Upper lobe predominance heterogeneity was found in 15 patients, and upper lobe plus apical segment of the lower lobe heterogeneity was found in the remaining. Pulmonary rehabilitation was not routinely performed pre-operatively because many patients lived far away from our hospital and cannot receive an adequate rehabilitation program with their local medical centres. All patients of both groups began rehabilitation immediately before and after operation. Our rehabilitative program included education in breathing techniques, anxiety control, muscle exercises, cycling and walking.
Electrocardiographic monitoring, and radial arterial and central venous cannulation were routine in all cases. An epidural catheter was placed to provide adequate post-operative analgesia and also for intra-operative anaesthetic management, in order to reduce inhalational anaesthetic and systemic narcotic drugs. Selective airway intubation with a left sided double lumen tube was used and a stand-by for high frequency jet ventilation was made in case of necessity.
Pulse oxymetry and capnography were monitored during the operation. All operations were unilateral in both groups and performed thoracoscopically. Three to four intercostal ports have been used to accomplish operations. Bullectomy and lung reduction were performed using 45 mm endoscopic staplers. Large bullae still hyperinflated were opened for deflation to gain more space and better visualization of the pleural cavity.
During the operation, all efforts were applied to prevent or minimize air leakage. Bovine pericardium, pleural tent or surgical glues were used singularly or in combination, to reduce the pleural space and to reinforce the mechanical sutures. In some cases lower pulmonary ligament was transected to allow a better lung re-expansion.
Two chest tubes were left in place and connected to a water seal chamber under mild suction. No intra-operative complications developed in either group. We had to convert thoracoscopy to thoracotomy in one patient during lung volume reduction because of complete obliteration of the pleural space.
This patient had a significant air leak after operation and developed empyema, re-intubation and mechanical ventilation for respiratory insufficiency and sepsis that caused his demise after 25 days after the operation. Our policy was to achieve immediate post-operative extubation, however all but one in the first group and all but two in the second group were extubated in the operating room.
The remaining two were extubated after 24 and 36 h, respectively. No patient required re-intubation and none died in the bullous group. One patient developed contralateral pneumothorax that required an emergency chest tube drainage.
Post-operative complications, reported in Table 2 , were similar in both groups. Air leak was the most frequent problem. The mean chest tube drainage time was 8. Both groups were homogeneous for demographic characteristics, pre-operative lung function data and degree of respiratory derangement.
Post-operative lung function data recorded after 6 and 12 months were available for 19 patients in Group I one patient died in the post-operative period and 17 patients in Group II one patient died of a stroke 10 months after the operation. Limited improvement in the diffusion capacity of carbon monoxide DLCO was also observed. The mean air oxygen tension did not change after the operation; slight reduction of the PaCO 2 level was observed. The mean six minutes walking distance increased markedly in both groups Tables 3 and 4.
No statistically significant differences of respiratory functional results, recorded after 6 and 12 months after the operation, were observed between the two groups Table 5. Comparison between pre-operative and 6 months post-operative respiratory function data of Group I a. Comparison between pre-operative and 6 months post-operative respiratory function data of Group II a. Comparison of post-operative functional data recorded at 6 and 12 months between the two groups a.
End-stage emphysema is a disabling disease associated with significant morbidity, mortality and poor quality of life.
Medical treatment has limited efficacy since it can not address the anatomical abnormalities that cause the physio-pathological changes seen in emphysema. Multiple observational studies have shown that even after adjustment for other risk factors, these patients develop COPD at a slightly younger age and with slightly lower levels of tobacco exposure compared to HIV-negative controls.
The pathogenesis of emphysema occurring in HIV is not clearly understood. HIV-positive smokers with emphysema have increased concentrations of inflammatory cytokines in the lung microenvironment and upregulated expression of matrix metalloproteinases, proteolytic enzymes involved in development of emphysema.
HIV infection leads to induction of both native and innate responses, and evidence indicates possible increased activity of both Th-1 and Th cellular immune responses. Oxidative stress, induction of microvascular endothelial cell apoptosis, malnutrition, and lung damage due to opportunistic infections, particularly PCP may play additional roles in the early development of emphysema in these patients. Bullous lung disease is typically diagnosed by chest imaging. Although there are no specific laboratory tests useful in its diagnosis, laboratory testing may be of some use in exploring etiology and assessing the risk of operative intervention.
The laboratory workup of a patient with bullous emphysema is not standardized, but it may include the following considerations:. HIV testing is indicated in patients with potential risk factors, particularly in those at a comparatively young age or with emphysema out of proportion to tobacco exposure. A CBC may exclude anemia as a contributor to dyspnea, and in severely affected patients, may occasionally reveal polycythemia associated with hypoxemia.
ABG can evaluate for hypercapnia in those with severe respiratory impairment; hypercapnia increases risks of operative intervention and may alter medical management. In rare cases, genetic testing may be considered in patients with disease onset at a young age and who have characteristic physical features of inherited connective tissue diseases, such as Marfans or Ehlers-Danlos syndrome. Chest imaging is the basis for diagnosing bullous lung disease.
Although CXRs may reveal focal areas of radiolucency surrounded by thin curvilinear density, suggesting the presence of bullae, this test is not very sensitive for bullous lung disease. Cross-sectional imaging using CT allows more detailed characterization of the number, size, and location of bullae, as well as the condition of the surrounding lung parenchyma.
Characteristic findings of the chest CT include:. Apical-predominant bullae, which are most commonly associated with emphysema in the surrounding lung parenchyma. Basilar-predominant disease may be associated with alpha-1 antitrypsin deficiency or IV drug use.
Thin, irregular, linear stranding within the bulla that represent residual strands of alveolar septae or blood vessels. Multiple, small, round, clearly demarcated airspaces in the lung parenchyma, particularly in the absence of surrounding emphysema, should raise suspicion for cystic lung disease e.
The clinical context and other imaging findings may help to narrow the differential. For example, multiple cysts in otherwise normal lungs of a young woman with a renal angiomyolipoma are highly suggestive of lymphangioleiomyomatosis. Langerhans cell histiocytosis, which may cause multiple, irregular, air-filled spaces in the upper lung zones of an older smoker, is often mistaken for the far more common bullous emphysema. The presence of multiple nodules or significant fibrosis between air-filled spaces may help distinguish Langerhans cell histiocytosis from bullous emphysema.
Thick-walled airspaces within the lung parenchyma or the presence of an air-fluid level within the cavity should prompt consideration of cavitating infection or malignancy with central necrosis.
Although bullae may rarely become secondarily infected, infected bullae are far less common than lung abscesses. Focal thickening in one wall of a bulla raises possibility of lung cancer arising in adjacent lung tissue. Significant hilar or mediastinal lymphadenopathy is not seen in uncomplicated bullous lung disease, so its presence may raise suspicion for cavitating infection, malignancy, or possibly fibrocavitary sarcoidosis.
On CXR, cystic bronchiectasis associated with cystic fibrosis may be mistaken for bullae, but CT scans clearly demonstrate that the air-filled spaces are dilated airways rather than holes in the parenchyma itself. A CXR in which an acute angle is observed where the edge of the air-filled space meets the chest wall may signal a pneumothorax rather than a bulla.
Typically, a bulla meets the chest wall at an obtuse angle. In severely symptomatic patients, certain imaging features may suggest a favorable outcome from surgical intervention. Patients that could benefit from lung volume reduction surgery are those with severe apical-predominant emphysema even without a dominant bulla and relative preservation of parenchyma in the mid and lower lung zones. Pulmonary function testing is not diagnostic of bullous lung disease, but it is critical in evaluating its functional significance, guiding medical therapy, and evaluating the likelihood of benefit from surgical intervention:.
Spirometry establishes the presence or absence of airflow obstruction and reflects its severity. The forced expiratory volume in 1 second FEV1 is used to grade severity, as well as selects appropriate candidates for surgical bullectomy see below. Measurement of lung volumes, specifically total lung capacity TLC and residual volume RV , is used to evaluate for hyperinflation and air-trapping respectively.
Because of the frequency of severe air trapping in patients with bullous lung disease, gas dilution methods may underestimate true lung volumes. Consequently, plethysmography when it is available is the preferred method for lung volume measurement.
A decreased diffusing capacity for carbon monoxide DLCO can support the diagnosis of emphysema or bullous disease, but is nonspecific.
The DLCO is also used to select candidates for surgical treatment see below. Diagnostic procedures like bronchoscopy and lung biopsies have essentially no role in the evaluation of bullous lung disease. In patients with severe respiratory impairment and those being considered for bullectomy or lung volume reduction surgery, cardiac testing like echocardiography, stress testing, and cardiac catheterization may be considered as appropriate, in evaluating for pulmonary arterial hypertension.
In addition, testing for coexistent ischemic heart disease may be warranted. These conditions may be contraindications for bullectomy and lung volume reduction surgery. Testing for alpha-1 antitrypsin deficiency is often performed in patients with bullous lung disease but is not necessary in every case. Clinical context should help guide the decision to test individual patients.
The patient with bullous disease should be educated about significance and possible complications related to the presence of bullae.
Possibility of spontaneous or traumatic pneumothorax needs to be discussed with the patient and the patient needs to be aware of the severity of this complication and risks of not reacting promptly with a visit to medical care.
Because of this, the condition tends to get diagnosed after it has advanced. During your appointment, your doctor will review your medical history and assess your symptoms. From there, your doctor may order a chest scan or X-ray to assess your lung function and look for visual abnormalities.
Your doctor will prescribe either a non-steroid or steroid inhaler. Non-steroid inhalers can help improve your ability to breathe. In severe instances, a lung transplant may be necessary.
Your doctor will work with you to develop a management plan that can reduce or alleviate your symptoms. Your projected life expectancy will depend on your individual diagnosis. Talk with your doctor about what this may mean for you. Sticking to your treatment plan can help slow the progression of the disease. Keep reading: Understanding emphysema treatments ».
Emphysema is often preventable. In many cases, avoidable lifestyle factors determine its likelihood. If emphysema runs in your family, have your doctor run tests to determine your genetic risk of developing the disease. In the case of subcutaneous emphysema, you should try to protect yourself against avoidable injuries. We'll go into detail about the condition's stages and how to manage symptoms.
Smoking is the leading cause of emphysema, a disease of the lungs that makes it hard to breathe. Learn more about how emphysema affects you and how….
Types of chronic lung disease range from congenital conditions like asthma to those caused by tissue damage, like emphysema and lung cancer. Learn the…. Chronic bronchitis is a form of COPD. A Real Improvement There are really only two lung cancer surgeries that actually restore lung function as well as relieve symptoms.
One is lung volume reduction surgery LVRS , and the other is a bullectomy—the removal of a giant bulla. Most patients report an increased ability to draw breath as well as relief from the symptoms of the bulla. Search Encyclopedia. Giant Bullae What are Giant Bullae? The Mechanics of Giant Bullae Emphysema causes a loss of elasticity in the walls of the small air sacs in the lung. Symptoms of Giant Bullae Because of its size, a giant bulla makes its presence known and produces symptoms.
Symptoms from a giant bulla can include: Pressure in the chest Difficulty drawing breath Soreness A bloated feeling General fatigue due to lack of oxygen Causes of Giant Bullae Smoking cigarettes is by far the most common cause of emphysema. Treating Giant Bullae In virtually every case, the treatment for a giant bulla is a bullectomy—surgical removal of the growth.
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