine if a sample of the fluid or complete drainage of the pleural space is desired. This step is influenced by the clinical history, the type and amount of fluid present, the Brunicardi_Ch19_p0661-p0750.indd 73601/03/19


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Surgery_Schwartz. fluid or complete drainage of the pleural space is desired. This step is influenced by the clinical history, the type and amount of fluid present, the Brunicardi_Ch19_p0661-p0750.indd 73601/03/19 7:01 PM


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Surgery_Schwartz. CHAPTER 19737CHEST WALL, LUNG, MEDIASTINUM, AND PLEURATable 19-33Leading causes of pleural effusion in the United States, based on data from patients undergoing thoracentesisCAUSEANNUAL INCIDENCETRANSUDATEEXUDATECongestive heart failure500,000YesNoPneumonia300,000NoYesCancer200,000NoYesPulmonary embolus150,000SometimesSometimesViral disease100,000NoYesCoronary artery bypass surgery60,000NoYesCirrhosis with ascites50,000YesNoData from Light RW: Pleural diseases, 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2001.nature of the collection (such as free-flowing or loculated), the cause, and the likelihood of recurrence. For small, free-flowing effusions, an outpatient diagnostic and/or therapeutic thora-centesis with a relatively small-bore needle or catheter (14to 16-gauge) can be performed (Fig. 19-50). The appearance of the fluid is informative: clear straw-colored fluid is often transuda-tive; turbid or bloody fluid is often exudative.The site of entry for drainage of a


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Surgery_Schwartz. be performed (Fig. 19-50). The appearance of the fluid is informative: clear straw-colored fluid is often transuda-tive; turbid or bloody fluid is often exudative.The site of entry for drainage of a pleural effusion or pneumothorax may be based on the CXR alone if the effu-sion is demonstrated to be free-flowing. For free-flowing effu-sions, a low approach at the eighth or ninth intercostal space in the posterior midclavicular line facilitates complete drainage. If the effusion is loculated, CTor ultrasound-guided drainage may be indicated. If the goal is complete drainage, a small-bore pigtail catheter is inserted and connected to a closed drainage system with applied suction (typically –20 cm H2O). In general, the smallest-bore drainage catheter that will effec-tively drain the pleural space should be chosen. Smaller-diam-eter catheters significantly decrease the pain associated with the placement of chest tubes but are more prone to clogging and twisting.174,175 For clinical


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Surgery_Schwartz. space should be chosen. Smaller-diam-eter catheters significantly decrease the pain associated with the placement of chest tubes but are more prone to clogging and twisting.174,175 For clinical situations requiring biopsy or for potential interventions such as adhesiolysis or pleurodesis, minimally invasive surgery may be indicated, using a VATS approach.Figure 19-50. Techniques for aspiration and drainage of a pleural effusion. A. Needle aspiration. With careful appraisal of the x-ray findings, the best interspace is selected, and fluid is aspirated with a needle and syringe. Large volumes of fluid can be removed with a little patience and a large-bore needle. B. Chest tube insertion. After careful skin preparation, draping, and administration of local anesthesia, a short skin incision is made over the correct interspace. The incision is deepened into the intercostal muscles, and the pleura is penetrated (usually with a clamp). When any doubt exists about the status of the pleural


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Surgery_Schwartz. is made over the correct interspace. The incision is deepened into the intercostal muscles, and the pleura is penetrated (usually with a clamp). When any doubt exists about the status of the pleural space at the site of puncture, the wound is enlarged bluntly to admit a finger, which can be swept around the immediately adjacent pleural space to assess the situation and break down any adhesions. The tube is inserted, with the tip directed toward the optimal position suggested by the chest X-rays. In general, a high anterior tube is best for air (pneumothorax), and a low posterior tube is best for fluid. A 28F to 32F tube is adequate for most situations. A 36F tube is preferred for hemothorax or for a viscous empyema. Many surgeons prefer a very small tube (16F to 20F) for drainage of simple pneumothorax. C. The tube is connected to a water-seal drainage system. Suction is added, if necessary, to expand the lung; it usually will be required in a patient with a substantial air leak


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Surgery_Schwartz. simple pneumothorax. C. The tube is connected to a water-seal drainage system. Suction is added, if necessary, to expand the lung; it usually will be required in a patient with a substantial air leak (bronchopleural fistula).Brunicardi_Ch19_p0661-p0750.indd 73701/03/19 7:01 PM 738SPECIFIC CONSIDERATIONSPART IITable 19-34Differential diagnosis of pleural effusions I. Transudative pleural effusions A. Congestive heart failure B. Cirrhosis C. Nephrotic syndrome D. Superior vena caval obstruction E. Fontan procedure F. Urinothorax G. Peritoneal dialysis H. Glomerulonephritis I. Myxedema J. Cerebrospinal fluid leaks to pleura K. Hypoalbuminemia L. Pulmonary emboli M. Sarcoidosis II. Exudative pleural effusions A. Neoplastic diseases 1. Metastatic disease 2. Mesothelioma 3. Body cavity lymphoma 4. Pyothorax-associated lymphoma B. Infectious diseases 1. Tuberculosis 2. Other bacterial infections 3. Fungal infections 4. Parasitic infections 5. Viral infections C. Pulmonary


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Surgery_Schwartz. cavity lymphoma 4. Pyothorax-associated lymphoma B. Infectious diseases 1. Tuberculosis 2. Other bacterial infections 3. Fungal infections 4. Parasitic infections 5. Viral infections C. Pulmonary embolization D. Gastrointestinal disease 1. Pancreatic disease 2. Subphrenic abscess 3. Intrahepatic abscess 4. Intrasplenic abscess 5. Esophageal perforation 6. After abdominal surgery 7. Diaphragmatic hernia 8. Endoscopic variceal sclerosis 9. After liver transplantation E. Heart diseases 1. After coronary artery bypass graft surgery 2. Post-cardiac injury (Dressler’s) syndrome 3. Pericardial disease F. Obstetric and gynecologic diseases 1. Ovarian hyperstimulation syndrome 2. Fetal pleural effusion 3. Postpartum pleural effusion 4. Megis’ syndrome 5. Endometriosis G. Collagen vascular diseases 1. Rheumatoid pleuritis 2. Systemic lupus erythematosus 3. Drug-induced lupus 4. Immunoblastic lymphadenopathy 5. Sjögren’s syndrome 6. Familial Mediterranean fever 7. Churg-Strauss


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Surgery_Schwartz. vascular diseases 1. Rheumatoid pleuritis 2. Systemic lupus erythematosus 3. Drug-induced lupus 4. Immunoblastic lymphadenopathy 5. Sjögren’s syndrome 6. Familial Mediterranean fever 7. Churg-Strauss syndrome 8. Wegener’s granulomatosis H. Drug-induced pleural disease 1. Nitrofurantoin 2. Dantrolene 3. Methysergide 4. Ergot alkaloids 5. Amiodarone 6. Interleukin-2 7. Procarbazine 8. Methotrexate 9. Clozapine I. Miscellaneous diseases and conditions 1. Asbestos exposure 2. After lung transplantation 3. After bone marrow transplantation 4. Yellow nail syndrome 5. Sarcoidosis 6. Uremia 7. Trapped lung 8. Therapeutic radiation exposure 9. Drowning 10. Amyloidosis 11. Milk of calcium pleural effusion 12. Electrical burns 13. Extramedullary hematopoiesis 14. Rupture of mediastinal cyst 15. Acute respiratory distress syndrome 16. Whipple’s disease 17. Iatrogenic pleural effusions J. Hemothorax K. ChylothoraxReproduced with permission from Light RW: Pleural diseases, 5th ed. Philadelphia, PA:


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Surgery_Schwartz. respiratory distress syndrome 16. Whipple’s disease 17. Iatrogenic pleural effusions J. Hemothorax K. ChylothoraxReproduced with permission from Light RW: Pleural diseases, 5th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2007.Complications of Pleural Drainage. The most common complications of invasive pleural procedures are inadvertent injury to adjacent organs, including lung, with air leakage and pneumothorax; subdiaphragmatic entry and damage to the liver, spleen, or other intra-abdominal viscera; intercostal ves-sel injury with subsequent bleeding or larger vessel injury; and even cardiac puncture. Sometimes, bleeding may be the result of an underlying coagulopathy or anticoagulant therapy. Other technical complications include loss of a catheter, guidewire, or fragment in the pleural space and infections. Occasionally, rapid drainage of a large effusion can be followed by shortness of breath, clinical instability, and a phenomenon referred to as postexpansion pulmonary


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Surgery_Schwartz. pleural space and infections. Occasionally, rapid drainage of a large effusion can be followed by shortness of breath, clinical instability, and a phenomenon referred to as postexpansion pulmonary edema. For this reason, it is recom-mended to drain only up to 1500 mL initially. Most complica-tions can be avoided by consulting with a clinician experienced in pleural drainage techniques.Pleural Fluid Analysis. Pleural fluid collections are generally classified as transudates and exudates (Table 19-34). Transu-dates are protein-poor ultrafiltrates of plasma that result from alterations in the systemic hydrostatic pressures or colloid Brunicardi_Ch19_p0661-p0750.indd 73801/03/19 7:01 PM


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Surgery_Schwartz. CHAPTER 19739CHEST WALL, LUNG, MEDIASTINUM, AND PLEURAosmotic pressures (for example, with congestive heart failure or cirrhosis). On gross visual inspection, a transudative effusion is generally clear or straw-colored. Exudates are protein-rich pleural fluid collections that generally result from inflamma-tion or pleural invasion by tumor. Grossly, they are often turbid, bloody, or purulent. Absent trauma, grossly bloody effusions are frequently malignant, but they may also occur in the setting of a pulmonary embolism or pneumonia.Transudates and exudates can be differentiated using Light’s criteria. An effusion is exudative if the pleural fluid-to-serum ratio of protein is greater than 0.5 and the LDH ratio is greater than 0.6 or the absolute pleural LDH level is greater than two-thirds of the normal upper limit for serum. If criteria suggest a transudate, a careful evaluation for congestive heart failure, cirrhosis, or conditions associated with transudates is under-taken. If


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Surgery_Schwartz. of the normal upper limit for serum. If criteria suggest a transudate, a careful evaluation for congestive heart failure, cirrhosis, or conditions associated with transudates is under-taken. If criteria suggest an exudate, further diagnostic studies may be helpful. If total and differential cell counts reveal a pre-dominance of neutrophils (>50% of cells), the effusion is likely associated with an acute inflammatory process (such as a para-pneumonic effusion or empyema, pulmonary embolus, or pan-creatitis). A predominance of mononuclear cells suggests a more chronic inflammatory process (such as cancer or tuberculosis). Gram stains and cultures should be obtained if possible, with inoculation into culture bottles at the bedside. Pleural fluid glu-cose levels are frequently decreased (<60 mg/dL) with complex parapneumonic effusions or malignant effusions. It is important to note that while the distinction between transudate and exudate can be diagnostically useful, the ultimate


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Surgery_Schwartz. (<60 mg/dL) with complex parapneumonic effusions or malignant effusions. It is important to note that while the distinction between transudate and exudate can be diagnostically useful, the ultimate decision for prolonged chest tube drainage or surgery depends on the effusion size and adequacy of drainage, presence of loculations, adequacy of lung reexpansion after drainage, and recurrence after initial drainage.A pleural effusion occurring in association with pleuritic chest pain, hemoptysis, or dyspnea out of proportion to the size of the effusion should raise concern for pulmonary embolism. These effusions may be transudative, but if an associated infarct near the pleural surface occurs, an exudate may be seen. If a pulmonary embolism is suspected in a postoperative patient, most clinicians would obtain a spiral CT scan. Alternatively, duplex ultrasonography of the lower extremities may yield a diagnosis of deep vein thrombosis, thereby indicating antico-agulant therapy and


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Surgery_Schwartz. clinicians would obtain a spiral CT scan. Alternatively, duplex ultrasonography of the lower extremities may yield a diagnosis of deep vein thrombosis, thereby indicating antico-agulant therapy and precluding the need for a specific diagnosis of pulmonary embolism. In some patients, a blood test for levels of d-dimer may be helpful; if a sensitive d-dimer blood test is negative, pulmonary embolism may be ruled out.Malignant Pleural EffusionMalignant pleural effusions may occur in association with a number of different malignancies, most commonly lung can-cer, breast cancer, and lymphomas, depending on the patient’s age and gender (Tables 19-35 and 19-36).176 Cytologic testing should be done on exudative effusions to rule out an associated malignancy; accuracy is 70% when associated with adenocarci-nomas, but it is less sensitive for mesotheliomas (<10%), squa-mous cell carcinomas (20%), or lymphomas (25% to 50%). If the diagnosis remains uncertain after drainage and fluid analy-sis,


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Surgery_Schwartz. adenocarci-nomas, but it is less sensitive for mesotheliomas (<10%), squa-mous cell carcinomas (20%), or lymphomas (25% to 50%). If the diagnosis remains uncertain after drainage and fluid analy-sis, thoracoscopy and direct biopsies are indicated.177,178 Malig-nant effusions are exudative and often tinged with blood. An effusion in the setting of a malignancy means a more advanced stage; mean survival ranges from 3 to 11 months, depending on the primary tumor location.Occasionally, effusions associated with a bronchogenic NSCLC are benign, and surgical resection may still be indicated.Table 19-35Primary organ site or neoplasm type in male patients with malignant pleural effusionsPRIMARY SITE OR TUMOR TYPENO. OF MALE PATIENTSPERCENTAGE OF MALE PATIENTSLung14049.1Lymphoma/leukemia6021.1Gastrointestinal tract207.0Genitourinary tract176.0Melanoma41.4Miscellaneous less common tumors103.5Primary site unknown3110.9Total285100.0Reproduced with permission from Johnston WW. The malignant


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Surgery_Schwartz. tract207.0Genitourinary tract176.0Melanoma41.4Miscellaneous less common tumors103.5Primary site unknown3110.9Total285100.0Reproduced with permission from Johnston WW. The malignant pleural effusion: a review of cytopathologic diagnoses of 584 specimens from 472 consecutive patients, Cancer. 1985 Aug 15;56(4):905-909.Table 19-36Primary organ site or neoplasm type in female patients with malignant pleural effusionsPRIMARY SITE OR TUMOR TYPENO. OF FEMALE PATIENTSPERCENTAGE OF FEMALE PATIENTSBreast7037.4Female genital tract3820.3Lung2815.0Lymphoma148.0Gastrointestinal tract84.3Melanoma63.2Urinary tract21.1Miscellaneous less common tumors31.6Primary site unknown179.1Total187100.0Reproduced with permission from Johnston WW. The malignant pleural effusion: a review of cytopathologic diagnoses of 584 specimens from 472 consecutive patients, Cancer. 1985 Aug 15;56(4):905-909.Effusion size and degree of associated dyspnea influence management. Symptomatic, moderate to large effusions should be


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Surgery_Schwartz. 584 specimens from 472 consecutive patients, Cancer. 1985 Aug 15;56(4):905-909.Effusion size and degree of associated dyspnea influence management. Symptomatic, moderate to large effusions should be drained by tunneled indwelling pleural catheter, tube thora-costomy (chest tube or pigtail catheter) with subsequent instilla-tion of a sclerosing agent, or VATS with talc instillation. Management is based on patient preference, degree of known or anticipated lung reexpansion, and patient tolerance for operative intervention. Lung entrapment by tumor or adhesions limits reexpansion and generally predicts a poor result with pleurode-sis; it is the primary indication for placement of indwelling pleu-ral catheters. Patient preference is also considered, as is their life expectancy. Tunneled indwelling pleural catheters have dramati-cally changed the management of end-stage cancer treatment Brunicardi_Ch19_p0661-p0750.indd 73901/03/19 7:01 PM 740SPECIFIC CONSIDERATIONSPART IITable


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Surgery_Schwartz. indwelling pleural catheters have dramati-cally changed the management of end-stage cancer treatment Brunicardi_Ch19_p0661-p0750.indd 73901/03/19 7:01 PM 740SPECIFIC CONSIDERATIONSPART IITable 19-37Pathogenesis of empyemaContamination from a source contiguous to the pleural space (50%–60%) Lung Mediastinum Deep cervical area Chest wall and spine Subphrenic areaDirect inoculation of the pleural space (30%–40%) Minor thoracic interventions Postoperative infections Penetrating chest injuriesHematogenous infection of the pleural space from a distant site (<1%)Reproduced with permission from Pearson FG, Cooper JD, Deslauriers J, et al: Thoracic Surgery, 2nd ed. New York, NY: Elsevier/Churchill Livingstone; 2002.Outpatient referral for management of MPEPlacement ofindwelling pleuralcatheterLoculatedfluid/trapped lungFree-flowing with fulllung expansion Excellent performancestatus/long life expectancyVATS pleurodesisPoor performancestatus/short life expectancyPlacement of


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Surgery_Schwartz. pleuralcatheterLoculatedfluid/trapped lungFree-flowing with fulllung expansion Excellent performancestatus/long life expectancyVATS pleurodesisPoor performancestatus/short life expectancyPlacement of indwellingpleural catheterDecubitus films and/or CT scan Figure 19-51. Treatment decision algorithm for the management of malignant pleural effusion (MPE). CT = computed tomography; VATS = video-assisted tho-racic surgery.because they substantially shorten the amount of time patients spend in the hospital during their final weeks of life.179 If the lung is expected to fully expand and the patient has a longer life expectancy (e.g., malignant effusions in the setting of breast cancer), drainage with sclerosis is the preferred option. The choice of sclerosant includes mechanical pleurodesis or pleurectomy, talc, bleomycin, or doxycycline. Success rates range from 60% to 90% and are highest with talc. Typically, talc is administered as an aerosolized powder during video-assisted


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Surgery_Schwartz. or pleurectomy, talc, bleomycin, or doxycycline. Success rates range from 60% to 90% and are highest with talc. Typically, talc is administered as an aerosolized powder during video-assisted thoracoscopy, whereas doxycycline or a talc slurry is infused at the bedside through a previously placed pigtail catheter or larger bore chest tube. Figure 19-51 presents a decision algorithm for the management of malignant pleural effusion.EmpyemaThoracic empyema is defined by a purulent pleural effusion. Patients of all ages can develop empyema, but the frequency is increased in older or debilitated patients. Common associ-ated conditions include a pneumonic process in patients with pulmonary disorders and neoplasms, cardiac problems, diabe-tes mellitus, drug and alcohol abuse, neurologic impairments, postthoracotomy problems, and immunologic impairments. The mortality of empyema frequently depends on the degree of severity of the comorbidity; it may range from as low as 1% to over 40% in


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Surgery_Schwartz. postthoracotomy problems, and immunologic impairments. The mortality of empyema frequently depends on the degree of severity of the comorbidity; it may range from as low as 1% to over 40% in immunocompromised patients.Pathophysiology. The most common causes are parapneu-monic, but postsurgical, posttraumatic, and GI-associated (e.g., subphrenic or hepatic abscess, perforation of esophagus or other viscus) empyema is also common (Table 19-37). The spectrum of organisms involved in pneumonic processes that progress to empyema is changing. Pneumococci and staphylococci continue to be the most common, but gram-negative aerobic bacteria and anaerobes are becoming more prevalent. Cases involving myco-bacteria or fungi are rare. Multiple organisms may be found in up to 50% of patients. Cultures may be sterile, however, if antibiotics were initiated before the culture or if the culture pro-cess was not efficient. It is also fairly common for Pneumococ-cus to grow in blood cultures but not to


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Surgery_Schwartz. may be sterile, however, if antibiotics were initiated before the culture or if the culture pro-cess was not efficient. It is also fairly common for Pneumococ-cus to grow in blood cultures but not to grow in the pleural fluid cultures. The choice of antibiotics, therefore, is guided 11by the clinical scenario and not just the organisms found on culture. Broad-spectrum coverage may be required even when cultures do not grow out an organism or if a single organism is grown when the clinical picture is more consistent with a mul-tiorganism process. For example, a polymicrobial gram stain, particularly including yeast, is strongly suggestive of esopha-geal perforation. Common gram-negative organisms include Escherichia coli, Klebsiella, Pseudomonas, and Enterobacte-riaceae. Anaerobic organisms may be fastidious and difficult to document by culture and are associated with periodontal dis-eases (especially Streptococcus species), aspiration syndromes, alcoholism, general anesthesia, drug


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Surgery_Schwartz. may be fastidious and difficult to document by culture and are associated with periodontal dis-eases (especially Streptococcus species), aspiration syndromes, alcoholism, general anesthesia, drug abuse, or other functional associations with gastroesophageal reflux.Organisms gain entry into the pleural cavity through con-tiguous spread from pneumonia, lung abscess, liver abscess, or another, adjacent infectious processes. Organisms may also enter the pleural cavity by direct contamination from thora-centesis, thoracic surgical procedures, esophageal injuries, Brunicardi_Ch19_p0661-p0750.indd 74001/03/19 7:01 PM


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Surgery_Schwartz. CHAPTER 19741CHEST WALL, LUNG, MEDIASTINUM, AND PLEURAor trauma. As organisms enter the pleural space, an influx of polymorphonuclear cells and fluid occurs, with subsequent release of inflammatory mediators and toxic oxygen radi-cals. These mechanisms lead to variable degrees of endothe-lial injury and capillary instability. This process overwhelms the normal pleural lymphatic drainage. This early effusion is watery and free-flowing in the pleural cavity. Thoracentesis at this stage yields fluid with a pH typically above 7.3, a glucose level greater than 60 mg/dL, and a low LDH level (<500 U/L). At this stage, the decision to use antibiotics alone or perform a repeat thoracentesis, chest tube drainage, thoracoscopy, or open thoracotomy depends on the amount of pleural fluid, its consis-tency, the clinical status of the patient, the degree of expansion of the lung after drainage, and the presence of loculated fluid in the pleural space (vs. free-flowing purulent fluid). Early in the


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Surgery_Schwartz. the clinical status of the patient, the degree of expansion of the lung after drainage, and the presence of loculated fluid in the pleural space (vs. free-flowing purulent fluid). Early in the parapneumonic process, when the purulent fluid is relatively thin, complete drainage with simple large-bore thoracentesis is possible. If complete lung expansion is obtained and the pneu-monic process is responding to antibiotics, no further drainage may be necessary. Pleural fluid with a pH lower than 7.2 and with a glucose level of less than 40 mg/dL means that a more aggressive approach to drainage should be pursued.The pleural fluid may become thick and loculated over the course of hours to days and may be associated with fibrinous adhesions (the fibrinopurulent stage). At this stage, chest tube insertion with closed-system drainage or drainage with thora-coscopy may be necessary to remove the fluid and adhesions and facilitate complete lung expansion.180 Further progression of the


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Surgery_Schwartz. tube insertion with closed-system drainage or drainage with thora-coscopy may be necessary to remove the fluid and adhesions and facilitate complete lung expansion.180 Further progression of the inflammatory process leads to the formation of a pleu-ral peel, which may be flimsy and easy to remove early on. However, as the process progresses, a thick pleural rind may develop, leaving a trapped lung; complete lung decortication by either thoracoscopy or thoracotomy would then be necessary.The use of intrapleural fibrinolytic therapy for manage-ment of empyema has been investigated in several large pro-spective trials. Intrapleural infusion of tissue plasminogen activator (t-PA) alone did not improve outcomes, whereas combined intrapleural t-PA and DNase was associated with a reduction in hospital stay of nearly 7 days, 77% fewer refer-rals for surgical intervention at 3 months, and more than double the reduction in the infected pleural fluid collection by CXR imaging.181 In this trial,


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Surgery_Schwartz. stay of nearly 7 days, 77% fewer refer-rals for surgical intervention at 3 months, and more than double the reduction in the infected pleural fluid collection by CXR imaging.181 In this trial, the medications were given twice daily by intrapleural injection; the dose was 5 mg for the DNase and 10 mg for t-PA. The chest drain was clamped for 1 hour after injection and released. This study suggests that the combination of fibrinolysis (t-PA) and cleavage of uncoiled DNA by DNase reduces fluid viscosity and facilitates pleural clearance.Management. If there is a residual space, persistent pleural infection is likely to occur. A persistent pleural space may be secondary to contracted, but intact, underlying lung; or it may be secondary to surgical lung resection. If the space is small and well drained by a chest tube, a conservative approach may be possible. This requires leaving the chest tubes in place and attached to closed-system drainage until symphysis of the vis-ceral and parietal


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Surgery_Schwartz. drained by a chest tube, a conservative approach may be possible. This requires leaving the chest tubes in place and attached to closed-system drainage until symphysis of the vis-ceral and parietal surfaces takes place. At this point, the chest tubes can be removed from suction; if the residual pleural space remains stable, the tubes can be cut and advanced out of the chest over the course of several weeks. If the patient is stable, tube removal can frequently be done in the outpatient setting, guided by the degree of drainage and the size of the residual space visualized on serial CT scans. Larger spaces may require open thoracotomy and decortication in an attempt to reexpand the lung to fill this residual space. If reexpansion has failed or appears too high risk, then open drainage, rib resection, and prolonged packing may be required, with delayed closure with muscle flaps or thoracoplasty.182 Most chronic pleural space problems can be avoided by early specialized thoracic


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Surgery_Schwartz. rib resection, and prolonged packing may be required, with delayed closure with muscle flaps or thoracoplasty.182 Most chronic pleural space problems can be avoided by early specialized thoracic surgi-cal consultation and complete drainage of empyema, allowing space obliteration by the reinflated lung.ChylothoraxChylothorax develops most commonly after surgical trauma to the thoracic duct or a major branch, but may be also associ-ated with a number of other conditions (Table 19-38).183 It is generally unilateral; for example, it may occur after dissection of the distal esophagus where the duct lies in close proximity to the esophagus as it enters the right chest from its origin in the Table 19-38Etiology of chylothoraxCongenital Atresia of thoracic duct Thoracic duct-pleural space fistula Birth traumaTraumatic and/or iatrogenic Blunt injury Penetrating injury Surgery Cervical Excision of lymph nodes Radical neck dissection Thoracic Correction of patent ductus


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Surgery_Schwartz. space fistula Birth traumaTraumatic and/or iatrogenic Blunt injury Penetrating injury Surgery Cervical Excision of lymph nodes Radical neck dissection Thoracic Correction of patent ductus arteriosus Correction of coarctation of the aorta Vascular procedure involving the origin of the left subclavian artery Esophagectomy Sympathectomy Resection of thoracic aneurysm Resection of mediastinal tumors Left pneumonectomy Abdominal Sympathectomy Radical lymph node dissection Diagnostic procedures Translumbar arteriography Subclavian vein catheterization Left-sided heart catheterizationNeoplasmsInfections Tuberculous lymphadenitis Nonspecific mediastinitis Ascending lymphangitis FilariasisMiscellaneous Venous thrombosis Left subclavian-jugular vein Superior vena cava Pulmonary lymphangiomatosisReproduced with permission from Sabiston DC, Spencer FC: Surgery of the Chest, 6th ed. Philadelphia, PA: Elsevier; 1995.Brunicardi_Ch19_p0661-p0750.indd 74101/03/19


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Surgery_Schwartz. cava Pulmonary lymphangiomatosisReproduced with permission from Sabiston DC, Spencer FC: Surgery of the Chest, 6th ed. Philadelphia, PA: Elsevier; 1995.Brunicardi_Ch19_p0661-p0750.indd 74101/03/19 7:01 PM 742SPECIFIC CONSIDERATIONSPART IIabdomen at the cisterna chyli (Fig. 19-52). If the mediastinal pleura are disrupted on both sides, bilateral chylothoraces may occur. Left-sided chylothoraces may develop after a left-sided neck dissection, especially in the region of the confluence of the subclavian and internal jugular veins. Chylothorax may also follow nonsurgical trauma, including penetrating or blunt inju-ries to the chest or neck area, central line placements, and other surgical misadventures. It may be seen in association with a variety of benign and malignant diseases that generally involve the lymphatic system of the mediastinum or neck.Pathophysiology. Most commonly, the thoracic duct origi-nates in the abdomen from the cisterna chyli, which is located in the midline,


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Surgery_Schwartz. involve the lymphatic system of the mediastinum or neck.Pathophysiology. Most commonly, the thoracic duct origi-nates in the abdomen from the cisterna chyli, which is located in the midline, near the level of the second lumbar vertebra. From this origin, the thoracic duct ascends into the chest through the aortic hiatus at the level of T10 to T12, and courses just to the right of the aorta (see Fig. 19-52). As the thoracic duct courses cephalad above the diaphragm, it most commonly remains in the right chest, lying just behind the esophagus, between the aorta and azygos vein. The duct continues superiorly, lying just to the right of the vertebral column. Then, at the fourth thoracic ver-tebra, it crosses behind the aorta and the aortic arch into the left posterior mediastinum and travels superiorly, staying near the esophagus and mediastinal pleura as it exits the thoracic inlet. As it exits the thoracic inlet, it passes to the left, just behind the carotid sheath and anterior to the


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Surgery_Schwartz. superiorly, staying near the esophagus and mediastinal pleura as it exits the thoracic inlet. As it exits the thoracic inlet, it passes to the left, just behind the carotid sheath and anterior to the inferior thyroid and vertebral bodies. Just medial to the anterior scalene muscle, it courses inferiorly and drains into the union of the internal jugular and subclavian veins. Given the extreme variability in the main duct and its branches, accumulation of chyle in the chest or flow from penetrating wounds may be seen after a variety of trau-matic and medical conditions.184The main function of the duct is to transport fat absorbed from the digestive system along with variable amounts of protein and lymphatic material (Table 19-39). Given the high volume of chyle that flows through the thoracic duct, signifi-cant injuries can cause leaks in excess of 2 L per day; if left untreated, protein, lymphocyte, and volume depletion can lead to serious metabolic effects and death. Thoracentesis is


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Surgery_Schwartz. duct, signifi-cant injuries can cause leaks in excess of 2 L per day; if left untreated, protein, lymphocyte, and volume depletion can lead to serious metabolic effects and death. Thoracentesis is usually grossly suggestive, revealing milky, nonpurulent pleural fluid. However, if the patient is taking nothing by mouth, the pleural fluid may not be grossly abnormal. Laboratory analysis of the pleural fluid shows the presence of chylomicrons, a high lym-phocyte count and high triglyceride levels. If the triglyceride level is greater than 110 mg/100 mL, a chylothorax is almost certainly present (a 99% accuracy rate). If the triglyceride level is less than 50 mg/mL, there is only a 5% chance of chylothorax. In many clinical situations, the accumulation of chyle may be slow because of minimal digestive fat flowing through the gas-trointestinal tract after major trauma or surgery, so the diagnosis may be more difficult to establish.Management. The treatment plan for any chylothorax depends


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Surgery_Schwartz. digestive fat flowing through the gas-trointestinal tract after major trauma or surgery, so the diagnosis may be more difficult to establish.Management. The treatment plan for any chylothorax depends on its cause, the amount of drainage, and the patient’s clinical status (Fig. 19-53). In general, most patients are treated with a short period of chest tube drainage, nothing by mouth (NPO) orders, total parenteral nutrition (TPN), and observation. In cen-ters with interventional radiology expertise, thoracic duct embo-lization as soon as possible after diagnosis should be considered. Thoracic d.Cisterna chyliFigure 19-52. Normal thoracic duct anatomy. The esophagus comes into close proximity with the thoracic duct as it enters the chest from its origin in the abdomen at the cisterna chyli.Table 19-39Composition of chyleCOMPONENTAMOUNT (PER 100 ML)Total fat0.4–5 g Total cholesterol65–220 mgTotal protein2.21–5.9 g Albumin1.1–4.1 g Globulin1.1–3.1 g Fibrinogen16–24 gSugars48–200


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Surgery_Schwartz. chyli.Table 19-39Composition of chyleCOMPONENTAMOUNT (PER 100 ML)Total fat0.4–5 g Total cholesterol65–220 mgTotal protein2.21–5.9 g Albumin1.1–4.1 g Globulin1.1–3.1 g Fibrinogen16–24 gSugars48–200 gElectrolytesSimilar to levels in plasmaCellular elements Lymphocytes400–6800/mm3 Erythrocytes50–600/mm3Antithrombin globulin>25% of plasma concentrationProthrombin>25% of plasma concentrationFibrinogen>25% of plasma concentrationReproduced with permission from Miller JI: Diagnosis and management of chylothorax, Chest Surg Clin N Am. 1996 Feb;6(1):139-148.Brunicardi_Ch19_p0661-p0750.indd 74201/03/19 7:02 PM


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Surgery_Schwartz. CHAPTER 19743CHEST WALL, LUNG, MEDIASTINUM, AND PLEURARadiationtherapyMedicallyunstablePleuralperitonealshuntDrainagepersists(Nonmalignant)Drainage persists(>500 mL/d)MalignantchylothoraxThoracentesisConfirm diagnosisMedicallystableThoracotomyChest tubeConservative management NPOChest tube to suctionCentral hyperalimentationWait 2 weeks*Drainage decrease(<250 mL/d)Continue1 weekThoracotomyDuct ligationMass ligationDecorticationPleurectomyDrainagestopsRemovechest tube Figure 19-53. Algorithm for the management of chylothorax. *If high output persists (>50 mL/d), early surgical ligation of the thoracic duct may be considered. NPO = nothing by mouth.Chest cavity drainage must be adequate to allow complete lung reexpansion. Somatostatin has been advocated by some authors, with variable results. If significant chyle drainage (>500 mL per day in an adult, >100 mL in an infant) continues despite TPN and good lung expansion, early surgical duct ligation or embo-lization is recommended (within


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Surgery_Schwartz. If significant chyle drainage (>500 mL per day in an adult, >100 mL in an infant) continues despite TPN and good lung expansion, early surgical duct ligation or embo-lization is recommended (within 4–7 days following diagnosis). Ligation can be approached best by right thoracotomy, and in some experienced centers, by right thoracoscopy. Chylothoraces due to malignant conditions often respond to radiation and/or chemotherapy and less commonly require surgical ligation. Significant nutritional and immunologic depletion results from untreated chylothorax; associated mortality is in excess of 50%. With early recognition and aggressive medical management as well as early surgical ligation or embolization for persistent leaks, the mortality rate of chylothorax is now less than 10%.Tumors of the PleuraMalignant mesothelioma is the most common type of primary tumor of the pleura, with approximately 3000 cases per year in the United States. Other, less common tumors include benign and


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Surgery_Schwartz. of the PleuraMalignant mesothelioma is the most common type of primary tumor of the pleura, with approximately 3000 cases per year in the United States. Other, less common tumors include benign and malignant fibrous tumors of the pleura, lipomas, and cysts.Malignant Mesothelioma. The only known risk factor for mesothelioma is exposure to asbestos, identified in over 50% of cases. Exposure is typically work-related in industries using asbestos in the manufacturing process, such as shipbuilding and brake pad linings. The risk extends to family members who are Brunicardi_Ch19_p0661-p0750.indd 74301/03/19 7:02 PM 744SPECIFIC CONSIDERATIONSPART IIexposed to the dust of the clothing or to the work environment. Asbestos exposure and smoking synergistically increase the risk for lung cancer, but smoking does not increase risk for malig-nant mesotheliomas. Male predominance is 2:1, and it occurs most commonly after the age of 40.Risk of developing mesothelioma after asbestos exposure


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Surgery_Schwartz. but smoking does not increase risk for malig-nant mesotheliomas. Male predominance is 2:1, and it occurs most commonly after the age of 40.Risk of developing mesothelioma after asbestos exposure differs depending on the physical characteristics of the asbestos and similar fibers (either serpentine or amphibole). The serpen-tine fibers are large and curly and are generally not able to travel beyond larger airways. However, the narrow, straight amphibole fibers, in particular the crocidolite fibers, may navigate distally into the pulmonary parenchyma and are most clearly associated with mesotheliomas. Like many carcinogens, the latency period between asbestos exposure and the development of mesothe-lioma is at least 20 years. The tumor generally is multicentric, with multiple pleural-based nodules coalescing to form sheets of tumor. This process initially involves the parietal pleura, gener-ally with early spread to the visceral surfaces and with a variable degree of invasion of


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Surgery_Schwartz. nodules coalescing to form sheets of tumor. This process initially involves the parietal pleura, gener-ally with early spread to the visceral surfaces and with a variable degree of invasion of surrounding structures. Autopsy studies have shown that most patients have distant metastases, but the natural history of the disease in untreated patients culminates in death due to local extension and effective strangulation of the lung.Clinical Presentation Most patients present with dyspnea and chest pain. Over 90% have a pleural effusion, but thora-centesis is diagnostic in less than 10% of patients. Frequently, a thoracoscopy or open pleural biopsy with special stains is required to differentiate mesotheliomas from adenocarcinomas (Table 19-40). Epithelial subtypes are associated with a more favorable prognosis, and long-term survival may be seen in rare patients with no treatment. Sarcomatous and mixed tumors share a more aggressive course.Management The treatment of malignant


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Surgery_Schwartz. a more favorable prognosis, and long-term survival may be seen in rare patients with no treatment. Sarcomatous and mixed tumors share a more aggressive course.Management The treatment of malignant mesotheliomas remains controversial. Treatment options include supportive care only, surgical resection, and multimodality approaches (using a combination of surgery, chemotherapy, and radia-tion therapy).186 Surgical approaches range from extrapleural pneumonectomy (removal of the lung, entire parietal pleural, ipsilateral pericardium, and hemidiaphragm with patch recon-struction), pleurectomy and decortication (removal of the vis-ceral and parietal pleura only), and palliative procedures such as talc pleurodesis and insertion of long-term tunneled indwelling pleural catheters.Table 19-40Differentiation of mesothelioma from adenocarcinoma MESOTHELIOMAADENOCARCINOMAImmunohistochemical results Carcinoembryonic antigenNegativePositive VimentinPositiveNegative Low molecular weight


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Surgery_Schwartz. 19-40Differentiation of mesothelioma from adenocarcinoma MESOTHELIOMAADENOCARCINOMAImmunohistochemical results Carcinoembryonic antigenNegativePositive VimentinPositiveNegative Low molecular weight cytokeratinsPositiveNegativeElectron microscopic featuresLong, sinuous villiShort, straight villi with fuzzy glycocalyxFibrous Tumors of the Pleura. Fibrous tumors of the pleura are unrelated to asbestos exposure or malignant mesotheliomas. They generally occur as a single pedunculated mass arising from the visceral pleura but can occasionally arise from the parietal pleura. They can grow to be quite large, with most ranging from 5 to 10 cm and 100 to 400 g in size by the time they are dis-covered. Architecturally, the most common microscopic feature is the “patternless pattern.” This is characterized by randomly situated areas of hypercellularity, containing spindle cells with bland, vesicular, ovoidal nuclei and scarce cytoplasm, and hypo-cellularity, with fibrous connective tissue,


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Surgery_Schwartz. by randomly situated areas of hypercellularity, containing spindle cells with bland, vesicular, ovoidal nuclei and scarce cytoplasm, and hypo-cellularity, with fibrous connective tissue, hemorrhage, myxoid, or necrosis. They can also have an hemangiopericytoma-like appearance. The neoplastic cells are immunoreactive for CD34 and CD99 but negative for cytokeratins and desmin. Immuno-reactivity for Bcl-2 is variably positive.187They are frequently discovered incidentally on routine CXRs, without an associated pleural effusion. They occur with equal frequency in males and females and are most common in the sixth to seventh decade of life. Fibrous tumors of the pleura may be benign or malignant.188 Symptoms such as cough, chest pain, and dyspnea occur in 30% to 40% of patients but are found in 75% of patients with malignant tumors. Malignant tumors are differentiated from benign tumors based on high cellularity, more than four mitotic figures per 10 high-power fields, nuclear


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Surgery_Schwartz. are found in 75% of patients with malignant tumors. Malignant tumors are differentiated from benign tumors based on high cellularity, more than four mitotic figures per 10 high-power fields, nuclear pleomorphism, tumor necrosis, and hemorrhage. They are more likely to arise from the parietal pleura of the chest wall, dia-phragm, or mediastinum, or in the fissures or invaginating into the lung parenchyma. Hypoglycemia, associated pleural effu-sion, and hypertrophic pulmonary osteoarthropathy (clubbed digits, long bone ossifying periostitis, and arthritis) are associ-ated with these lesions in approximately 25% of patients. Less common are fever and hemoptysis.Symptoms resolve with surgical resection. Given the well-circumscribed and often pedunculated nature of fibrous tumors of the pleura, all benign lesions and approximately 50% of malignant lesions are cured by complete surgical resection.188 Incompletely resected malignant tumors may recur locally or metastasize, and more than 50%


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Surgery_Schwartz. all benign lesions and approximately 50% of malignant lesions are cured by complete surgical resection.188 Incompletely resected malignant tumors may recur locally or metastasize, and more than 50% of patients with malignant tumors will die from the disease; frequently, they are fatal within 2 to 5 years.REFERENCESEntries highlighted in bright blue are key references. 1. Cusimano RJ, Pearson FG. Anatomy, physiology, and embry-ology of the upper airway. In: Pearson FG, Cooper JD, Deslauriers J, et al, eds. Thoracic Surgery. 2nd ed. New York: Churchill Livingstone; 2002:215. 2. Grillo HC. Surgical treatment of postintubation tracheal inju-ries. J Thorac Cardiovasc Surg. 1979;78(6):860-875. 3. Nouraei SA, Ma E, Patel A, et al. Estimating the population incidence of adult post-intubation laryngotracheal stenosis. Clin Otolaryngol. 2007;32(5):411-412. 4. Couraud L, Ballester MJ, Delaisement C. Acquired tracheo-esophageal fistula and its management. Semin Thorac Cardio-vasc Surg.


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Surgery_Schwartz. laryngotracheal stenosis. Clin Otolaryngol. 2007;32(5):411-412. 4. Couraud L, Ballester MJ, Delaisement C. Acquired tracheo-esophageal fistula and its management. Semin Thorac Cardio-vasc Surg. 1996;8(4):392-399. 5. Mathisen DJ, Grillo HC, Wain JC, Hilgenberg AD. Manage-ment of acquired nonmalignant tracheoesophageal fistula. Ann Thorac Surg. 1991;52(4):759-765. 6. Bhattacharyya N. Contemporary staging and prognosis for primary tracheal malignancies: a population-based analysis. Otolaryngol Head Neck Surg. 2004;131:639-642.Brunicardi_Ch19_p0661-p0750.indd 74401/03/19 7:02 PM


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Surgery_Schwartz. CHAPTER 19745CHEST WALL, LUNG, MEDIASTINUM, AND PLEURA 7. Gaissert HA, Grillo HC, Shadmehr MB, et al. Uncommon primary tracheal tumors. Ann Thorac Surg. 2006;82(1): 268-272. 8. Regnard JF, Fourquier P, Levasseur P. Results and prognostic factors in resections of primary tracheal tumors: a multicenter retrospective study. The French Society of Cardiovascular Surgery. J Thorac Cardiovasc Surg. 1996;111:808-813; discussion 813. 9. Chow DC, Komaki R, Libshitz HI, Mountain CF, Ellerbroek N. Treatment of primary neoplasms of the trachea. The role of radiation therapy. Cancer. 1993;71(10):2946-2952. 10. Rice TW. Anatomy of the lung. In: Pearson FG, Cooper JD, Deslauriers J, et al, eds. Thoracic Surgery. 2nd ed. New York: Churchill Livingstone; 2002:427. 11. Jeremy George P, Banerjee AK, Rea CA, et al. Surveillance for the detection of early lung cancer in patients with bronchial dysplasia. Thorax. 2007;62(1):43-50. 12. Wang GF, Lai MD, Yang RR, et al. Histological types and significance


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Surgery_Schwartz. CA, et al. Surveillance for the detection of early lung cancer in patients with bronchial dysplasia. Thorax. 2007;62(1):43-50. 12. Wang GF, Lai MD, Yang RR, et al. Histological types and significance of bronchial epithelial dysplasia. Mod Pathol. 2006;19:429-437. 13. Gould VE, Warren WH. Epithelial tumors of the lung. Chest Surg Clin N Am. 2000;10(4):709-728. 14. Fu JB, Kau TY, Severson RK, Kalemkerian GP. Lung cancer in women: analysis of the national Surveillance, Epidemiology, and End Results database. Chest. 2005;127(3):768-777. 15. Travis WD, Brambilla E, Noguchi M, et al. International Association for the Study of Lung Cancer/American Tho-racic Society/European Respiratory Society international multidisciplinary classification of lung adenocarcinoma. J Thorac Oncol. 2011;6(2):244-285. 16. Schmidt L, Myers J. Bronchioloalveolar carcinoma and the significance of invasion: predicting biologic behavior. Arch Pathol Lab Med. 2010;134:1450-1454. 17. Cerilli LA, Ritter JH, Mills SE,


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Surgery_Schwartz. AK, Law MR, Wald NJ. The accumulated evidence on lung cancer and environmental tobacco smoke. BMJ. 1997;315(7114):980-988. 23. Aberle DR, Adams AM, Berg CD, et al. Reduced lung-cancer mortality with low-dose computed tomographic screening. N Engl J Med. 2011;365(5):395-409. 24. Gould MK, Fletcher J, Iannettoni MD, et al. Evaluation of patients with pulmonary nodules: when is it lung cancer? ACCP evidence-based clinical practice guidelines (2nd edition). Chest. 2007;132(3 suppl):108S-130S. 25. Marten K, Grabbe E. The challenge of the solitary pulmonary nodule: diagnostic assessment with multislice spiral CT. Clin Imaging. 2003;27(3):156-161. 26. Remy-Jardin M, Remy J, Giraud F, Marquette CH. Pulmonary nodules: detection with thick-section spiral CT versus conven-tional CT. Radiology. 1993;187(2):513-520. 27. Naidich DP. Helical computed tomography of the thorax: clinical applications. Radiol Clin North Am. 1994;32(4): 759-774. 28. Stroobants S, Verschakelen J, Vansteenkiste J. Value


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Surgery_Schwartz. DP. Helical computed tomography of the thorax: clinical applications. Radiol Clin North Am. 1994;32(4): 759-774. 28. Stroobants S, Verschakelen J, Vansteenkiste J. Value of FDG-PET in the management of non-small cell lung cancer. Eur J Radiol. 2003;45(1):49-59. 29. Cahan WG, Shah JP, Castro EB. Benign solitary lung lesions in patients with cancer. Ann Surg. 1978;187(3):241-244. 30. Davidson RS, Nwogu CE, Brentjens MJ, Anderson TM. The surgical management of pulmonary metastasis: current con-cepts. Surg Oncol. 2001;10(1-2):35-42. 31. Pastorino U, Buyse M, Friedel G, et al. Long-term results of lung metastasectomy: prognostic analyses based on 5206 cases. J Thorac Cardiovasc Surg. 1997;113(1):37-49. 32. McCormack PM, Bains MS, Begg CB, et al. Role of vid-eoassisted thoracic surgery in the treatment of pulmonary metastases: results of a prospective trial. Ann Thorac Surg. 1996;62(1):213-216; discussion 216-217. 33. Rivera MP, Mehta AC; American College of Chest Physi-cians. Initial


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Surgery_Schwartz. the treatment of pulmonary metastases: results of a prospective trial. Ann Thorac Surg. 1996;62(1):213-216; discussion 216-217. 33. Rivera MP, Mehta AC; American College of Chest Physi-cians. Initial diagnosis of lung cancer: ACCP evidence-based clinical practice guidelines (2nd edition). Chest. 2007;132 (3 suppl):131S-148S. 34. Ost D, Fein AM, Feinsilver SH. Clinical practice. The solitary pulmonary nodule. N Engl J Med. 2003;348(25): 2535-2542. 35. Toloza EM, Harpole L, McCrory DC. Noninvasive staging of non-small cell lung cancer: a review of the current evidence. Chest. 2003;123(1 suppl):137S-146S. 36. Goldberg M, Unger M. Lung cancer. Diagnostic tools. Chest Surg Clin N Am. 2000;10(4):763-779. 37. Vaz AP, Fernandes G, Souto Moura C, Bastos P, Queiroga H, Hespanhol V. Integrated PET/CT in non small cell lung cancer staging: clinical and pathological agreement. Rev Port Pneu-mol. 2012;18(3):109-114. 38. Iskender I, Kapicibasi HO. Comparison of integrated positron emission


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Surgery_Schwartz. PET/CT in non small cell lung cancer staging: clinical and pathological agreement. Rev Port Pneu-mol. 2012;18(3):109-114. 38. Iskender I, Kapicibasi HO. Comparison of integrated positron emission tomography/computed tomography and mediastinos-copy in mediastinal staging of non-small cell lung cancer:analysis of 212 patients. Acta Chir Belg. 2012;112:219-225. 39. Li X, Zhang H, Xing L, et al. Mediastinal lymph nodes staging by 18F-FDG PET/CT for early stage non-small cell lung cancer: a multicenter study. Radiother Oncol. 2012;102:246-250. 40. Lv YL, Yuan DM. Diagnostic performance of integrated posi-tron emission tomography/computed tomography for medi-astinal lymph node staging in non-small cell lung cancer: a bivariate systematic review and meta-analysis. J Thorac Oncol. 2011;6(8):1350-1358. 41. Mountain CF, Dresler CM. Regional lymph node classification for lung cancer staging. Chest. 1997;111:1718-1723. 42. Barrera R, Shi W, Amar D, et al. Smoking and timing of ces-sation: impact


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Surgery_Schwartz. CF, Dresler CM. Regional lymph node classification for lung cancer staging. Chest. 1997;111:1718-1723. 42. Barrera R, Shi W, Amar D, et al. Smoking and timing of ces-sation: impact on pulmonary complications after thoracotomy. Chest. 2005;127:1977-1983. 43. Nakagawa M, Tanaka H, Tsukuma H, Kishi Y. Relationship between the duration of the preoperative smoke-free period and the incidence of postoperative pulmonary complications after pulmonary surgery. Chest. 2001;120:705-710. 44. Colice GL, Shafazand S, Griffin JP, Keenan R, Bolliger CT; American College of Chest Physicians. Physiologic evaluation of the patient with lung cancer being con-sidered for resectional surgery: ACCP evidenced-based clinical practice guidelines (2nd ed). Chest. 2007;132(3 suppl):161S-177S. 45. Richards TB, Henley SJ, Puckett MC, et al. Lung cancer sur-vival in the United States by race and stage (2001-2009): Find-ings from the CONCORD-2 study. Cancer. 2017;123(suppl 24): 5079-5099. 46. Raz DJ, Zell JA, Ou


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Surgery_Schwartz. SJ, Puckett MC, et al. Lung cancer sur-vival in the United States by race and stage (2001-2009): Find-ings from the CONCORD-2 study. Cancer. 2017;123(suppl 24): 5079-5099. 46. Raz DJ, Zell JA, Ou SH, Gandara DR, Anton-Culver H, Jablons DM. Natural history of stage I non–small cell lung cancer: implica-tions for early detection. Chest. 2007;132(1):193-199. 47. Ginsberg RJ, Rubinstein LV. Randomized trial of lobec-tomy versus limited resection for T1 N0 non–small cell lung cancer. Lung Cancer Study Group. Ann Thorac Surg. 1995;60(3):615-622. 48. Warren WH, Faber LP. Segmentectomy versus lobectomy in patients with stage I pulmonary carcinoma. Five-year survival Brunicardi_Ch19_p0661-p0750.indd 74501/03/19 7:02 PM 746SPECIFIC CONSIDERATIONSPART IIand patterns of intrathoracic recurrence. J Thorac Cardiovasc Surg. 1994;107(4):1087-1093; discussion 1093-1094. 49. Bedetti B, Bertolaccini L, Rocco R, Schmidt J, Solli P, Scarci M. Segmentectomy versus lobectomy for stage I non-small cell


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Surgery_Schwartz. J Thorac Cardiovasc Surg. 1994;107(4):1087-1093; discussion 1093-1094. 49. Bedetti B, Bertolaccini L, Rocco R, Schmidt J, Solli P, Scarci M. Segmentectomy versus lobectomy for stage I non-small cell lung cancer: a systematic review and meta-analysis. J Thorac Dis. 2017;9(6):1615-1623. 50. Schuchert MJ, Pettiford BL, Keeley S, et al. Anatomic seg-mentectomy in the treatment of stage I non-small cell lung cancer. Ann Thorac Surg. 2007;84(3):926-932; discussion 932-923. 51. Sienel W, Stremmel C, Kirschbaum A, et al. Frequency of local recurrence following segmentectomy of stage IA non-small cell lung cancer is influenced by segment localisation and width of resection margins–implications for patient selec-tion for segmentectomy. Eur J Cardiothorac Surg. 2007;31(3): 522-527; discussion 527-528. 52. Shapiro M, Weiser TS, Wisnivesky JP, Chin C, Arustamyan M, Swanson SJ. Thoracoscopic segmentectomy compares favorably with thoracoscopic lobectomy for patients with small stage I lung cancer.


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Surgery_Schwartz. cysts of the mediastinum. J Thorac Cardiovasc Surg. 1995;109(5):1003-1010. 170. St-Georges R, Deslauriers J, Duranceau A, et al. Clinical spec-trum of bronchogenic cysts of the mediastinum and lung in the adult. Ann Thorac Surg. 1991;52(1):6-13. 171. Agostoni E. Mechanics of the pleural space. In: Fisherman AP, Macklem PT, Mead J, et al, eds. Mechanics of Breathing: Handbook of Physiology. Vol 3. Bethesda, MD: American Physiological Society; 1986. 172. Lawrence GH. Considerations of the anatomy and physiology of the pleural space. In: Lawrence GH, ed. Problems of the Pleural Space. Philadelphia: WB Saunders; 1983. 173. Rusch VW. Pleural effusion: benign and malignant. In: Pear-son FG, ed. Thoracic Surgery. 2nd ed. New York: Churchill Livingstone; 2002:1157. 174. Gammie JS, Banks MC, Fuhrman CR, et al. The pigtail cath-eter for pleural drainage: a less invasive alternative to tube thoracostomy. JSLS. 1999;3(1):57-61. 175. Luketich JD, Kiss M, Hershey J, et al. Chest tube insertion: a


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Surgery_Schwartz. CR, et al. The pigtail cath-eter for pleural drainage: a less invasive alternative to tube thoracostomy. JSLS. 1999;3(1):57-61. 175. Luketich JD, Kiss M, Hershey J, et al. Chest tube insertion: a prospective evaluation of pain management. Clin J Pain. 1998;14(2):152-154. 176. Johnston WW. The malignant pleural effusion. A review of cytopathologic diagnoses of 584 specimens from 472 consecu-tive patients. Cancer. 1985;56(4):905-909.Brunicardi_Ch19_p0661-p0750.indd 74801/03/19 7:02 PM


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Surgery_Schwartz. CHAPTER 19749CHEST WALL, LUNG, MEDIASTINUM, AND PLEURA 177. Ocaña I, Martinez-Vazquez JM, Segura RM, et al. Adenosine deaminase in pleural fluids. Test for diagnosis of tuberculous pleural effusion. Chest. 1983;84(1):51-53. 178. Lee YC, Rogers JT, Rodriguez RM, Miller KD, Light RW. Adenosine deaminase levels in nontuberculous lymphocytic pleural effusions. Chest. 2001;120(2):356-361. 179. Tremblay A, Michaud G. Single-center experience with 250 tunneled pleural catheter insertions for malignant pleural effu-sion. Chest. 2006;129(2):362-368. 180. Light RW. Parapneumonic effusions and empyema. Clin Chest Med. 1985;6(1):55-62. 181. Rahman NM, Maskell NA, West A, et al. Intrapleural use of tissue plasminogen activator and DNase in pleural infection. N Engl J Med. 2011;365:518-526. 182. Miller JI Jr. The history of surgery of empyema, thoracoplasty, Eloesser flap, and muscle flap transposition. Chest Surg Clin N Am. 2000;10(1):45-53. 183. Miller JI Jr. Diagnosis and management of


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Surgery_Schwartz. JI Jr. The history of surgery of empyema, thoracoplasty, Eloesser flap, and muscle flap transposition. Chest Surg Clin N Am. 2000;10(1):45-53. 183. Miller JI Jr. Diagnosis and management of chylothorax. Chest Surg Clin N Am. 1996;6(1):139-148. 184. Malthaner RA, Inculet RI. The thoracic duct and chylotho-rax. In: Pearson FG, ed. Thoracic Surgery. 2nd ed. New York: Churchill Livingstone; 2002:1228. 185. Rusch VW. A proposed new international TNM staging system for malignant pleural mesothelioma. From the International Mesothelioma Interest Group. Chest. 1995;108(4):1122-1128. 186. Khalil MY, Mapa M, Shin HJ, Shin DM. Advances in the management of malignant mesothelioma. Curr Oncol Rep. 2003;5(4):334-341. 187. Fletcher CDM, Unni KK, Mertens F. World Health Organization Classification of Tumours. Pathology and Genetics of Tumours of Soft Tissue and Bone. Lyon, France: IARC Press; 2002. 188. England DM, Hochholzer L, McCarthy MJ. Localized benign and malignant fibrous tumors of the


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Surgery_Schwartz. of Tumours. Pathology and Genetics of Tumours of Soft Tissue and Bone. Lyon, France: IARC Press; 2002. 188. England DM, Hochholzer L, McCarthy MJ. Localized benign and malignant fibrous tumors of the pleura. A clinicopathologic review of 223 cases. Am J Surg Pathol. 1989;13(8):640-658.Brunicardi_Ch19_p0661-p0750.indd 74901/03/19 7:02 PM


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Surgery_Schwartz. Congenital Heart DiseaseRaghav Murthy, Tabitha G. Moe, Glen S. Van Arsdell, John J. Nigro, and Tara Karamlou20chapterINTRODUCTIONCongenital heart surgery is a dynamic and evolving field. The last 20 years have brought about rapid developments in technol-ogy, emphasis on a multidisciplinary approach to treatment, and a more thorough understanding of both the anatomy and patho-physiology of congenital heart disease, leading to the improved care of these challenging patients.These advancements have created a sustained paradigm shift in the field of congenital heart surgery. The traditional strategy of initial palliation followed by definitive correction at a later age, which had pervaded the thinking of most surgeons, began to evolve into emphasizing early repair. Defects such as hypoplastic left heart syndrome (HLHS) are now successfully managed with staged palliation, resulting in excellent survival outcomes for these children.The goal in most cases of congenital heart disease (CHD) is


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Surgery_Schwartz. left heart syndrome (HLHS) are now successfully managed with staged palliation, resulting in excellent survival outcomes for these children.The goal in most cases of congenital heart disease (CHD) is appropriate timing of complete repair. Rather than subdivid-ing lesions into cyanotic or noncyanotic lesions, a more appro-priate classification divides defects into three categories based on the feasibility of achieving complete repair: (a) defects that have no reasonable palliation and for which repair is the only option; (b) defects for which repair is not possible and for which palliation is the only option; and (c) defects that can either be repaired or palliated in infancy. It bears mentioning that all defects in the second category are those in which the appropriate anatomic components either are not present, as in hypoplastic left heart syndrome, or cannot be created from existing structures, i.e., unguarded tricuspid orifice.1Eight out of every 1000 live births will have some


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Surgery_Schwartz. either are not present, as in hypoplastic left heart syndrome, or cannot be created from existing structures, i.e., unguarded tricuspid orifice.1Eight out of every 1000 live births will have some form of CHD, most of which, however, are mild.1 In the United States nearly 40,000 infants are affected each year.2 As of 2010, it is estimated that there are about 2 million people living with CHD in the United States, and as of 2011 there are more adults (>18) than children.2 CHD is the most common birth defect and the most common cause of infant death related to birth defects, accounting for 28% of deaths due to birth defects in the first month of life. There are currently 127 centers in North America that perform congenital heart surgery. The Society for Thoracic Surgeons (STS) reports an overall national mortality of 3.1%.3DEFECTS AMENABLE TO COMPLETE REPAIRAtrial Septal DefectAn atrial septal defect (ASD) is defined as discontinuity of the interatrial septum that permits direct mixing


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Surgery_Schwartz. national mortality of 3.1%.3DEFECTS AMENABLE TO COMPLETE REPAIRAtrial Septal DefectAn atrial septal defect (ASD) is defined as discontinuity of the interatrial septum that permits direct mixing of blood between the systemic venous and pulmonary venous circulations.Embryology. The atrial and ventricular septa form between the third and sixth weeks of fetal development. After the paired heart tubes fuse into a single tube folded onto itself, the distal por-tion of the tube indents to form the roof of the common atrium. Near this portion of the roof, the septum primum originates and descends in a crescentic formation toward the atrioventricular (AV) junction. The ostium primum is situated superiorly to the crux of the heart at the atrioventricular junction. Prior to completion of endocardial cushion fusion with the septum pri-mum, a sequence of fenestrations appear that coalesce into the Introduction 751Defects Amenable to Complete Repair 751Atrial Septal Defect / 751Aortic Stenosis /


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Surgery_Schwartz. cushion fusion with the septum pri-mum, a sequence of fenestrations appear that coalesce into the Introduction 751Defects Amenable to Complete Repair 751Atrial Septal Defect / 751Aortic Stenosis / 755Patent Ductus Arteriosus / 759Aortic Coarctation / 761Truncus Arteriosus / 764Total Anomalous Pulmonary Venous Connection / 765Cor Triatriatum / 768Aortopulmonary Window / 769Vascular Rings and Pulmonary Artery Slings / 769Defects Requiring Palliation 770Tricuspid Atresia / 770Hypoplastic Left Heart Syndrome / 773Defects That May be Palliated or Repaired 777Ebstein’s Anomaly / 777Transposition of the Great Arteries / 780Double-Outlet Right Ventricle / 783Double-Outlet Right Ventricle With Noncommitted Ventricular Septal Defect / 783Double-Outlet Right Ventricle With Subaortic or Doubly Committed Ventricular Septal Defect Without Pulmonary Stenosis / 784Double-Outlet Right Ventricle With Subaortic or Doubly Committed Ventricular Septal Defect With Pulmonary Stenosis /


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Surgery_Schwartz. or Doubly Committed Ventricular Septal Defect Without Pulmonary Stenosis / 784Double-Outlet Right Ventricle With Subaortic or Doubly Committed Ventricular Septal Defect With Pulmonary Stenosis / 784Taussig–Bing Syndrome Without Pulmonary Stenosis / 784Taussig–Bing Syndrome With Pulmonary Stenosis / 784Tetralogy of Fallot / 784Ventricular Septal Defect / 786Atrioventricular Canal Defects / 789Interrupted Aortic Arch / 790Pediatric Mechanical Circulatory Support / 790Pediatric Heart Transplantation / 791Public Reporting and the STS Database in Congenital Heart Surgery / 792Future Directions / 793Brunicardi_Ch20_p0751-p0800.indd 75122/02/19 2:54 PM 752ostium secundum. During this coalescence, the septum secun-dum grows downward from the roof of the atrium, parallel to and to the right of the septum primum. The septum primum does not fuse, but creates an oblique pathway, called the foramen ovale, within the interatrial septum. After birth, the increase in left atrial pressure


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Surgery_Schwartz. right of the septum primum. The septum primum does not fuse, but creates an oblique pathway, called the foramen ovale, within the interatrial septum. After birth, the increase in left atrial pressure associated with an increase in SVR relative to PVR typically closes this pathway in approximately 80% of the population, obliterating the interatrial communication.Anatomy. ASDs can be classified into three different types (Fig. 20-1): (a) ostium secundum type defect (Fig. 20-1B,C) (deficiency of septum primum), which are the most prevalent subtype, comprising 80% of all ASDs; (b) ostium primum defects (Fig. 20-1A), which may also be described as partial or transitional AV canal defect; and (c) sinus venosus type defects, comprising approximately 5% to 10% of all ASDs.4Pathophysiology. ASDs result in an increase in pulmonary blood flow secondary to primarily left-to-right shunting through the defect. The direction of the intracardiac shunt is predomi-nantly determined by the compliance of