1

What is a pneumothorax (Figure 1)?

A pneumothorax is defined as air within the pleural space (between the visceral and parietal pleura) separating the lung from the chest wall.

It may cause secondary collapse of the ipsilateral lung or haemodynamic compromise (associated with a tension pneumothorax).

2

How are pneumothoraces classified?

Pneumothoraces can be classified according to the:

a)

presence of an open chest wound – closed vs. open;

b)

presence of a tension pneumothorax – simple vs. tension;

c)

presence of trauma – spontaneous vs. traumatic.

Spontaneous pneumothorax – occurs in the absence of any trauma:

a)

primary – occurs in the absence of any known underlying pulmonary disease;

b)

secondary – related to the presence of underlying pulmonary disease.

Traumatic pneumothorax – occurs following injury to the visceral or parietal pleura:

a)

iatrogenic;

b)

penetrating chest trauma;

c)

blunt chest trauma.

3

What is the aetiology of a pneumothorax?

Primary spontaneous pneumothorax is caused by the rupture of apical blebs, which lie just under the visceral pleura (Figures 2 and 3). Their exact aetiology is unclear but it is thought that these blebs may represent a form of interstitial emphysema. They are usually less than 3cm in size and are located at the apex of the upper and lower lobes. Primary spontaneous pneumothorax has been linked to genetic disorders, such as Marfan syndrome, Birt-Hogg-Dube syndrome and homocystinuria.

Secondary spontaneous pneumothorax is caused by ruptured bullae following pathological destruction of the pulmonary parenchyma in patients with:

a)

airway disease – chronic obstructive pulmonary disease (COPD), emphysema, cystic fibrosis;

b)

pulmonary infection – tuberculosis, pneumocystis pneumonia;

c)

interstitial lung disease – sarcoidodsis, pulmonary fibrosis, histiocytosis X;

d)

tumours – lung cancer or metastases;

e)

catamenial – focal endometrial deposits on the visceral pleura;

f)

connective tissue disorders – Marfan syndrome, Ehlers Danlos syndrome, rheumatoid arthritis.

Traumatic iatrogenic pneumothorax can be caused following a diagnostic or therapeutic medical intervention, such as a lung biopsy, thoracocentesis, thoracic surgery, central line insertion or associated with mechanical ventilation-induced barotrauma.

Penetrating chest trauma can cause a pneumothorax following a stab wound or gunshot wound to the chest, or be associated with an oesophageal or tracheal perforation.

Blunt chest trauma can cause a pneumothorax, secondary to a rib fracture-induced pulmonary parenchymal tear.

4

What is the epidemiology of a pneumothorax?

The incidence of spontaneous pneumothoraces has a bimodal age distribution, with a peak in the young (aged 20-30) for primary pneumothoraces and a peak in the eldery (aged 60-65) for secondary pneumothoraces.

Primary spontaneous pneumothoraces are more common in tall men (male to female ratio 6:1) and over 80% are smokers. Smoking increases the risk by 10-20-fold, with the risk increasing proportionally to the number of cigarettes smoked.

Catamenial pneumothoraces occur in women (usually aged 25-45) within 3 days of menstruation. They are usually right-sided, often recurrent and may be associated with an ipsilateral haemothorax.

5

What is the pathophysiology of a pneumothorax (Figure 4)?

The lungs remain inflated within the thoracic cavity because the intrapleural pressure remains negative throughout the respiratory cycle.

A pneumothorax occurs when air is allowed to enter through the chest wall or the lung, thereby connecting the pleural space to atmospheric pressure and removing the fixed negative intrathoracic pressure.

As the ingress of air continues into the pleural space, the lung separates from the chest wall.

Once the defect in the chest wall or lung has been closed, air within the pleural cavity is gradually resorbed.

Tension pneumothorax is caused by the presence of a one-way valve mechanism allowing air inflow to the pleural space but no outflow. This results in increasing intrapleural pressure (greater than atmospheric pressure) and subsequent ipsilateral lung collapse, causing hypoxia. As the pressure increases further, progressive mechanical mediastinal shift causes compression on the contralateral lung and cardiovascular structures, resulting in impaired venous return (caval compression) and reduced cardiac output.

6

What are the complications of a pneumothorax (Figure 5)?

Lung collapse (and subsequent respiratory compromise).

Persistent air leak (bronchopleural fistula) – caused by failure of the pulmonary or chest wall defect to seal.

Haemothorax – caused by tearing of vascular adhesions between the lung and chest wall, when the lung collapses.

Pneumomediastinum – caused by dissection of air along the bronchovascular structures.

Recurrence of pneumothorax.

Contralateral pneumothorax.

Subcutaneous emphysema.

7

What is the natural history of a pneumothorax?

Most uncomplicated pneumothoraces resolve within 10 days, at the rate of 1.25-2.2% of the volume of the cavity per day.

Most recurrences usually occur within the first 2 years.

The 5-year recurrence rate for primary spontaneous pneumothorax is 30% and for secondary spontaneous pneumothorax is 43%.

Predictors of recurrence include age, smoking, emphysema and pulmonary fibrosis.

Approximately 10% of patients develop a pneumothorax on the contralateral side.

8

What are the symptoms of a pneumothorax?

Spontaneous pneumothorax usually develops at rest but may be precipitated by heavy lifting or following other activities that increase the intrathoracic pressure.

Symptoms can vary from being asymptomatic to respiratory distress and depend on:

a)

age of the patient;

b)

presence of underlying lung disease;

c)

extent of the pneumothorax.

Symptoms tend to be more severe in patients with secondary spontaneous pneumothorax, as the contralateral lung is affected by the underlying pulmonary disease and hence the patient is not able to tolerate loss of function on the affected side.

The commonest symptoms include sudden onset:

a)

chest pain – which is severe, stabbing, worse on inspiration (pleuritic) and radiates to the shoulder. The chest pain occasionally resolves within the first 24 hours, even whilst the pneumothorax remains;

b)

shortness of breath.

It is also important to elicit any history of a previous pneumothorax (in cases of recurrence) or underlying pulmonary disease (in cases of secondary pneumothorax).

Patients with a tension pneumothorax present with extreme cardiorespiratory distress or confusion (secondary to hypoxia and hypotension).

9

What are the signs of a pneumothorax?

As with the symptoms, the signs of a pneumothorax can vary depending on the extent of the pneumothorax and subsequent cardiorespiratory compromise. They may include:

a)

tachypnoea;

b)

asymmetric lung expansion;

c)

reduced or absent breath sounds;

d)

decreased vocal resonance;

e)

hyper-resonance on percussion;

f)

respiratory distress.

As well as the above signs of a simple pneumothorax, the following signs indicate the presence of a tension pneumothorax:

a)

tachycardia;

b)

tracheal shift;

c)

pulsus paradoxus;

d)

hypotension;

e)

jugular venous distention (may be absent if hypovolaemia is present).

10

What are the chest radiological features of a pneumothorax (Figure 6)?

A chest radiograph (CXR) may demonstrate:

a)

linear shadow of visceral pleura parallel to the chest wall;

b)

lack of lung markings peripheral to the linear shadow, indicative of a collapsed lung.

The size of the pneumothorax can be estimated by measuring the distance of the lung edge from the chest wall, with a 2.5cm margin corresponding approximately to a 30% pneumothorax (Figure 7).

The CXR may also indicate underlying parenchymal disease on the contralateral side.

Tension pneumothorax represents a medical emergency and patients with this condition should undergo prompt decompression with a needle thoracocentesis before any CXR.

In cases where a CXR has been performed, the radiographical findings of a tension pneumothorax include (Figure 8):

a)

ipsilateral lung collapse;

b)

widened intercostal spaces on the ipsilateral side;

c)

tracheal and mediastinal shift to the contralateral side;