The pleural cavity is a closed, potential space without air. Under normal circumstances, the pleural cavity is under negative pressure. Any condition that allows air to enter the pleural cavity, resulting in an accumulation of air, is termed pneumothorax. Pneumothorax can be classified into spontaneous pneumothorax, traumatic pneumothorax, and iatrogenic pneumothorax. Spontaneous pneumothorax is further divided into primary spontaneous pneumothorax and secondary spontaneous pneumothorax. The former occurs in healthy individuals without underlying lung diseases, while the latter commonly affects patients with underlying lung diseases. Traumatic pneumothorax results from direct or indirect injury to the chest wall due to external trauma. Iatrogenic pneumothorax is caused by diagnostic or therapeutic procedures. Pneumothorax is a common medical emergency, with a higher incidence in males than in females. The incidence of primary spontaneous pneumothorax is (18-28)/100,000 in males and (1.2-6)/100,000 in females. After the occurrence of pneumothorax, the negative pressure within the pleural cavity can turn into positive pressure, impeding venous return and leading to cardiopulmonary dysfunction.
Etiology and pathogenesis
Under normal circumstances, there is no air in the pleural cavity because the total gas pressure in the capillary blood is only 706 mmHg, which is 54 mmHg lower than the atmospheric pressure. The total gas pressure in the pleural capillaries is lower than the atmospheric pressure, so there is no air in the pleural cavity. Additionally, due to the outward expansion force of the thoracic cage and the inward recoil force of the lung tissue, the pressure in the pleural cavity is negative throughout the respiratory cycle.
Air enters the pleural cavity only in three situations:
- Damage between the alveoli and the pleural cavity
- Communication between the chest wall and the external environment due to trauma
- Presence of gas-producing microorganisms in the pleural cavity
Clinically, the first two causes are most common. In pneumothorax, the traction effect of the negative pressure in the pleural cavity on the lung is lost, and even positive pressure may compress the lung, preventing the lung from expanding, which results in reduced lung volume, decreased vital capacity, and reduced maximum ventilation, leading to restrictive ventilatory dysfunction. Due to the reduction in lung volume, blood flow does not initially decrease, leading to a decrease in the ventilation-perfusion ratio, leading to arteriovenous shunt and hypoxemia. In massive pneumothorax, the negative pressure that attracts venous blood back to the heart is absent, and even the positive pressure in the pleural cavity compresses the blood vessels and heart, reducing cardiac filling and output, leading to tachycardia, hypotension, and even shock. Tension pneumothorax can cause mediastinal shift, circulatory disturbances, asphyxiation，and even death.
Primary spontaneous pneumothorax (PSP)
PSP occurs in healthy individuals without underlying lung diseases, but the rupture of subpleural blebs and bullae may be the primary mechanism of pneumothorax. Studies have shown that cigarette smoking, body type, and family history are risk factors. This type is more common in tall, thin, young males. Routine chest x-ray shows no significant abnormalities, but there may be subpleural blebs, mostly in the lung apex. The cause of these subpleural blebs is not clear, possibly related to cigarette smoking, height, and small airway inflammation, or possibly related to nonspecific inflammatory scars or congenital elastic fiber dysplasia.
Secondary spontaneous pneumothorax (SSP)
SSP is most common and mostly in patients with underlying lung diseases. Partial obstruction and distortion of bronchioles caused by lesions result in the formation of one-way valve, leading to local overinflation of alveoli, destruction and fusion of alveolar walls, and the formation of bullae. When the intrapulmonary pressure suddenly increases, the bullae rupture under the visceral pleura, forming pneumothorax. Conditions include pulmonary tuberculosis, chronic obstructive pulmonary disease (COPD), lung cancer, lung abscess, pulmonary fibrosis, eosinophilic granuloma, sarcoidosis, pneumoconiosis, and lymphangioleiomyomatosis. Due to the presence of underlying lung diseases, patients with secondary spontaneous pneumothorax have more severe clinical symptoms and lower tolerance to pneumothorax compared to those with primary spontaneous pneumothorax, so most patients require active intervention.
Special pneumothorax
Catamenial pneumothorax
Catamenial pneumothorax is recurrent pneumothorax associated with the menstrual cycle, accounting for 0.9% of female spontaneous pneumothorax patients. Catamenial pneumothorax occurs only within 24 - 72 hours before or after menstruation. The pathogenesis is not clear, but it is mainly due to the rupture of ectopic endometrial nodules on the lung, pleura, or diaphragm.
Pneumothorax in pregnancy
This condition occurs in patients with each pregnancy, and based on the time to occurrence, it can be divided into early pneumothorax (3 - 4 months of pregnancy) and late pneumothorax (over 8 months of pregnancy). The pathogenesis is unclear, possibly related to hormonal changes and alterations in thoracic compliance.
Clinical classification
Based on the condition of the visceral pleural rupture and its impact on the intrathoracic pressure, spontaneous pneumothorax is typically classified into the following three types.
Closed (simple) pneumothorax
The pleural rupture is small and closes as the lung collapses, preventing further air from entering the pleural cavity. The pressure in the pleural cavity is close to or higher than atmospheric pressure, and does not increase after aspiration.
Open (communicating) pneumothorax
The rupture is large or persists due to adhesions or traction between the two layers of the pleura, allowing air to freely enter and exit the pleural cavity during inhalation and exhalation. The pressure in the pleural cavity fluctuates around 0 cm H2O; after aspiration, it may turn negative, but in few minutes, the pressure returns to the level before aspiration.
Tension (high-pressure) pneumothorax
The rupture acts as a one-way valve or piston. During inhalation, the thoracic cavity expands, pleural cavity pressure decreases, and air enters through the rupture. During exhalation, the thoracic cavity contracts, increasing the pleural pressure and closing the valve, trapping air within the pleural cavity. This causes the pressure in the pleural cavity to continuously rise, compressing the lung and shifting the mediastinum to the healthy side, affecting venous return to the heart. The pressure in the pleural cavity in this type often exceeds 10 cm H2O, and can even reach 20 cm H2O. After aspiration, the pressure in the pleural cavity may decrease, but it quickly rises again. This type has the most significant impact on respiratory and circulatory functions and requires emergency treatment.
Clinical manifestations
The severity of symptoms is related to the presence of underlying lung diseases and their functional status, the speed of pneumothorax development, and the amount of air and pressure in the pleural cavity.
The severity of dyspnea is closely related to the baseline lung function, the degree of lung collapse, and the speed of onset. Young individuals with normal lung function may not experience significant dyspnea, while patients with severe underlying lung diseases, such as COPD, may have significant dyspnea even with mild lung compression. In chronic pneumothorax, the healthy lung has already compensated, often presenting with mild tachypnea. Patients with mediastinal emphysema may have more pronounced dyspnea, and even cyanosis.
There is usually sudden, sharp, stabbing pain in the anterior chest or axilla on one side, lasting for a short period and exacerbating with inspiration, sometimes radiating to the shoulder, back, or upper abdomen. The severity of thoracodynia is unrelated to the degree of lung compression.
Irritative dry cough is caused by pleural irritation from air, generally mild, with no or little sputum, sometimes bloody.
Secondary spontaneous pneumothorax often presents with more severe symptoms than primary spontaneous pneumothorax. In tension pneumothorax, the sudden increase in pleural cavity pressure compresses the lung and shifts the mediastinum, rapidly causing severe respiratory and circulatory disturbances. Patients may experience extreme anxiety, chest tightness, restlessness, cyanosis, diaphoresis, tachycardia, collapse, arrhythmia, and even unconsciousness and respiratory failure.
Signs depend on the amount of air in the pleural cavity. Small amounts of pneumothorax may have no obvious signs, especially in patients with emphysema, where reduced breath sounds are particularly important. In large pneumothorax, the trachea shifts to the healthy side, the affected chest bulges, respiratory movements and tactile fremitus are reduced, percussion reveals hyperresonance or tympany, and cardiac or hepatic dullness may be diminished or absent. Breath sounds are reduced or absent on auscultation. In small pneumothorax on the left side or mediastinal emphysema, a ticking or crackling sound synchronized with the heartbeat may sometimes be heard at the left cardiac border, which is termed Hamman sign. In hydropneumothorax, there is a splashing sound (succussion splash) in the chest. In hemopneumothorax, excessive blood loss can cause hypotension, and even hemorrhagic shock.
Imaging and other examinations
Chest x-ray
A posteroanterior (PA) upright chest x-ray is a crucial method for diagnosing pneumothorax. It can reveal the degree of lung compression, the presence of lung lesions, and whether there is pleural adhesion, pleural effusion, or mediastinal shift. The typical sign of pneumothorax is convex, curvilinear opacity, which is the boundary line between the lung tissue and the air in the pleural cavity, known as pneumothorax line. Inside this line is the compressed lung tissue, while outside the line, the lucency increases, and there is no lung tissue. In case of massive pneumothorax, the lung is compressed to the hilum, showing a spherical opacity, often accompanied by mediastinal shift towards the healthy side.
Figure 1 Right pneumothorax on the frontal chest x-ray
Pulmonary tuberculosis or chronic inflammation of the lungs can cause multiple pleural adhesions, resulting in localized encapsulation of pneumothorax, and sometimes multiple lesions can interconnect with each other. If pneumothorax extends to the lower part of the thoracic cavity, the costophrenic angle becomes sharp. In case of concurrent pleural effusion, air-fluid level can be seen. Localized pneumothorax can be easily missed on PA chest x-ray, but lateral chest x-ray can assist in diagnosis.
Clinically, the degree of lung compression after pneumothorax can be estimated using chest x-ray films. For example, the size of pneumothorax can be estimated from the pneumothorax line at the apex of the lung to the top of the thoracic cavity. A distance ≥ 3 cm indicates a large pneumothorax, while the distance < 3 cm indicates a small pneumothorax. At the level of the hilum, 1 cm from the lateral chest wall to the lung edge represents approximately 25% of the volume of the unilateral thoracic cavity, and 2 cm represents about 50%. Therefore, a distance ≥ 2 cm from the lateral chest wall to the lung edge represents a large pneumothorax, while the distance < 2 cm represents a small pneumothorax.
Figure 2 Pneumothorax volume measurement
Chest CT
Chest CT is more sensitive and accurate than chest x-ray for detecting small and localized pneumothorax and distinguishing between pulmonary bullae and pneumothorax. It also provides more accurate assessment of the size of pneumothorax. The findings include the presence of extremely hypodense gas opacity in the pleural cavity, accompanied by lung compression.
Blood gas analysis and pulmonary function test
Most patients with pneumothorax have abnormal arterial blood gas analysis, characterized by decreased PaO2 and usually normal or decreased PaCO2. Pulmonary function test is not very helpful in detecting the occurrence or volume of pneumothorax, and is not recommended for routine clinical evaluation.
Diagnosis
Pneumothorax can generally be confirmed based on clinical symptoms, signs, and imaging findings. The presence of pneumothorax line on x-ray or CT is the definitive basis for diagnosis. If patient develops sudden dyspnea and cannot be moved for imaging, prompt thoracentesis should be performed at the site with the most prominent signs on the affected side. If gas is aspirated, the diagnosis of pneumothorax can be confirmed.
Differential diagnosis
Spontaneous pneumothorax, especially in older patients or those with preexisting chronic heart or lung diseases, can resemble other cardiac and pulmonary emergencies and requires careful differentiation.
Asthma and chronic obstructive pulmonary disease (COPD)
Both conditions can present with dyspnea during acute exacerbations, similar to spontaneous pneumothorax. Asthma patients often have a history of recurrent paroxysmal wheezing episodes, while COPD patients typically experience a long-term, progressive dyspnea. If asthma or COPD patients suddenly develop severe dyspnea, diaphoresis, and restlessness, with poor response to bronchodilators and antibiotics, and symptoms exacerbate, the possibility of concurrent pneumothorax should be considered. Chest x-ray or CT scans can aid in differentiation.
Acute myocardial infarction
Patients presents with sudden thoracodynia, chest tightness, and even syspnea and shock, often with a history of hypertension, atherosclerosis, and coronary artery disease. Physical examination, ECG, x-ray or CT, and serum enzyme test can aid in diagnosis.
Acute pulmonary embolism
Large pulmonary embolism can present with acute dyspnea, thoracodynia, restlessness, panic, or impending doom sensation, analogous to spontaneous pneumothorax. However, patients may also have hemoptysis, low-grade fever, and syncope, often with a history of deep vein thrombosis, fractures, postoperative conditions, stroke, or atrial fibrillation. This condition occurs also in older bedridden patients. CT pulmonary angiography can help differentiate.
Pulmonary bullae
Peripheral pulmonary bullae, especially giant bullae, can be mistaken for pneumothorax. Pulmonary bullae typically develop slowly and do not cause severe dyspnea, while pneumothorax suddenly occurs. On imaging, pulmonary bullae show round or oval air-filled cavities with fine linear markings, which are remnants of lung lobules or blood vessels. Pulmonary bullae expand peripherally, compressing the lung towards the apical region, costophrenic angle, and cardiophrenic angle. Pneumothorax shows lucent band on the lateral chest wall with no visible lung markings. Chest x-ray from different angles shows pulmonary bullae as circular lucent areas without pneumothorax line. The pressure inside pulmonary bullae is close to atmospheric pressure, and aspiration does not significantly alter their volume. Misdiagnosed aspiration from pulmonary bullae can lead to pneumothorax.
Other conditions
Other conditions include perforated peptic ulcers, pleurisy, costochondritis, lung cancer, and diaphragmatic hernia. Occasionally, sudden thoracodynia, upper abdominal pain, and dyspnea may present and should also be differentiated from spontaneous pneumothorax.
Severity assessment
To facilitate clinical observation and management, spontaneous pneumothorax is classified into stable spontaneous pneumothorax and unstable spontaneous pneumothorax based on clinical presentation.
Stable spontaneous pneumothorax meets all the following criteria:
- Respiratory rate < 24 breaths per minute
- Heart rate of 60 - 120 beats per minute
- Normal blood pressure
- SaO2 > 90% while breathing room air
- Ability to speak in full sentences between breaths
Otherwise, the condition is unstable spontaneous pneumothorax.
Treatment
The goals are to promote reexpansion of the affected lung, eliminate the cause, and reduce recurrence. Common treatment methods include conservative treatment, thoracic decompression and air evacuation (thoracentesis and closed thoracic drainage), pleurodesis, and surgical treatment. The specific treatment should be based on the type and cause of pneumothorax, frequency of episodes, degree of lung compression, clinical status, and presence or absence of complications.
Factors affecting lung reexpansion include the age, underlying lung disease, type of pneumothorax, duration of lung collapse, and treatment measures. Lung reexpansion generally requires more time in older patients; open pneumothorax requires more time than closed pneumothorax; patients with underlying lung disease or prolonged lung collapse also require more time; and bed rest alone results in slower reexpansion compared to closed thoracic drainage or thoracentesis. Conditions such as bronchopleural fistula, thickened visceral pleura, and bronchial obstruction can hinder lung reexpansion and may lead to chronic persistent pneumothorax.
Conservative treatment
Indications for conservative treatment typically include:
- Stable small pneumothorax with lung compression less than 20% and no significant symptoms
- First occurrence with no obvious lung bullae on CT
- No hemothorax
Patients should rest in bed, be observed, receive oxygen therapy, and be given sedatives or analgesics as needed while waiting for the air to be resorbed spontaneously.
In spontaneous pneumothorax patients, the resorption rate of air per 24 hours (as seen on chest x-ray) is 1.25% - 2.20%. High-concentration oxygen can increase PaO2 in blood, reducing nitrogen partial pressure, thereby increasing the nitrogen pressure gradient between the pleural cavity and blood, promoting the transfer of nitrogen from the pleural cavity into the blood (nitrogen-oxygen exchange), accelerating air resorption, and promoting lung reexpansion. Inhaling oxygen at a rate of 10 L/min through nasal cannula or mask can be effective. Patients under conservative treatment should be closely monitored, especially within 24 - 48 hours after pneumothorax occurrence. In older patients, patients with underlying lung diseases such as COPD, and patients with slow healing of pleural rupture and severe symptoms, conservative treatment is generally not recommended even if pneumothorax is small.
Air evacuation treatment
When lung compression due to pneumothorax exceeds 20%, especially in patients with poor lung function or underlying lung disease, air evacuation is the primary measure. Tension pneumothorax and open pneumothorax require emergency air evacuation.
Thoracentesis is indicated in closed pneumothorax patients with unilateral pneumothorax with 20% - 50% lung compression, mild dyspnea, and good cardiopulmonary function. The puncture site is usually the second intercostal space along the midclavicular line on the affected side, or the fourth, fifth, or sixth intercostal space in the anterior axillary area. Localized pneumothorax requires CT-guided puncture. After skin disinfection, a pneumothorax needle or fine catheter is used to puncture the chest cavity, connected to a 50ml or 100ml syringe for air evacuation until dyspnea is relieved. The maximum air volume removed should not exceed 1,000 ml, and air can be evacuated daily or every other day based on lung reexpansion. In tension pneumothorax, rapid decompression is necessary to prevent severe complications. In emergencies without thoracic drainage equipment, a large needle can be used to quickly puncture the pleural cavity for decompression.
Closed thoracic drainage is indicated in unstable pneumothorax patients with significant dyspnea, severe lung compression, open or tension pneumothorax, and recurrent pneumothorax. Regardless of pneumothorax volume, early closed thoracic drainage is recommended. Secondary pneumothorax patients require drainage but may have poorer outcomes than primary pneumothorax patients, sometimes needing repeated drainage. The insertion site is typically the second intercostal space lateral to the midclavicular line or the fourth to fifth intercostal space along the anterior axillary line. For localized pneumothorax or pleural effusion drainage, the site is chosen based on x-ray or CT findings. Under local anesthesia, a 1.5 - 2 cm skin incision is placed parallel to the upper edge of the rib, a trocar needle is used to puncture the pleural cavity, and a sterile catheter is inserted through the trocar. Alternatively, intercostal tissue is bluntly dissected to the pleura, and the catheter is directly inserted. A 16 - 22F catheter is suitable for most patients, while a 24 - 28F catheter is recommended for bronchopleural fistula or mechanical ventilation patients. The catheter is connected to a water-sealed bottle 1 - 2 cm below the water surface, maintaining pleural pressure at -1 to -2 cm H2O. Successful insertion results in continuous bubbling, rapid dyspnea relief, and lung reexpansion within hours to days. In patients with severe or prolonged lung compression, the drainage tube should be clamped for intermittent drainage to prevent reexpansion pulmonary edema caused by sudden reduction in intrapleural pressure. If no air bubbles are observed and dyspnea resolves, the tube can be clamped for 24 hours after 24 - 48 hours of observation, and if the condition remains stable or x-ray shows full lung reexpansion, the catheter can be removed. Approximately 70% of patients achieve lung reexpansion after three days of closed drainage. If bubbling persists but symptoms do not improve, catheter obstruction or partial dislodgement from the pleural cavity should be considered, and catheter replacement or other interventions are required.
Figure 3 Water-sealed bottle closed thoracic drainage
PSP often achieves full lung reexpansion with catheter drainage, but SSP may require multiple catheters due to septation. Bilateral pneumothorax may require bilateral drainage. If the pleural rupture does not heal after water-sealed drainage, continuous bubbling indicates the need for negative pressure drainage. Low negative pressure suction is recommended, and if the suction pressure is too high, a pressure-regulating bottle can be used to adjust the pressure, typically -10 to - 20 cm H2O. If the negative pressure exceeds the set value, air enters the pressure-regulating bottle, ensuring the suction pressure in the pleural cavity does not exceed the set value, avoiding excessive suction damage to the lung.
Figure 4 Negative pressure suction water bottle
Continuous negative pressure suction is preferred; if lung reexpansion is not achieved in 12 hours, the cause should be investigated. Absence of bubbles indicates lung reexpansion, allowing suction cessation and observation for 2 - 3 days. If chest x-ray confirms no pneumothorax recurrence, the drainage tube can be removed. The water-sealed bottle should be placed below the patient's chest to prevent backflow into the pleural cavity. During catheter drainage, sterilization should be ensured to prevent infection.
Pleurodesis
Due to the high recurrence rate of pneumothorax, sclerosing agents can be injected into the pleural cavity to induce sterile pleuritis, causing adhesion between visceral and parietal pleura, eliminating the pleural space, and preventing recurrence.
Pleurodesis is indicated in patients who are not candidates for or refuse surgery, including:
- Persistent or recurrent pneumothorax
- Bilateral pneumothorax
- Concurrent lung bullae
- Impaired lung function, inability to tolerate surgery
Common sclerosing agents include talc, povidone-iodine, doxycycline, and tetracycline, diluted in 60-100 ml saline and injected through the thoracic catheter. The catheter is clamped for 1 - 2 hours before drainage, or talc can be sprayed under thoracoscopic guidance. Before injection of the sclerosing agent, full lung reexpansion should be achieved with closed thoracic drainage. To avoid local pain from the agent, lidocaine can be injected, allowing the patient to change positions for pleural anesthesia, and the sclerosing agent is injected in 15 - 20 minutes. If one injection is ineffective, repeated injections can be performed. After injection, 1 - 3 days of observation are required, and if chest x-ray confirms pneumothorax resorption, the drainage tube can be removed. Main side effects include thoracodynia and fever. Talc can cause acute respiratory distress syndrome, requiring caution.
Endobronchial occlusion
Microballoons or emboli are used to occlude the bronchus, causing distal lung atelectasis to close the bullous rupture. This should be performed under intercostal drainage. After microballoon insertion (silicone balloon), bubbling in the water-sealed bottle can be observed. If bubbling stops, the position is correct. After several days of observation, the balloon is released to check for bubbling; absence indicates closure. Endobronchial embolization can use silicone plugs, fibrin glue, and autologous blood.
Surgical treatment
While most patients can be temporarily cured with thoracentesis or closed thoracic drainage, over 30% of patients experience persistent or recurrent pneumothorax. The likelihood of recurrence increases with each episode. Effective treatment for recurrent spontaneous pneumothorax is surgical resection of lung bullae in combination with pleurodesis. Surgery is also indicated in chronic pneumothorax, hemopneumothorax, bilateral pneumothorax, recurrent pneumothorax, failed tension pneumothorax drainage, pleural thickening causing incomplete lung expansion, and imaging showing multiple lung bullae. Surgical treatment has a high success rate and low recurrence rate.
Complications
Pyopneumothorax
Pyopneumothorax can result from pneumonia, lung abscesses, and caseous pneumonia caused by Staphylococcus aureus, Klebsiella pneumoniae, Pseudomonas aeruginosa, Mycobacterium tuberculosis, and various anaerobic bacteria, and can also result from iatrogenic infections during thoracentesis or intercostal drainage. The condition is often severe, frequently leading to bronchopleural fistula formation. Pathogens can be detected in the pus. Besides antibiotic treatment, catheter drainage and pleural lavage with saline are recommended. Surgery may be considered based on the specific situation.
Hemopneumothorax
Pneumothorax with hemorrhage into the pleural cavity is often related to the rupture of blood vessels within pleural adhesions. Hemorrhage typically stops spontaneously once the lung fully reexpands. If hemorrhage persists, in addition to air evacuation, fluid drainage, and appropriate blood transfusion, surgical intervention to ligate the blood vessels should be considered.
Mediastinal and subcutaneous emphysema
Air escaping from ruptured alveoli can enter the lung interstitium, forming interstitial emphysema. This air can travel along vascular sheaths into the mediastinum and even into subcutaneous tissues of the neck, chest, or abdomen, resulting in subcutaneous emphysema. After thoracentesis or closed drainage of tension pneumothorax, subcutaneous emphysema can occur along needle tracks or incisions, potentially spreading throughout the body or into the mediastinum. Most patients are asymptomatic, though neck swelling due to subcutaneous air accumulation may occur. Air accumulation in the mediastinal space can compress major vessels, causing dry cough, dyspnea, emesis, and retrosternal pain radiating to the shoulders or arms. Pain is often exacerbated by breathing or swallowing. Symptoms include cyanosis, jugular vein distention, tachycardia, hypotension, diminished or absent cardiac dullness, and distant heart sounds. Chest x-ray may show a lucent band along the mediastinum or cardiac border (mainly the left heart border). Subcutaneous and mediastinal emphysema usually resolve spontaneously as thoracic air is evacuated and pressure is relieved. High-concentration oxygen inhalation can increase mediastinal oxygen concentration, aiding in emphysema resolution. If mediastinal emphysema is severe enough to affect respiration and circulation, incision and drainage in the suprasternal notch can be performed.
Prevention
The best prevention is to eliminate the cause and properly treat the primary condition. Patients with pneumothorax should avoid air travel, as high altitudes can exacerbate the condition and lead to serious consequences. Flying is generally safe one week after full lung reexpansion. It is recommended patients who have not undergone surgical treatment should avoid air travel for one year after pneumothorax occurrence.