| disease | Pulmonary Bulla |
| alias | Emphysematous Bleb |
Bullae refer to bullous lung qi swelling, a localized lung qi swelling. The alveoli are highly distended, and the alveolar walls rupture and fuse together, usually caused by valvular obstruction of small bronchi.
bubble_chart Pathological Changes
The wall of a pulmonary bulla is very thin, composed of flattened epithelial cells of the alveoli, or it may consist solely of a fibrous membrane. It can coexist with various types of lung emphysema, commonly seen adjacent to the septa or lobules, and may be accompanied by carbon deposition, such as in coal miners' pneumoconiosis, or without carbon deposition, as in scar tissue emphysema. Based on pathological morphology, pulmonary bullae are classified into three types.
**Type I**: Narrow-necked bulla. It protrudes from the lung surface and is connected to the lung by a narrow band. The enlargement of the bulla is due to collateral alveolar ventilation and gas trapping caused by valvular obstruction from bronchial scar tissue. The wall of a Type I bulla is thin, often formed by the pleural membrane and connective tissue. It predominantly occurs in the middle lobe or lingula but is also common in the upper lobe, possibly due to the higher negative intrathoracic pressure in these regions. Conventional chest X-rays can detect the presence of such bullae.
**Type II**: Broad-based superficial bulla. Located superficially in the lung, between the visceral pleura and emphysematous lung tissue. Connective tissue septa may be visible within the bulla cavity, but they do not form the wall of the bulla. This type can occur in any part of the lung.
**Type III**: Broad-based deep bulla. Structurally similar to Type II but located deeper, surrounded entirely by emphysematous lung tissue. The bulla may extend toward the hilum and can be found in any lobe.
When a bulla enlarges, it compresses the surrounding lung tissue and causes displacement of the lung. On chest X-rays, the compressed lung tissue appears as an area of increased density around the bulla. All three types are observed in chronic bronchitis. Centrilobular emphysema does not complicate bullae formation. Bullae in the lower lobes are commonly seen in complicated coal miners' pneumoconiosis and confluent silicosis.bubble_chart Clinical Manifestations
Small bullae themselves do not cause symptoms, and patients with simple bullae often have no symptoms. Some bullae may remain unchanged for many years, while others may gradually enlarge. The enlargement of bullae or the appearance of new bullae in other areas can lead to impaired lung function and the gradual onset of symptoms. Giant bullae may cause patients to experience chest tightness and shortness of breath. Sudden enlargement or rupture of a bulla can result in spontaneous pneumothorax, leading to severe dyspnea, and may also cause chest pain resembling colicky pain.
Patients with bullae often have concurrent chronic bronchitis, bronchial asthma, or pulmonary emphysema, and the clinical symptoms are primarily caused by these conditions. However, after the formation of bullae, the clinical symptoms may worsen further. Secondary infection of bullae can cause cough, sputum production, shivering, and fever, and in severe cases, cyanosis may occur. If the draining bronchus becomes obstructed, the bulla cavity may fill with inflammatory material, causing the cavity to disappear. Clinically, it is possible for the infection symptoms to resolve after treatment, while the bulla shadow on the chest X-ray persists for weeks or months without subsiding.
Chest X-ray is the best method for diagnosing pulmonary bullae. Bullae in the apical region of the lungs appear as thin, translucent cavities at the edges of the lung fields, which may be round, oval, or flattened rectangular in shape, varying in size. In larger bullae, transverse septa may sometimes be observed. Multiple bullae clustered together can form a polyhedral appearance. Generally, they do not directly communicate with larger bronchi, lack fluid levels, and bronchographic contrast agents cannot enter them. Bullae at the base of the lungs are often difficult to visualize on frontal chest radiographs. Some may lie entirely below the level of the diaphragmatic dome, while others may only partially extend above it. If the wall of the bulla is not displayed as a continuous ring-like shadow, it can easily be mistaken for tent-like pleural adhesions. Giant bullae typically exhibit tension, with a surrounding layer of compressive atelectasis that makes the bulla wall appear thicker, and those adjacent to the chest wall may be indistinct. Nearby lung tissue is compressed, leading to partial atelectasis, convergence of lung markings, and reduced translucency. Bullae can merge to form very large bullae, resembling localized pneumothorax. Bullae may also rupture, resulting in localized pneumothorax.
The key points for differentiating bullae from localized pneumothorax are: bullae expand outward in all directions, so compressed lung tissue can be seen in the apical region, costophrenic angle, or cardiophrenic angle; whereas localized pneumothorax primarily compresses lung tissue inward, usually showing the compressed lung edge retracting toward the hilum, a phenomenon not seen with bullae. Therefore, although linear septa may be observed in both conditions, they can still be distinguished.
Fluoroscopy and expiratory-phase chest radiographs help in detecting bullae, as air trapping during expiration makes the bullae appear relatively larger and their edges more distinct. Tomography is also useful for clarifying the contours of bullae and revealing compression and displacement of surrounding lung tissue. When coexisting with lobular emphysema, tomographic images can also display abnormal pulmonary vascular patterns.
CT scans can detect subpleural bullae smaller than 1 cm in diameter, which are difficult to visualize on conventional chest radiographs.
Pulmonary angiography can accurately depict the extent of pulmonary vascular damage and the compression of surrounding vessels by bullae.
bubble_chart Treatment Measures
Asymptomatic pulmonary bullae do not require treatment. For patients with chronic bronchitis or lung qi swelling, the primary focus is treating the underlying condition. Antibiotics should be used in cases of secondary infection.
For patients with large pulmonary bullae occupying 70–100% of one hemithorax, exhibiting clinical symptoms, and without other lung lesions, surgical removal of the bullae can lead to re-expansion of the compressed lung tissue, increased respiratory surface area, elimination of intrapulmonary shunting, improved oxygen partial pressure in stirred pulse, reduced airway resistance, and increased ventilation. Symptoms such as chest tightness, shortness of breath, and other respiratory difficulties can be alleviated.
During surgery, as much healthy lung tissue as possible should be preserved, aiming to perform only bulla resection and suturing or local wedge resection of lung tissue to avoid unnecessary loss of pulmonary function.
Spontaneous pneumothorax caused by ruptured pulmonary bullae can be cured through non-surgical therapies such as thoracentesis or closed thoracic drainage. However, recurrent spontaneous pneumothorax should be treated surgically. During surgery, the bullae should be ligated or sutured, and tetracycline or 2% iodine can be applied to the pleural cavity to induce pleural adhesion and fixation, preventing recurrence of pneumothorax.
Patients with combined hemopneumothorax may present with severe clinical symptoms, often including chest pain and dyspnea, along with signs of internal bleeding. Close monitoring of the patient's condition is essential. If non-surgical measures such as blood transfusion or thoracentesis do not significantly improve symptoms within a short period, exploratory thoracotomy should be performed decisively. In such cases, there is often significant active bleeding, and prolonged observation with non-surgical treatment may delay care, resulting in a poorer prognosis compared to surgical hemostasis.
Spontaneous pneumothorax is the most common complication of pulmonary bullae, followed by infection and spontaneous hemopneumothorax.
1. Spontaneous pneumothorax: Pulmonary bullae may not cause any symptoms. During sudden exertion, such as severe coughing, heavy lifting, or sports activities, the pressure suddenly increases, causing the pulmonary bullae to rupture. Gas from the lungs enters the pleural cavity, forming a spontaneous pneumothorax. Symptoms may include dyspnea, shortness of breath, flusteredness, and increased pulse rate. Pneumothorax eliminates the negative pressure in the pleural cavity, compressing the lung tissue and causing it to collapse toward the hilum. The degree of collapse depends on the amount of gas entering the pleural cavity and the pathological condition of the lung and pleura. If a large amount of gas enters the pleural cavity and the lung tissue has mild pre-existing lesions with good compliance, the lung may collapse significantly, sometimes up to 90% of one side of the pleural cavity. Rapid entry of gas into the pleural cavity and sudden collapse of the lung tissue can lead to severe symptoms, even cyanosis. If the patient also has conditions such as pulmonary emphysema, pulmonary fibrosis, or long-term chronic lung infections, the collapse of the lung tissue may be less severe when the bullae rupture, but symptoms can still be significant due to pre-existing reduced lung function. X-rays may show a pneumothorax line formed by the compressed lung. If adhesions are present, the pneumothorax line may appear irregular. After the rupture of a pulmonary bulla, a small portion of the rupture may close on its own as the lung tissue collapses, stopping the fistula and allowing the pleural gas to gradually absorb. The negative pressure in the pleural cavity is restored, and the lung re-expands and heals.
2. Tension pneumothorax: If a valve-like mechanism forms after the rupture of a pulmonary bulla, during inhalation, the negative pressure in the pleural cavity increases, allowing gas to enter. During exhalation, the valve closes, preventing gas from escaping. This is especially pronounced during coughing, when the glottis closes, increasing airway pressure and allowing gas to enter the pleural cavity. When the glottis opens, the airway pressure decreases, and the rupture closes again. Each breath and cough increases the amount of gas in the pleural cavity, leading to tension pneumothorax. In tension pneumothorax, the affected lung tissue collapses completely, and the mediastinum is pushed toward the healthy side. While the healthy lung tissue is also compressed, the heart and major blood vessels shift, and large veins become twisted, impairing blood return and causing severe respiratory and circulatory dysfunction. Patients may experience dyspnea, rapid pulse, decreased blood pressure, or even asphyxia and shock. The affected side of the chest may bulge, often accompanied by subcutaneous emphysema, and the trachea may shift significantly toward the healthy side. This is a critical condition that often requires emergency treatment.
3. Spontaneous hemothorax: Spontaneous hemothorax caused by pulmonary bullae usually results from bleeding due to the tearing of adhesions between bullae in the lung apex or surrounding lung tissue and the chest wall. The small vessels in the adhesion bands can have diameters up to 0.2 cm. These vessels originate from the systemic circulation and have higher pressure. Additionally, the negative pressure in the pleural cavity further increases the tendency to bleed. Moreover, due to the defibrinating effect of lung, heart, and diaphragm movements, the blood in the pleural cavity does not clot, making it difficult for bleeding to stop automatically. Clinical symptoms vary depending on the rate of bleeding. With slow bleeding, patients may experience gradually worsening chest tightness and dyspnea. X-rays may show blunting of the costophrenic angle or a parabolic shadow of pleural effusion. With rapid bleeding, shock symptoms may appear in a short period.
4. Spontaneous hemopneumothorax: When adhesions between pulmonary bullae and surrounding lung tissue and the chest wall are torn, if vessels in the adhesion bands rupture and the lung tissue is also injured, spontaneous hemopneumothorax occurs.
In recent years, some scholars have pointed out that the range of diaphragmatic movement may play a decisive role in the occurrence of spontaneous hemopneumothorax. During strenuous activities such as breath-holding or exertion, the amplitude of diaphragmatic movement increases, exerting sudden direct or indirect traction on the adhesive bands at the apex of the chest. Since lung tissue is looser than the pleura, it is prone to tearing on the lung side, resulting in hemopneumothorax that involves both bleeding and fistulous air leakage. If the tear occurs on the parietal side or central segment of the band, only hemothorax occurs. Tall and slender young individuals have a greater range of diaphragmatic movement and, due to their lean physique, often underdeveloped chest muscles, relying more on abdominal breathing. However, after middle age, the gradual accumulation of intra-abdominal fat limits diaphragmatic movement to varying degrees, so even with the aforementioned pathological changes, the condition rarely develops. Women primarily rely on thoracic breathing, resulting in a lower incidence. The right lung has three lobes, and its interlobar fissures provide some buffering effect against sudden downward traction. Additionally, the liver beneath the right lung may contribute to the lower incidence on the right side. Therefore, patients with spontaneous hemopneumothorax are typically young, more often male than female, more frequently affected on the left side than the right, and commonly have a tall and slender body type. Bilateral spontaneous pneumothorax also occurs occasionally, usually with the left side affected first and the right side later, though in rare cases, both sides may be affected simultaneously, presenting a critical and potentially life-threatening condition.
5. Secondary infection of pulmonary bullae In most cases, pulmonary bullae occur distal to the eighth-level bronchi and are generally not infected. However, if the draining bronchus becomes obstructed and the bronchus of the pulmonary bulla is filled with inflammatory secretions, the patient may exhibit infection symptoms such as fever, cough, and sputum production. Sometimes, after anti-infection treatment, the clinical symptoms improve, but the signs of infection on the chest X-ray may persist for an extended period.
