I. Overview
Pulmonary alveoli refers to large alveolar emphysema, which is a type of restrictive emphysema. The alveoli are highly inflated and formed by rupture and fusion of the alveolar walls with each other, usually caused by live-valve obstruction of small bronchioles.
II. Diagnosis
Chest x-ray is the best way to diagnose pulmonary maculoplasm. Apical pulmonary blisters appear as very thin translucent cavities located at the edges of the lung fields, which can be round, oval, or flatter rectangular in size, and in larger blisters, sometimes transverse intervals can be seen. Multiple pulmonary blisters can be multifaceted when brought together. They are usually not in direct communication with the larger bronchi, have no fluid level, and are not accessible to bronchial contrast agents. Pulmonary blisters at the base of the lungs are often not easily seen on the orthopantomogram, some can be located completely below the level of the diaphragm apex, while others are only partially above the diaphragm apex. Giant pulmonary blisters are usually tense and may be surrounded by a layer of compressive atelectasis, making the wall of the blister appear thick and indistinct close to the chest wall. The nearby lung is pushed and causes partial atelectasis, with a clustered lung texture and reduced translucency. Pulmonary blisters may fuse with each other to form a very large, space-occupying pulmonary blister, resembling a confined pneumothorax. Pneumomediastinum can also rupture and produce a restrictive pneumothorax.
The main point of differentiation between pulmonary blisters and restrictive pneumothorax is that pulmonary blisters expand in all directions, so compressed lung tissue can be seen in the apical region, septal angle or diaphragm angle, whereas restrictive pneumothorax mainly pushes the lung tissue into the lung, and the edge of the compressed lung is usually seen to shrink toward the lung door, which is not seen in pulmonary blisters. Therefore, although striated septa are seen in both, a distinction can still be made.
Fluoroscopy and whistle-phase plethysmography are helpful in detecting pulmonary bullae, which appear relatively larger and more clearly margined because of gas retention during whistling. Tomography is also helpful in defining the contours of the pulmonary blister and showing compression and displacement of the surrounding lung tissue. In cases of coexisting lobar emphysema, tomograms may also show abnormalities in the shape of the pulmonary vessels.
CT examination may reveal subpleural pulmonary blisters less than 1 cm in diameter that are not easily visualized on ordinary chest radiographs.
Pulmonary angiography can accurately show the degree of pulmonary vascular damage and the compression of blood vessels around pulmonary blisters.
Third, treatment measures
Asymptomatic pulmonary blisters do not require treatment. Patients with chronic bronchitis or emphysema are treated primarily for the primary lesion. In case of secondary infection, antibiotics are applied.
Patients with large pulmonary blisters, occupying 70% to 100% of one side of the chest cavity, clinically symptomatic and without other pulmonary lesions, surgical removal of pulmonary blisters can result in reopening of the compressed lung tissue, increased whistling area, disappearance of intrapulmonary shunts, increased partial pressure of arterial blood oxygen, decreased airway resistance, increased ventilation, and patients with chest tightness, shortness of breath and other symptoms of whistling difficulties can be improved.
As much healthy lung tissue as possible should be preserved during surgery, and strive to perform only pulmonary herpetotomy suture, or local wedge resection of lung tissue to avoid unnecessary loss of lung function.
Spontaneous pneumothorax caused by ruptured pulmonary blisters can be cured by non-surgical treatments such as thoracentesis and closed thoracic flow, but spontaneous pneumothorax that occurs repeatedly should be treated by surgical methods. During surgery, ligation or suture of the pulmonary blister can be performed, while tetracycline or 2% iodine can be applied to the chest cavity to fix the pleural adhesions and prevent the recurrence of pneumothorax.
Patients with combined hemopneumothorax sometimes have very heavy clinical symptoms, often with chest pain and inspiratory difficulties, and also a series of manifestations of internal bleeding. Clinically, changes in the condition should be closely observed and non-operative measures, such as blood transfusion and thoracentesis, should be taken within a short period of time, and when symptoms do not improve significantly, open-chest exploration should be performed decisively. At this time, there is often a large active bleeding, and the observation time of non-operative treatment is often too long to delay the disease, and the prognosis is not as good as surgical hemostasis.
Fourth, pathological changes
The wall of the pulmonary blister is very thin and consists of flattened epithelial cells of the alveoli, or it may only be a fibrous membrane. They can coexist with a variety of emphysematous conditions, commonly parapneumonic or parafollicular emphysema, with or without carbon deposition, such as coal miner’s pneumoconiosis, and with scar tissue emphysema. Pulmonary maculopathy is classified into three types based on pathological morphology.
Type I: Narrow-necked pulmonary blister. It protrudes from the lung surface and has a narrow band attached to the lung. The increase in the size of the alveoli is due to alveolar side branch ventilation and gas retention because of live valve obstruction formed by bronchial scar tissue. Type I pulmonary blisters are thin-walled, often formed by pleura and connective tissue, and occur mostly in the middle or lingual lobes, but also commonly in the upper lobe of the lung.
Type II: Wide basal superficial pulmonary blisters. It is located in the superficial lung layer, between the dirty pleura and emphysematous lung tissue. A connective tissue septum is visible within the lumen of the pulmonary blister, but it does not form the wall of the blister and can be seen anywhere in the lung.
Type III: Deeply located pulmonary blister with a wide base. The structure is similar to type II, but the site is deeper, surrounded by emphysematous lung tissue, and the pulmonary blister can extend to the hilum and can be seen in any lung lobe.
When the size of the pulmonary blister increases, the surrounding lung tissue is compressed and causes displacement of the lung. The compressed lung tissue appears as an increased density shadow around the pulmonary blister on an X-ray chest radiograph. All three types are seen in chronic bronchiectasis. Small lobe central emphysema is not complicated by pulmonary bullae. Lower lobe pulmonary blisters are commonly seen in coal miners with complications of pneumoconiosis and fused silicosis.
V. Clinical manifestations
Small pulmonary blisters themselves do not cause symptoms, and patients with simple pulmonary blisters are often asymptomatic, and some pulmonary blisters may remain unchanged for many years, while some may gradually increase in size. The enlargement of pulmonary blisters or the appearance of new pulmonary blisters in other parts of the body can cause pulmonary dysfunction and gradually develop symptoms. Large pulmonary blisters can cause chest tightness and shortness of breath. The sudden enlargement and rupture of a pulmonary blister can produce a spontaneous pneumothorax, which can cause severe inspiratory distress, or chest pain similar to angina.
Patients with pulmonary herpes are often combined with chronic bronchitis, bronchial asthma, and emphysema, and the clinical symptoms are mainly caused by these diseases, only to be further aggravated by the formation of pulmonary herpes. Secondary infection of pulmonary herpes can cause cough, cough, chills and fever, and in severe cases, cyanosis. If the draining bronchus is obstructed and the lung blister cavity is filled with inflammatory material, the cavity may disappear. It may occur clinically that the symptoms of infection disappear with treatment, while the pulmonary maculopapillary shadows on chest radiographs persist for weeks or months without resolving.
Pulmonary signs are often a manifestation of preexisting pulmonary disease.
VI. Complications
Spontaneous pneumothorax is the most common complication of pulmonary maculoplasm, followed by infection and spontaneous hemopneumothorax.
1.Spontaneous pneumothorax
Pneumomediastinum can have no symptoms. The degree of atrophy depends on the amount of gas entering the chest cavity and the pathology of the original lesions of the lung and pleura. If the patient has emphysema, pulmonary fibrosis, long-term chronic infection of lung tissue, etc. in addition to pulmonary herpes, when the pulmonary herpes ruptures, although some of the gas enters the chest cavity, and the degree of lung tissue atrophy can be less, but because the patient’s original lung function has been reduced, the symptoms are also more serious. After the rupture of the pulmonary blister, a small part of the fissure is small, and the fissure closes by itself after the lung tissue atrophy, the air leakage stops, the pneumothorax is gradually absorbed, the negative chest pressure is restored, and the lung reopening is healed.
2.Tension pneumothorax
If the lung blister ruptures and forms a live valve, the negative pressure in the chest cavity increases when inhaling, gas enters the chest cavity, the live valve closes when whistling, gas cannot be discharged, especially when coughing, the airway pressure increases when the vocal valve is closed, gas enters the chest cavity, the vocal valve opens, the airway pressure decreases, the fissure closes again, and the amount of gas in the chest cavity increases with each whistle and cough, forming a tension pneumothorax. In tension pneumothorax, the lung tissue on the affected side is completely atrophied and the mediastinum is pushed to the healthy side, while the lung tissue on the healthy side is also compressed, the large blood vessels of the heart are displaced and the large veins are distorted and deformed, which affects the blood return and causes serious obstruction to the whistling circulation. The affected side of the thorax is elevated, mostly accompanied by subcutaneous emphysema on the affected side, the trachea is obviously displaced to the healthy side, the condition is critical and often requires emergency treatment.
3.Spontaneous hemothorax
Spontaneous hemothorax caused by pulmonary herpes, mostly bleeding from the apical pulmonary herpes or pulmonary tissues around the herpes with adhesions to the apex of the chest and adhesions tearing activity. The diameter of small arteries in the adhesion zone can reach 0 or 2 cm, and the vessels originate from the body circulation with higher pressure, while the thoracic cavity is under negative pressure, which increases the tendency of bleeding. In addition, the bleeding is difficult to stop automatically because the blood in the thoracic cavity does not coagulate due to the defibrotic effect of lung, heart and diaphragm movements. Clinical symptoms may vary depending on the speed of bleeding. When bleeding is slow, patients may present with gradually increasing chest tightness, difficulty in whistling, blunting of the diaphragm angle visible on X-ray, or parabolic images of pleural effusion. When the bleeding is rapid, there can be shock performance in a short period of time.
4.Spontaneous hemopneumothorax
When the adhesions between the pulmonary blister and the surrounding lung tissues and chest wall are torn, if there is a rupture of blood vessels in the adhesion zone and the lung tissues are also damaged, spontaneous hemopneumothorax is formed.
In recent years, some scholars have pointed out that the amplitude of diaphragm activity may play a decisive role in the occurrence of spontaneous hemopneumothorax, and that the amplitude of diaphragm activity increases during strenuous activities such as rejection of air and force, resulting in a sudden direct or indirect pull on the adhesive band at the top of the chest. If the tear is on the wall side or central part of the cord, only a hemothorax will occur. The diaphragm is more active in long and lean young people, and is more dependent on abdominal whistling because of the underdeveloped thoracic muscles, but the accumulation of fat in the abdominal cavity gradually increases after middle age, limiting the diaphragm activity to varying degrees, so even though the above pathological changes exist, they rarely develop. In women, the predominantly thoracic whistle has a lower incidence. The right lung is triple-lobed, and its lobe space plays a buffering role against the fierce downward pull, and there is still a liver under the right lung, which may be the reason why the right side has less morbidity. Therefore, patients with spontaneous hemopneumothorax are characterized by young age, more males than females, more left side than right side, and more long and lean body type. Bilateral spontaneous pneumothorax also occurs from time to time, mostly the left side first and the right side later, and in individual cases it occurs bilaterally at the same time, and the condition is critical and even life-threatening.
5.Pneumothorax secondary infection
In most cases, pulmonary blisters occur at the distal end of the bronchus above the eighth level, and most of them are not infected, but if the draining bronchus is blocked and the bronchus of pulmonary blisters is filled with inflammatory secretions, the patient may have fever, cough, sputum and other symptoms of infection, and sometimes after anti-infection treatment, the clinical symptoms improve, but the signs of infection on chest X-ray can still last for a longer period of time.