disease | Pneumothorax |
alias | Spontaneouxpneumothorax |
The pleural cavity is a sealed space that does not contain gas. The accumulation of air in the pleural cavity due to any cause is collectively referred to as pneumothorax. When alveoli and the visceral pleura spontaneously rupture on the basis of chronic lung disease, allowing air to enter the pleural cavity, it is called spontaneous pneumothorax, which is the most common clinical presentation. A large amount of pleural air causing severe lung compression and collapse can lead to respiratory and circulatory dysfunction. The main clinical manifestations of pneumothorax include sudden chest pain, chest tightness, and shortness of breath. In severe cases, patients may experience restlessness, cyanosis, cold sweating, or even shock.
bubble_chart Etiology
It is classified into the following types based on different causes.
Surgical and autopsy findings confirm that spontaneous pneumothorax, whether secondary or idiopathic, often involves thin subpleural bullae at the lung margins, which serve as the foundation for pneumothorax. Under triggering factors such as cold air or inflammatory irritation, bronchospasm and increased airway resistance, or sudden rises in intrapulmonary pressure, can overinflate these bullae, increasing their tension. Severe coughing with glottal closure or rebound impact on already tense bullae can further elevate tension, causing the bullae and visceral pleura to rupture suddenly. This allows gas from the airways and alveoli to rapidly enter the pleural cavity, forming pneumothorax.
According to the condition of the pleural membrane rupture and the pressure in the pleural cavity, it can be divided into the following types.
bubble_chart Clinical Manifestations
Typical spontaneous pneumothorax often presents with sudden chest pain, followed by irritative cough, chest tightness, shortness of breath, wheezing, difficulty lying flat, and a preference for lying on the unaffected side. If there is pre-existing extensive lung disease, symptoms may be significant even with a small amount of air accumulation.
Tension pneumothorax, due to its rapid onset, large volume of air accumulation, severe lung compression, and mediastinal shift with compression of major blood vessels, often manifests as severe chest pain that may radiate to the shoulders, back, and forearms, accompanied by severe dyspnea, anxiety, forced upright posture, cyanosis, cold sweating, a sense of suffocation, and even respiratory failure, shock, and impaired consciousness.
If pneumothorax develops slowly, with a small amount of air accumulation, or if the tear heals quickly, or if there is no or only grade I lung disease, symptoms may be minimal or only mild chest tightness, and pneumothorax may only be detected on X-ray examination.
bubble_chart Auxiliary Examination
In the analysis of blood qi aspects, PaO2 and PaCO2 may decrease.
X-ray examination is the most important method for diagnosing pneumothorax, as it can reveal the amount of accumulated air, the degree of lung compression, the type of pneumothorax, pleural adhesions, pleural effusion, mediastinal shift, and more. It also allows monitoring of lung re-expansion during treatment, making it an indispensable diagnostic tool. In typical pneumothorax cases, a translucent band of accumulated air can be observed in the outer zone, devoid of lung markings, while the inner zone shows increased density due to compressed lung tissue. A distinct curved boundary, known as the pneumothorax compression line, separates these two zones. In cases of massive pleural air accumulation, the lung tissue may collapse toward the hilum, forming a mass-like structure with an arc-shaped or lobulated outer edge, often indicative of tension pneumothorax. A hydropneumothorax typically presents with a classic air-fluid level. For minor air accumulation confined to the lung apex, the pneumothorax compression line may be indistinct, making it easy to misdiagnose as fistula disease if not carefully examined. Combining chest fluoroscopy to observe increased lung retraction density at the end of expiration can help identify the compression line. In cases of localized or multiloculated pneumothorax, a simple posteroanterior X-ray may be confused with lung qi cysts or bullae, necessitating observation from different angles for accurate diagnosis.
bubble_chart Treatment Measures
1. Pneumothorax Therapy
If the patient's condition permits, a chest X-ray should first be performed to assess the volume of pneumothorax and the degree of lung compression. The intrapleural pressure should be measured using an artificial pneumothorax apparatus to determine the type of pneumothorax. Generally, if the lung is compressed by more than 20% and the intrapleural pressure is positive with dyspnea, pneumothorax drainage should be performed. There are various methods available, and the appropriate one can be selected based on the patient's condition.
Tension pneumothorax is a critical condition. Immediate drainage can be performed using a pneumothorax apparatus to measure pressure and aspirate air simultaneously, rapidly reducing the intrapleural pressure to equilibrium (zero) or negative pressure before further treatment. Alternatively, a large syringe connected to a three-way stopcock or rubber tube can be used for thoracentesis and air aspiration. Closed drainage can also be directly installed (method described later). In emergencies, a thick needle with a rubber finger cot (with a small slit) tied to its end can be inserted into the pleural cavity at the conventional pneumothorax puncture site to allow unidirectional air drainage. When a large amount of air is expelled and the pleural pressure drops to negative, the finger cot collapses, preventing external air from flowing back into the pleural cavity. This serves as a simple and effective temporary drainage method.
The treatment of open pneumothorax and further management of tension pneumothorax require the installation of closed thoracic drainage to ensure continuous and effective air removal, allowing the compressed lung to re-expand as quickly as possible. The method involves making a 2–3 cm transverse incision along the upper edge of the rib at the second intercostal space in the midclavicular line (the conventional pneumothorax puncture site) or the 4th–5th intercostal space in the anterior axillary line under routine disinfection and local anesthesia. A trocar is inserted into the pleural cavity, the stylet is removed, and a sterile rubber tube is advanced about 3–4 cm into the pleural cavity. The outer sheath is then withdrawn. Alternatively, after skin incision, blunt dissection is performed to reach the pleura, and the rubber tube is directly inserted into the pleural cavity using forceps to puncture the pleura. The forceps are then withdrawn, and the rubber tube remains in the pleural cavity, secured with sutures. Another rubber tube is connected to a water-seal bottle, with the tube submerged 1–2 cm underwater. When the intrapleural pressure exceeds this level, air is expelled through the water-seal bottle. A silicone tube is preferred for intrapleural drainage, with its tip cut into a duckbill shape and two side holes to prevent blockage and facilitate drainage. During closed drainage installation, ensure the skin incision is not too small to avoid subcutaneous emphysema. Monitor the drainage tube for patency and address any blockages promptly. If pneumothorax is accompanied by pleural effusion, the tube should be inserted one intercostal space above the fluid level as indicated by X-ray, using a double-bottle closed drainage system—the first bottle collects pleural fluid, and the second bottle drains air. After drainage, if symptoms improve, no air bubbles are observed, and X-ray confirms full lung re-expansion, the tube can be clamped for observation. If the lung remains well-expanded after 24 hours, the tube can be removed.
If the lung fails to re-expand after 2–3 days of closed drainage, continuous negative-pressure suction can be applied. This involves adding a pressure-regulating bottle connected to the suction device to the standard closed drainage system. The pressure-regulating tube should be submerged 8–12 cm underwater. When the suction negative pressure falls below -8 to -12 cm H₂O, room air enters the pressure-regulating bottle to prevent excessive negative pressure, avoiding complications such as lung tissue injury or re-expansion pulmonary edema. Continuous negative-pressure suction for 2–3 days usually allows pleural tears to heal. After lung re-expansion, the tube can be removed following standard closed drainage procedures (Figure 2-12-1).
For closed pneumothorax with a significant air volume, thoracentesis and air aspiration can be performed once or several times at the conventional pneumothorax puncture site (second intercostal space in the midclavicular line) using an artificial pneumothorax apparatus or a large syringe. The remaining small amount of air can be absorbed spontaneously. For localized pneumothorax, aspiration under X-ray guidance or based on X-ray localization is safer and more reliable.
2. Treatment of Complications
(1) Pneumomediastinum
Pneumomediastinum is primarily caused by high intrapleural pressure, so the key is prompt decompression. If a large volume of air accumulates in the mediastinum with organ compression symptoms, a transverse incision can be made at the suprasternal fossa for drainage. For mild cases without significant symptoms, rest and symptomatic treatment are sufficient, as the air will be absorbed spontaneously once the pneumothorax resolves.
(2) Pyopneumothorax and Hemopneumothorax
For patients with concurrent empyema, thorough drainage should be performed, and effective antibiotics should be selected based on the infecting bacteria, which can be used both systemically and locally. For cases that do not heal over a long period and develop into chronic empyema, surgery may be considered. Hemopneumothorax is often caused by the tearing of blood vessels in the pleural adhesion band; bleeding usually stops spontaneously after lung re-expansion. If the bleeding is severe, blood transfusion should be administered, and surgical ligation of the blood vessels may be necessary to stop the bleeding.
(3) Patients with bronchopleural fistula, or persistent pneumothorax that cannot be re-expanded after the above treatments, or recurrent pneumothorax in a short period, as well as those with giant bullae, may consider surgical treatment. If surgery is not suitable, pleural adhesion therapy can be used, which involves injecting sterile tetracycline or hypertonic glucose into the pleural cavity, or insufflating talc powder or kaolin to induce sterile pleuritis, thereby sealing the pleural cavity and preventing recurrence of pneumothorax.
3. Disease causes and symptomatic treatment
Patients with pneumothorax should rest in bed, preferably in a semi-recumbent position. For closed pneumothorax with lung compression <20%, if there are no obvious symptoms, air extraction may not be necessary, as rest often leads to spontaneous absorption within 1–2 weeks. However, patients with pre-existing impaired lung function may experience significant symptoms even with minimal air accumulation and should undergo air evacuation. To prevent secondary infection of pneumothorax, appropriate antibiotics such as penicillin (800,000 units, intramuscularly twice daily) may be administered. Patients with obvious dyspnea and hypoxia should receive oxygen therapy. Cough suppressants and sedatives may also be prescribed to facilitate rest. It is important to maintain bowel regularity to avoid straining. Underlying conditions should be actively treated.
Most cases of pneumothorax can be cured with active treatment. However, tension pneumothorax or cases with severe complications may be life-threatening if not treated promptly and properly. Recurrent pneumothorax can impair lung function.
Spontaneous pneumothorax, especially when the pleural membrane tear does not heal quickly or treatment is inadequate, can easily lead to pleural effusion; prolonged non-healing may result in a bronchopleural fistula; severe pleural infection or pulmonary abscess rupturing into the pleural cavity can cause pyopneumothorax; tearing of pleural adhesions or cancerous infiltration and rupture can lead to hemopneumothorax; mediastinal emphysema is a more severe complication of pneumothorax, often caused by tension pneumothorax gas entering the pulmonary interstitium, traveling along vascular sheaths or peribronchial spaces through the hilum into the mediastinum, frequently complicating left-sided pneumothorax. Severe cases may lead to respiratory and circulatory failure due to compression of mediastinal organs, also known as mediastinal air tamponade syndrome. Common manifestations include subcutaneous emphysema in the neck and anterior chest, which may extend to the face, abdomen, and even the whole body, with a typical crepitus sensation. Sometimes, Hamman's sign may be present, characterized by a crunching or crackling sound synchronous with the heartbeat heard over the precordium or lower sternum, caused by the heart beating against air-filled mediastinal tissues. X-ray imaging reveals gas-filled lucent bands around the mediastinum, heart, and major blood vessels.