obstruction.28 A chest CT scan is the optimal test to diagnose bronchiectasis (Fig. 80-25), and once the
diagnosis is made, the search for an etiology should begin, including obtaining sputum cultures and
blood tests for autoimmune markers such as rheumatoid factor.29
The treatment of the disease includes antibiotic therapy to control infection, the treatment of
underlying diseases if they exist, reducing inflammation, improving secretion clearance, and surgery to
remove focally damaged areas or transplantation if needed for more diffuse, severe disease. Antibiotic
therapy includes inhaled tobramycin and gentamicin.29 Macrolide antibiotics have been increasingly
studied for their nonantibiotic effects. Erythromycin and clarithromycin have anti-inflammatory
benefits. They disrupt the biofilm produced in Pseudomonas infections resulting in decreased sputum
volume and improved symptoms.30 Secretion removal is also essential to improving symptoms. Besides
the standard treatments of percussive therapy and postural drainage, the use of nebulized
acetylcysteine29 or hypertonic saline30 has been shown to improve mucus clearance.
Figure 80-24. Division of the scalene muscles and the first rib. A: Mobilization of the scalene muscles off of the first rib. B:
Exposure of the subclavian vessels. C: Mobilization of the first rib, protecting the vessels. (Reproduced with permission from ScottConner CE, Dawson DL, Shirazi MK, et al. Operative Anatomy. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2008.)
Surgical intervention may occur at many stages of the disease process. Bronchoscopy can be useful to
clear secretions or to manage hemoptysis. If the bronchiectasis is localized to a single lobe, resection
can eliminate the disease and the source of chronic infection. If a patient has a genetic disease such as
cystic fibrosis, a double lung transplant may be the best treatment if the patient’s symptoms are severe
enough.29 Pulmonary tuberculosis can have similar indications for surgical intervention when it results
in bronchiectasis or hemoptysis.31 The rise of more multidrug-resistant tuberculosis strains has led to the
increasing need for surgical intervention.32
Hemoptysis
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4 Hemoptysis is often used to describe any blood streaking associated with cough. True hemoptysis may
only be a few drops of blood, and it requires investigation. Massive hemoptysis is acutely life
threatening, not from blood or volume loss, but rather from suffocation secondary to blood in the
airway. The immediate goals when this is encountered are airway control, improved oxygenation, and
resuscitation if needed. Intubation may or may not be necessary, depending on the volume of blood in
the airway and the patient’s ability to cough.33 If the bleeding is able to be lateralized, the patient
should be placed in a lateral decubitus position with the bleeding site in the dependent position. The
causes of hemoptysis include cancer, infections/bronchiectasis, vascular injuries, vasculitides, and
coagulopathies.34
In patients with hemoptysis, any coagulopathy should be corrected. Early bronchoscopy is essential
and the goals are to lateralize the site of bleeding and identify the site and cause of the bleeding.
Flexible bronchoscopy may be done, but rigid bronchoscopy is the best approach to maintain airway
control, in particular in the setting of large volume hemoptysis. Initial treatment may include topical
therapy such as cold saline lavage, bronchial tamponade, and intubation of the contralateral good lung.
Double-lumen endotracheal tubes may also be useful to isolate and protect the uninvolved lung from
blood from the contralateral side obstructing its lumen.33 If a patient is stable, a chest CT scan is useful
to identify tumors or other potential sources of bleeding.34
Algorithm 80-1. Algorithm for management of lung abscess. (Adapted from Shields TW, ed. General Thoracic Surgery, 6th ed.
2005.)
Once a patient is stabilized and appropriate diagnostic tests performed, the treatment of continued
bleeding includes the use of interventional radiology and bronchial artery embolization (BAE).35 First
introduced in 1973, BAE is the best nonsurgical treatment of massive hemoptysis, with a success rate of
upto 98% within 24 hours.34 Surgery is reserved to treat the underlying condition once the patient has
been stabilized and bleeding controlled by other methods. Emergent surgery to treat bleeding may have
a mortality rate as high as 38%,35 and increase to 59% in the setting of malignancy.34 Depending on the
patient’s baseline lung function, a lobectomy, let alone a pneumonectomy, may not be tolerated. A risk
assessment of the benefits of surgery must be performed. In the setting of a vascular etiology of the
hemoptysis such as a ruptured aortic aneurysm, surgical repair is essential and should not be delayed
once the patient is hemodynamically stable and the airway is controlled.34 A detailed algorithm in the
assessment and treatment of hemoptysis is shown in Algorithm 80-2.
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Figure 80-25. CT scan of bronchiectatic lungs. (Reproduced with permission from Shields TW, ed. General Thoracic Surgery, 6th
ed.)
COPD and Lung Volume Reduction
COPD includes a broad group of diseases that result in airflow obstruction and hyperinflation. Medical
therapy involves smoking cessation, bronchodilator treatment, steroids, home oxygen, and antibiotics as
needed. Despite improvements in the medical management of this condition, patients continue to suffer
severe limitations due to their breathing and exercise capacity. As a result, surgical interventions have
continued to play a role in trying to ameliorate symptoms and improving survival in these patients.36,37
There is a more than 50-year history in the literature recording a variety of surgical approaches to
help treat COPD. Interest was diminished, however, because of the high mortality associated with
surgical intervention in this patient population. In the 1990s, a renewed interest in lung volume
reduction surgery (LVRS) was observed following reports that this procedure was associated with a low
published mortality rate and a significant improvement in FEV1 seen on pulmonary function testing.
There was a national increase in interest in the procedure, as many centers began offering it. Despite
continued publication of low mortality rates, evaluation of Medicare data in 1996 showed a mortality of
23% in surgically treated patients at 12 months, and Medicare reimbursement for the procedure
stopped. This led to the development of the National Emphysema Treatment Trial (NETT), a prospective
randomized trial to evaluate the outcomes of LVRS compared to optimal medical treatment.36
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Algorithm 80-2. Hemoptysis management. (Adapted from Jean-Baptiste E. Crit Care Med 2000;28(5):1642–1647.)
The goal of the NETT study was to evaluate short- and long-term survival, lung function, exercise
capacity, and quality of life. Centers used both median sternotomy and bilateral video-assisted
thoracoscopic surgery (VATS) approaches to perform the operative procedure. Interim analysis
identified a high-risk subgroup with a higher mortality. These patients had low FEV1
(less than 20%
predicted) and either a homogenous pattern of emphysema in both upper and lower lungs or a low
carbon monoxide diffusing capacity (DLCO) (less than 20% predicted). The mortality at 30 days was
16% and the risk was felt to be prohibitive. As the study continued, two preoperative factors appeared
to be associated with decreased mortality; dominant upper-lobe emphysema and having a higher
preoperative exercise capacity. Using these factors, patients were divided into four subgroups. Patients
with upper-lobe disease and a low exercise capacity, defined as achieving less than the 40th percentile
on exercise testing, 25 watts for women and 40 watts for men, showed a survival advantage and
improved exercise capacity after surgery. Patients with upper-lobe disease and high exercise capacity,
achieving more than the 40th percentile cutoff, showed no survival advantage, but did have improved
long-term exercise capacity. Patients with nonupper-lobe disease and low exercise capacity had no
survival or exercise improvements, but did note an improved quality of life at 24 months. The
remaining patients with nonupper-lobe disease and high exercise capacity had a higher risk of death and
no significant improvement in exercise capacity or quality of life. The 30-day mortality in the nonhighrisk subgroup was 5.5%. Long-term follow-up showed the same results in all subgroups except in the
nonupper-lobe disease and low exercise capacity group. The quality of life improvement had
disappeared by 3 years (Algorithm 80-3).36 This subgroup analysis has allowed surgeons to better
counsel patients as to the benefits of LVRS, based upon which group they fall in.
When the different surgical approaches where evaluated, there was no difference in mortality or
benefit from sternotomy versus VATS approaches. Sternotomy patients had a longer hospital stay and
higher costs noted at 6 months. The cost effectiveness of LVRS was also evaluated. The mean cost for
LVRS was much higher at 1 year than for the medical therapy group, $71,515 versus $23,371,
respectively.38 In the subgroup with upper-lobe disease and low exercise capacity, at 2 years of followup, there was a cost of $98,000 per quality-adjusted life-year (QALY). This was predicted to fall to
$21,000 at 10 years. In comparison, coronary artery bypass graft surgery has a cost of $64,000 per
QALY.38,39
A new technique aimed to provide the same benefit of LVRS but without the surgical risk is the
placement of one-way endobronchial valves. These are designed to allow air to escape the hyperinflated
apical regions and not allow air to reenter. Endobronchial stents have been designed to cross
bronchioles into hyperinflated regions of the lung and allow decompression. Other approaches being
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tested include the bronchoscopic introduction of biologic substances such as trypsin or thrombin into
hyperinflated regions of the lung with the goal of causing local scarring and reduce the hyperinflation.38
Other surgical procedures in the treatment of COPD include bullectomy in selected patients and lung
transplants in patients with end-stage disease.37
Algorithm 80-3. LVRS candidate workup. (Adapted from Martinez FJ, Chang A. Semin Respir Crit Care Med 2005;26(2):167–191.)
Tracheobronchial Foreign Body Aspiration
Tracheobronchial foreign body (TFB) aspiration occurs most often in children, but upto 20% of cases
have been reported in adults. Risk factors in adults include older age, as elderly patients have a higher
incidence of neurologic disease and an impaired cough reflex. Symptoms usually involve an episode of
choking, followed by a protracted cough. Fever, dyspnea, and wheezing can also be present.40 Chest xray may aid in the diagnosis if the aspirated TFB is radio-opaque or if there is associated air trapping,
atelectasis, or pneumonia, however, the TFB is visible less than a quarter of the time as most foods are
not radio-opaque.41 Chest CT scans are a more sensitive imaging modality, but not necessarily more
specific. Bronchoscopy should be performed if TFB aspiration is suspected. Removal of the TFB can
usually be accomplished by flexible bronchoscopy but may require rigid bronchoscopy in difficult
cases.40,41
Pneumothorax
Pneumothoraces are classified as spontaneous, primary or secondary, traumatic, or iatrogenic. Primary
spontaneous pneumothoraces occur in patients with no known lung disease, whereas secondary
spontaneous ones occur in patients with underlying lung pathology thought to predispose those patients
to a pneumothorax. Iatrogenic pneumothoraces may occur in either the postsurgical or postprocedural
setting, typically following central line placement or thoracentesis.42 Traumatic pneumothoraces are
covered elsewhere in this text.
Primary spontaneous pneumothoraces occur more frequently in men than women, with an incidence
of 7 to 18 cases per 100,000 people for men, compared to an incidence rate of 1 to 6 cases per 100,000
people in women. Most cases occur in males younger than 30 years of age, and they rarely occur in
people over the age of 40. Even though many patients with primary pneumothoraces do not have
apparent lung disease, almost all are found to have subpleural bullae, the pathophysiology of which is
unknown.42 Most bullae are apical in location.43 Patient symptoms can range from minimal to severe,
and usually include pleuritic pain, dyspnea, or both. Tachycardia may also be present, and if a person is
tachycardic and hypotensive, a tension pneumothorax must be high on the differential and appropriate
needle decompression considered. A tension pneumothorax occurs when air entering the pleural cavity
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cannot escape and the air compresses the vena cava and even the heart, resulting in hemodynamic
instability (Fig. 80-26). Urgent needle decompression followed by chest tube placement is the preferred
treatment. Most spontaneous pneumothoraces occur while patients are at rest.42,44
5 Observation is often the treatment of a stable, small pneumothorax, defined as being less than 3 cm
from the apex. For a larger pneumothorax, chest tube placement is the standard treatment, though some
advocate a trial of aspiration. Most patients will have a complete resolution of their pneumothorax and
not need further treatment. In the group of patients who have a persistent air leak from the initial
pneumothorax, or the 30% who have a recurrent pneumothorax, usually within 2 years, further
treatment is warranted. This involves some form of pleurodesis, chemical or mechanical, either via a
chest tube (talc infusion), or during a thoracoscopic evaluation where apparent blebs can also be
resected (Algorithm 80-4).43,44
Secondary spontaneous pneumothoraces can occur due to a variety of lung diseases, but COPD is the
most common.45 While primary pneumothoraces can be mild clinical events, secondary ones are much
more concerning because of the baseline lung disease and poor pulmonary reserve. Observation has no
role in this patient population who should undergo definitive treatment to prevent a recurrence during
the first event. Here a thoracoscopic approach may be more effective in establishing an adequate
pleurodesis and allow the evaluation for sources of air leaks.44 Iatrogenic pneumothoraces can result
from transthoracic needle lung biopsies, central line placement, thoracentesis, transbronchial lung
biopsies, pleural biopsies, and positive pressure ventilation. Patients with underlying lung disease are at
a higher risk of developing a pneumothorax after these procedures. Treatment should follow the same
paradigm as for spontaneous pneumothoraces. Patients with a small, asymptomatic, stable
pneumothorax and no underlying lung disease may be safely observed, while all others should undergo
placement of a chest tube.44 Some studies have suggested immediate aspiration of air after a CT-guided
lung biopsy resulting in a pneumothorax, with an 85% success rate in avoiding the need for chest tube
placement.43
Figure 80-26. A: A 40% left-sided spontaneous pneumothorax (arrow). B: Progression of simple pneumothorax to a tension
pneumothorax, showing the characteristic radiographic findings – virtual collapse of the entire involved lung, shift of the
mediastinum to the contralateral side, and compression of the contralateral lung. Subcutaneous air dissecting along the left chest
wall is also evident.
Congenital Lung Disease
Congenital malformations of the lung develop during fetal lung growth. They may be identified during
an in-utero evaluation, present as respiratory distress in the newborn, or be completely asymptomatic
and found in patients as adults. They can frequently occur with other congenital malformations and may
be life-threatening. Lung development begins during week 3 from the foregut. It progresses through
birth to approximately 2 years of age when alveolar development is complete. The five stages of lung
development have been divided into the embryonic, pseuodglandular, acinar, saccular, and alveolar
stages (Table 80-2). Malformations may occur at each step and lead to different pathologic conditions.46
Four separate conditions will be discussed here; pulmonary sequestration, lobar emphysema, congenital
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cystic adenomatoid malformation (CCAM), and bronchogenic cysts.47
Algorithm 80-4. Algorithm to treat pneumothorax. (Adapted from Baumann MH, Noppen M. Respirology 2004;9(2):157–164.)
Table 80-2 Phases of Lung Development Classification
Pulmonary Sequestrations
Pulmonary sequestrations are defined as pieces of parenchymal lung separated from the respiratory
tree, with the sequestration receiving its blood supply from an anomalous artery arising from the aorta,
rather than having the blood supply arising from the pulmonary artery. Sequestrations have been
further subdivided into extralobar and intralobar lesions, with very distinct anatomic alterations and
clinical presentations. Extralobar sequestrations reside outside of the true pleural space. Venous
drainage is usually into the azygos or hemiazygos veins. They are most often on the left side between
the left lower lobe and diaphragm (Fig. 80-27). Upto 80% of extralobar sequestrations occur in males.
Most patients present with dyspnea in the first 6 months of life. They may be diagnosed by fetal
ultrasound or after birth by chest x-ray. Other congenital abnormalities are found in upto two-thirds of
patients, with congenital diaphragmatic hernias present in a quarter of patients.46 Intralobar lesions
reside within the normal lung and within the normal pleura. They are almost always in the lower lobes
and occur in the left side just over 50% of the time. Venous drainage is usually through the pulmonary
vein. It is suggested that intralobar sequestration may be an acquired disease, caused by repeated
episodes of inflammation that lead to bronchiole narrowing and scarring. Ultimately the “lobe” becomes
isolated and may develop new feeding blood vessels from collateral arteries in the inferior pulmonary
ligament. A complete assessment of a sequestered lesion must be performed prior to resection, and
should include assessment of any potential airway or gut connection, determining the vascular supply of
the sequestration, and determining if there are any other congenital malformations.46
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Figure 80-27. Abnormal radiograph of the chest of a newborn with respiratory distress (A). Ultrasound identified the anomalous
vessel coursing through the diaphragm and entering the sequestration (B). This computed tomographic scan clearly demonstrates
the anomalous artery arising from the thoracic aorta and entering the sequestered lung (C). (Reproduced with permission from
Shields TW, ed. General Thoracic Surgery. 6th ed. 2005.)
Figure 80-28. Radiograph of a newborn with lobar emphysema involving the right middle lobe. Note the compressed right lower
lobe and mediastinal shift. (Reproduced with permission from Shields TW, ed. General Thoracic Surgery. 6th ed. 2005.)
Congenital Lobar Emphysema
Lobar emphysema is the cause of half of the episodes of newborn respiratory distress that are due to
structural anomalies. Two-thirds of the cases occur in males. Distension of the distal lung occurs from
obstruction of the airway, either from an intrinsic cause, such as meconium or torsion, or an extrinsic
cause, such as obstructing lymph nodes. In upto half of the cases, no cause can be found. Almost all
cases occur in the upper lobes, with almost equal distribution between sides. Half of the lesions will
present in newborns, and the remaining 50% will reveal themselves by 6 months. Chest x-rays are
diagnostic (Fig. 80-28).46 Surgical resection may not be immediately necessary, and may be delayed
until the child has grown, or until they develop a failure to thrive. Even after surgical resection, patients
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