Etiology

A primary spontaneous pneumothorax (PSP) occurs without preceding trauma or precipitating event, and develops in a person without clinically apparent pulmonary disease. Patients most at risk are those with a history of cigarette smoking, Marfan syndrome, homocystinuria, or family history of pneumothorax. Patients with PSP tend to be tall, slender, and young males.[12][13][14][15][16][17]

A secondary spontaneous pneumothorax occurs as a complication of an underlying pulmonary disease. COPD from cigarette smoking is the most common predisposing condition in the US and accounts for approximately 70% of these pneumothoraces. Other predisposing respiratory conditions include Pneumocystis jirovecii respiratory infection, cystic fibrosis, and tuberculosis. The severity of the patient's lung dysfunction correlates with the likelihood of developing a secondary spontaneous pneumothorax.[18][19][20][21] Catamenial pneumothorax occurs secondary to thoracic endometriosis.

A traumatic pneumothorax results from either penetrating or blunt injury to the chest or abdomen, and can be accompanied by hemothorax.

A tension pneumothorax can complicate primary and secondary spontaneous pneumothoraces as well as traumatic pneumothoraces.

Pathophysiology

Pneumothorax refers to gas within the pleural space. In a normal respiratory cycle, the alveolar pressure is greater than the intrapleural pressure, while the intrapleural pressure is less than atmospheric pressure. Therefore, if a communication develops between an alveolus and the pleural space, or between the atmosphere and the pleural space, gases will follow the pressure gradient and flow into the pleural space. This flow will continue until the pressure gradient no longer exists or the abnormal communication has been sealed. Because the thoracic cavity is normally below its resting volume, and the lung is above its resting volume, the thoracic cavity enlarges and the lung becomes smaller when a pneumothorax develops.[1]

A tension pneumothorax is a medical emergency and occurs when the intrapleural pressure exceeds atmospheric pressure, especially during expiration, and results from a ball valve mechanism that promotes inspiratory accumulation of pleural gases. This leads to a decrease in arterial partial pressure of oxygen and an increase in alveolar-arterial oxygen difference which lead to clinical decompensation. Increased intrathoracic pressure impairing venous return and limiting cardiac output also likely plays a role, as cardiac index has been observed to drop in tension pneumothorax.[1][22][23]​​

The pathophysiology of catamenial pneumothoraces is not well-described. There are four proposed theories for why it occurs, but none have been proven. The most widely accepted theory is diaphragmatic passage of air from the abdomen and genital tract through diaphragmatic fenestrations into the pleural cavity.[24] Other theories include: 1) a high concentration of prostaglandin F2 during menses leading to blood vessel/bronchiolar construction and alveolar rupture, 2) migration of endometrial cells through the diaphragm into the chest wall and visceral pleura, and 3) metastatic spread or pulmonary microembolization of endometrial cells from blood or lymph vessels (can also cause hemoptysis).[25]

Classification

Clinical classification[2]​​

Spontaneous pneumothoraces: occur without preceding trauma or precipitating event. This type of pneumothorax is further subdivided into the following, though this distinction is not as prominent as previously thought, given widespread utilization of high-resolution computed tomography and discovery of more blebs:[3]

  • Primary pneumothoraces: occur without clinically apparent pulmonary disease

  • Secondary pneumothoraces: occur as a complication of an underlying pulmonary disease, including catamenial pneumothorax secondary to thoracic endometriosis.

Traumatic pneumothorax: results from either penetrating or blunt injury to the chest. These may be the result of accidental or nonaccidental injury. Iatrogenic pneumothoraces are a form of accidental traumatic pneumothorax, and occur as a result of complications related to medical interventions. These include:

  • Transcutaneous needle aspiration of lung lesions, thoracentesis, bronchoscopic transbronchial lung biopsy, central venous catheter placement, and barotrauma as a sequelae of positive pressure mechanical ventilation.

Tension pneumothorax: occurs when the intrapleural pressure exceeds atmospheric pressure throughout expiration and often during inspiration. It is a medical emergency that requires prompt intervention.

Pneumothorax ex vacuo: is a rarely described form of pneumothorax and occurs via one of two mechanisms. 1) When rapid collapse of the lung (i.e., from mucus plugging) produces a decrease in the intrapleural pressure. It is most commonly seen in atelectasis of the right upper lobe. The increased negative intrapleural pressure causes gaseous nitrogen molecules to migrate from the pulmonary capillaries into the pleural space.[4] 2) When inflammatory pleural effusions cause thickening of the visceral pleura and prevent lung re-expansion after pneumothorax. It is commonly seen in malignant pleural effusions and can be a barrier to pleurodesis.[5]​​

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