Spontaneous Pneumothorax

Etiology

Spontaneous pneumothorax is categorized into 2 primary types: PSP and SSP, based on the presence or absence of underlying lung pathology. PSP occurs in individuals without clinically apparent lung disease, most commonly affecting young adults between the ages of 15 and 40 years. This condition is frequently associated with subpleural bleb rupture, often in tall, thin men. The annual incidence of PSP ranges from 7.4 to 24 per 100,000 in men and 1.2 to 6 per 100,000 in women.[5]

SSP, by contrast, occurs in patients with established pulmonary disease. Common causes include coronary obstructive pulmonary disease, asthma, cystic fibrosis, necrotizing pneumonia, Pneumocystis jirovecii infection, pulmonary abscess, tuberculosis, malignancy, and various forms of interstitial lung disease (eg, idiopathic pulmonary fibrosis, sarcoidosis, lymphangioleiomyomatosis). Additional etiologies include connective tissue disorders (eg, Marfan syndrome, Ehlers-Danlos syndrome, rheumatoid arthritis), pulmonary infarction, foreign body aspiration, and rare conditions such as Birt-Hogg-Dubé syndrome and catamenial pneumothorax secondary to thoracic endometriosis. SSP tends to affect older adults and carries a higher risk of morbidity due to underlying pulmonary compromise. Epidemiologic studies report an annual incidence of SSP of 6.3 per 100,000 in men and 2.0 per 100,000 in women.[6]

Epidemiology

Spontaneous pneumothorax occurs more frequently in adults than in children and is significantly more common in men than women across all age groups. In the United States, the estimated annual incidence of PSP in adults is 7.4 to 18 per 100,000 population in men and 1.2 to 6.0 per 100,000 in women.[7][8] SSP, which occurs in the context of underlying pulmonary disease, has a reported annual incidence of 6.3 per 100,000 men and 2.0 per 100,000 women. Spontaneous pneumothorax is relatively rare in the pediatric population, with an estimated annual incidence of 4.0 per 100,000 in boys and 1.1 per 100,000 in girls.[8] Risk factors for PSP include smoking, which significantly increases risk across age groups, and a tall, thin body habitus, especially in adolescent and young adult men.[7]

Epidemiologic trends underscore the clinical and healthcare impact of this condition. Results from a large-scale study in the United Kingdom (2017–2023) reported approximately 72,000 hospital admissions for spontaneous pneumothorax, highlighting its substantial burden on health systems.[9] Recurrence is a major concern, particularly in PSP, where rates reach approximately 32%, with 21% to 54% recurring within 1 to 2 years after the initial event. SSP tends to recur less frequently (13%–39%), but its association with significant underlying disease often results in more complex management and higher morbidity.[9]

Pathophysiology

The development of spontaneous pneumothorax arises from the accumulation of gas within the pleural space, a process driven by complex and multifactorial pathophysiological mechanisms. Central to this is the disruption of the alveolar-pleural barrier, typically caused by acute increases in transpulmonary pressure that exceed the tensile strength of the alveolar walls. These sudden pressure surges—commonly triggered by coughing, straining, or Valsalva maneuvers—can lead to alveolar rupture and air leakage into the pleural cavity.[10] 

Both primary and secondary spontaneous pneumothoraces are linked to elevated alveolar pressure exceeding pulmonary interstitial pressure, facilitating alveolar rupture and subsequent pleural air leakage. Structural weaknesses in the visceral pleura, including subpleural blebs, bullae, lung necrosis, and connective tissue abnormalities, predispose alveoli to rupture, although the precise mechanisms remain incompletely understood. Notably, intact bullae without overt visceral pleural defects have been associated with spontaneous pneumothorax. Histopathological and scanning electron microscopic analyses suggest that sloughing of pleural mesothelial cells may significantly contribute to pneumothorax pathogenesis.[11][12]

In PSP, rupture typically occurs at pre-existing sites of weakness such as subpleural blebs and bullae—lesions present in up to 77% of cases on imaging and histology. These lesions may develop secondary to alveolar overdistension, microvascular ischemia, or inflammatory remodeling, often linked to tobacco exposure.[10] Conversely, SSP occurs in the context of underlying lung disease, including COPD, interstitial lung disease, or necrotizing infections, which cause architectural distortion, alveolar wall thinning, and focal necrosis, compromising the alveolar-pleural interface.[6]

Additionally, the formation of alveolar–pleural fistulae or bronchopleural fistulae has been implicated in acute pneumothorax and persistent air leaks. These fistulous tracts represent direct communications between the alveolar or bronchial spaces and the pleural cavity. They are more frequently seen in SSP but can occur in advanced cases of PSP as well. The current understanding of spontaneous pneumothorax emphasizes not only mechanical rupture due to pressure gradients but also structural and microscopic defects in the pleura, airway remodeling, and inflammatory damage as key contributors to its onset and recurrence.

History and Physical

Spontaneous pneumothorax most commonly occurs at rest and without an exertional trigger. Patients typically present with sudden-onset, sharp, pleuritic chest pain on the affected side and acute dyspnea. Increased work of breathing is especially pronounced in those with SSP due to underlying lung disease. Tachycardia is one of the most frequent physical exam findings, although in smaller pneumothoraces (less than 15% of the hemithorax), the exam may be unremarkable. In larger cases (over 15%), clinicians may observe reduced chest wall movement, ipsilateral decreased or absent breath sounds, hyperresonance to percussion, decreased tactile fremitus, jugular venous distension, and pulsus paradoxus. A tension pneumothorax, though rare, represents a life-threatening complication characterized by hypoxemia, hypotension, and tracheal deviation away from the affected side.[13]

Evaluation

The diagnosis of spontaneous pneumothorax is often suggested by the patient’s history and physical exam findings, which can be confirmed by imaging. Chest radiography characteristically shows the displacement of the visceral pleural line with a space devoid of lung markings in between (see Image. Pneumothorax on Chest Radiography). While upright films are preferred, there is evidence that expiration does not necessarily increase the diagnostic yield. Ultrasound has also shown diagnostic potential. There is evidence that ultrasound has greater sensitivity than chest radiography; however, both modalities are limited in how well they estimate the size of a pneumothorax.

The use of chest computed tomography (CT) for diagnosing spontaneous pneumothorax has been debated. The high sensitivity and specificity of CT can be of value when there is a high index of suspicion for spontaneous pneumothorax, and initial imaging is negative or equivocal. While arterial blood gas measurements are not necessary for diagnosing spontaneous pneumothorax, they can be useful in assessing acute respiratory alkalosis and increases in the alveolar-arterial oxygen gradient when tension physiology is present.[14]

Treatment / Management

The main goal for the treatment of spontaneous pneumothorax is to evacuate the gas from the pleural space and prevent recurrences. The guidelines from the American College of Chest Physicians (ACCP) and the British Thoracic Society are focused mainly on managing pneumothorax in adults, but not specifically pediatric cases. Nevertheless, it is appropriate to initiate 100% oxygen via a nonrebreather mask and continuous cardiopulmonary monitoring for patients with spontaneous pneumothorax. Oxygen increases the rate of absorption of the gas from the pleural space up to 4-fold compared to the absorption of 1% to 2% of the volume per day without oxygen. Clinically unstable individuals with severe symptoms or symptoms suggestive of tension pneumothorax can be treated with emergent needle decompression as a bridge to tube thoracostomy placement.[15][16][17]

For stable patients presenting with a small PSP for the first time, conservative management with supplemental oxygen and observation of at least 6 hours is recommended. Suppose a repeat chest radiograph shows evidence of a stable pneumothorax and the patient has access to adequate follow-up. In that case, the patient can be discharged with strict return precautions for a 24-hour recheck. The British Thoracic Society suggests that certain asymptomatic individuals with large PSP may be considered for observation without active intervention. The ACCP recommends aspiration for large or symptomatic PSP with a small-bore catheter (14F or smaller) or admission with a chest tube (16F to 22F) if the initial aspiration fails. Larger PSP can be further managed with video-assisted thoracoscopic surgery (VATS) or thoracotomy to perform bullectomy, pleurectomy, and mechanical pleurodesis (ie, dry gauze abrasion). VATS is less invasive than thoracotomy and is an effective measure in the treatment and prevention of spontaneous pneumothorax recurrence.

Patients with recurrent PSP should be admitted with thoracostomy tube placement as a bridge to VATS. In patients who are unwilling to undergo VATS, are poor surgical candidates, or are being managed in an institution where VATS is not readily available, chemical pleurodesis can be performed with the introduction of irritants such as tetracyclines (ie, doxycycline, minocycline) or talc via the thoracostomy tube. The inflammatory processes associated with chemical pleurodesis lead to the formation of pleural adhesions that effectively obliterate the pleural space.

In adults presenting with SSP, both the ACCP and the British Thoracic Society recommend admission with supplemental oxygen and a repeat chest radiograph. The organizations also recommend placement of a pleural catheter or thoracostomy tube if the SSP is large, the patient is symptomatic, or the SSP is bilateral. Observation alone is not recommended, as there is an increased risk of mortality in SSP. Referral to a thoracic specialist is recommended, but not until the patient is stabilized with a chest drain.[3]

Differential Diagnosis

The differential diagnoses for spontaneous pneumothorax include:

• Myocardial infarction
• Aortic dissection
• Acute pericarditis
• Pulmonary embolism
• Rib and chest trauma

Prognosis

PSP generally has an excellent survival prognosis, with low associated mortality and prompt recovery in most individuals. However, recurrence is a substantial clinical concern. Recent epidemiological data from South Korea found a 5-year recurrence rate of about 20.3%, with significantly higher rates in men (eg, 20.8% in men vs 10.9% in women); intriguingly, those treated with conservative therapy had lower recurrence (7.9%) compared to those undergoing early surgical intervention (23.7%)—a finding that contrasts with traditional expectations and highlights the importance of personalized treatment decisions. Broad systematic reviews confirm a 32% overall recurrence rate, with most recurrences occurring within the first year following the initial episode. Significantly, recurrence likelihood is influenced by age (ie, younger than 20), presence of blebs/bullae, male sex, and conservative management without intervention.[18] Surgical approaches—especially VATS combined with pleurodesis—can substantially reduce the long-term risk, often lowering recurrence to under 10%. 

In contrast, SSP carries a more guarded prognosis, reflecting higher morbidity, mortality, recurrence, and healthcare resource use. One large retrospective cohort reported a 2.3% in-hospital mortality rate and a 9% overall recurrence rate, with both adverse events strongly associated with poor functional status, comorbidities, and larger pneumothorax size.[19] Data also show that up to 41% of those with SSP experience complications, including persistent air leaks in 13.5%. Compared to PSP, patients with SSP endure more extended hospital stays, more frequent persistent leaks, and less favorable recovery trajectories. Surgical repair via VATS is associated with a mortality rate of approximately 2% to 4% and significantly reduced recurrence rates (0%–15.8%). However, patients with interstitial lung disease have higher postoperative mortality, reaching up to 15%, compared with those who have chronic obstructive pulmonary disease.

Complications

Spontaneous pneumothorax, while often manageable in otherwise healthy individuals, can lead to a range of complications that significantly impact morbidity and clinical outcomes, particularly in cases of SSP. One of the most common and well-documented complications is recurrence, with PSP showing a 5-year recurrence rate of approximately 30% and SSP recurrence rates approaching 43%. The risk of recurrence is higher in younger male patients and those treated with nonsurgical approaches. Another significant complication is the development of a persistent air leak (PAL), defined as continued air passage through a chest tube beyond 5 to 7 days, or 48 hours in patients with SSP. PALs are reported in approximately 16% of PSP and over 30% of SSP patients managed with tube thoracostomy.[20] Persistent leaks can be caused by bronchopleural or alveolopleural fistula, often necessitating prolonged hospital stays or advanced interventions such as surgical repair or endobronchial valve placement.

Although rare, tension pneumothorax remains the most life-threatening complication. This condition presents with hypotension, hypoxemia, tracheal deviation, and mediastinal shift, requiring immediate needle decompression followed by definitive chest tube placement. Reexpansion pulmonary edema is another serious but infrequent complication, occurring when a large or longstanding pneumothorax is rapidly evacuated, particularly if the lung has been collapsed for over 72 hours or if more than 2 liters of air are removed quickly. This complication can manifest as sudden hypoxia and respiratory distress, and has been reported in up to 46% of delayed cases.

Infectious complications can also arise, particularly in patients with indwelling chest tubes. These may include empyema, pleuritis, or even pyopneumothorax, especially if sterile technique is compromised or drainage is prolonged. In addition, bronchopleural and alveolopleural fistulae—the underlying mechanism behind many PALs—are reported in nearly 35% of spontaneous pneumothorax cases, particularly in those with structural lung disease or necrosis. 

Finally, complications related to thoracostomy procedures themselves include bleeding, hemothorax, intercostal nerve injury, subcutaneous emphysema, and localized infection. Although rare, these can add significant morbidity, especially in elderly or comorbid populations. As newer strategies like ambulatory catheter systems and surgical pleurodesis gain traction, complication profiles may shift. Still, the core risks, especially persistent air leak and recurrence, remain pivotal in determining long-term outcomes.