Aetiology
General risk factors for spontaneous pneumothorax include:
Smoking[8]
This is the most important risk factor; men who smoke increase their risk of a first pneumothorax 22-fold and women 9-fold compared with non-smokers[7]
Family history of pneumothorax[9]
Tall and slender body build[8]
Male sex[8]
Young age[8]
However, secondary spontaneous pneumothorax is more common in people aged >55 years
Presence of underlying lung disease such as:
COPD
Severe asthma
Tuberculosis
Pneumocystis jirovecii infection
Cystic fibrosis
Structural abnormalities (e.g., Marfan syndrome, Ehlers-Danlos syndrome)[10]
Homocystinuria[9]
Menstruation
A traumatic pneumothorax results from either penetrating or blunt injury to the chest.[12]
A tension pneumothorax can complicate primary and secondary spontaneous pneumothoraces as well as traumatic pneumothoraces. It is also more likely in patients with the following risk factors:
Ventilated patients
Following trauma (especially penetrating chest wounds) or cardiopulmonary resuscitation
Lung disease, especially acute presentations of asthma and bullous COPD, or in long-standing underlying lung disease such as cystic fibrosis, bronchiectasis, fibrotic lung diseases, or lung cancer
Blocked chest drain
Patients receiving non-invasive ventilation (NIV)
Other (e.g., hyperbaric oxygen treatment)
Pneumothorax ex vacuo may occur following an invasive medical procedure (e.g., drainage of pleural effusion or CT-guided lung biopsy).[13][14]
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.
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.[15][16]
The pathophysiology of catamenial pneumothoraces is not fully understood. 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.[17] Other theories include:[18]
A high concentration of prostaglandin F2 during menses leading to blood vessel/bronchiolar construction and alveolar rupture
Migration of endometrial cells through the diaphragm into the chest wall and visceral pleura
Metastatic spread or pulmonary microembolisation of endometrial cells from blood or lymph vessels (can also cause haemoptysis).
Classification
Clinical classification[1]
Spontaneous pneumothorax: occurs without preceding trauma or precipitating event. This type of pneumothorax is further subdivided into the following:
Primary pneumothorax: occurs without clinically apparent pulmonary disease
Secondary pneumothorax: occurs as a complication of an underlying pulmonary disease, including COPD, asthma, and thoracic endometriosis (catamenial pneumothorax).
The distinction between primary and secondary spontaneous pneumothorax is becoming increasingly blurred in practice. Seek senior or specialist advice if you are in any doubt about which type of pneumothorax your patient has.
In theory, a patient with any underlying respiratory diagnosis should be considered to have a secondary, rather than primary, spontaneous pneumothorax. Most cases of secondary spontaneous pneumothorax are in patients with COPD.[2]
However, in practice, a patient with a history of only very mild respiratory disease might be managed as a primary spontaneous pneumothorax - for example, a patient with mild, intermittent asthma with no exacerbation of symptoms at presentation with the pneumothorax.
Traumatic pneumothorax: results from either penetrating or blunt injury to the chest. These may be the result of accidental or non-accidental injury.
Iatrogenic pneumothorax is a form of accidental traumatic pneumothorax, and occurs 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 decompression.
Pneumothorax ex vacuo: a rarely described form of pneumothorax that occurs via one of two mechanisms:
When rapid collapse of the lung (i.e., from mucous 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.
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.[3]
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