Pleural conditions

Normal pleural physiology (Fig. 47.28)

There is a potential space between the parietal and visceral pleura that contains only about S ml of pleural fluid at any one time. The amount of pleural fluid is governed by the factors producing and absorbing it (capillary hydrostatic pressure, capillary permeability, lymphatic drainage and colloid osmotic pressure). The turnover of fluid in the human pleural space is about 1 litre in 24 hours. Protein-depleted fluid is filtered into the pleural space from the capillaries in the parietal pleura. The fluid is then mostly absorbed into the pulmonary capillaries, with only about 10 per cent being absorbed by the pleural lymphatics.

Any disturbance of the equilibrium will lead to the development of a pleural effusion. There are two described types depending on the protein content of the fluid, although the distinction is not always clear.

Accumulation of protein in the pleural space results if the lymphatic drainage is deranged. This alters the osmotic pressure within the space and leads to the formation of an effusion. There is usually in excess of 30 g of protein per litre and this is termed an effusion. The underlying pathological mechanisms are:

  increased capillary permeability — capillary damage or inflammation;

  lymphatic obstruction;

venous obstruction.

The most common pathologies associated with exudative effusions are:

  malignancy;

  infection;

  connective tissue disease;

  pulmonary infarction.

A transudate has less than 30 g/litre of protein and is the result of low colloid osmotic pressure from liver cirrhosis or high hydrostatic pressure from cardiac failure or a combination of both.

Presentation

The clinical signs depend on the rate of effusion growth. Rapidly developing effusions may cause severe dyspnoea, whereas slowly developing ones may be very large but asymptomatic. On clinical examination there are reduced breath sounds on the affected side with tracheal deviation to the opposite side. The chest is stony dull to percussion. A pleural effusion may be the initial presentation of a systemic malignancy in up to 30 per cent of cases.

Investigation

Radiology

A chest radiograph will determine the size of the effusion and may give a clue as to the aetiology (coexistent tuberculosis, hilar shadow, etc.). Further information about the lung may be obtained by CT it the lung is the primary pathology. Pleural thickening is best distinguished from fluid by ultrasonography.

Aspiration

Pleurocentesis (Fig. 47.29) is performed under local anaesthesia using aseptic precautions. The needle is introduced just above a rib (to avoid the neurovascular bundle) at the point of maximal dullness. Fluid is drawn for diagnosis (cytology and biochemistry) and symptomatic relief. It is important not to remove too much fluid because pulmonary oedema may ensue. Biochemistry will determine whether the fluid is an exudate. If it is then diagnostic efforts must be directed at finding the cause.

Cytology

Histological examination of the aspirated fluid may be useful but the absence of malignant cells does not rule out malignancy. The yield may be increased by pleural biopsy (using an Abram’s needle) taken at the same time.

Thoracoscopy

This is a more invasive technique performed under general anaesthesia. The patient is positioned and draped as for a thoracotomy. A small incision is made over an intercostal space down to the pleura. The pleura is opened and the effusion drained by suction. The thoracoscope is introduced and the parietal pleural and lung are inspected thoroughly. Any suspicious nodules or plaques may be biopsied and in the case of a recurrent malignant pleural effusion, definitive pleurodesis may be done.

Treatment

The prognosis for malignant pleural effusion is very poor and therefore the treatment should be simple and effective if the patient is to enjoy a reasonable quality of life. Simple aspiration is a temporary solution in the symptomatic patient, because the effusion usually re accumulates and repeated aspiration merely results in loculation of the fluid. Treatment of the underlying malignancy may lead to resolution of the effusion but the distressing dyspnoea will be prolonged. A much better method of palliation is aspiration of the effusion and pleurodesis. 

Three requirements must be met for successful pleurodesis: 

The pleura must be aspirated to dryness, the pleural surfaces must be kept apposed and the fluid must not be allowed to re accumulate. This can be achieved by tube drainage with underwater seal and 5 mmHg of suction pressure, and the introduction of a sclerosing agent. There is a variety of sclerosing agents, including tetracycline, bleomycin and iodised talc. Pleurodesis may be carried out on the ward but the success rate is higher if the procedure is performed under general anaesthesia with talc insufflation and thoracoscopic inspection to ensure that the pleural surface is completely covered. At the end of the procedure, basal and apical drains are inserted and left on suction to ensure that the pleural surfaces are apposed. Theme is an intense inflammatory reaction which is very uncomfortable for the patient. Adequate analgesia (avoiding nonsteroidal anti-inflammatory drugs) is therefore essential while the drains are in place. The success rate is over 75 per cent for this form of treatment and failures usually result from failure of the underlying lung to expand, lung metastases or lymphangitis. Pleurectomy is hard to justify because it is a major procedure in a patient with a very limited life expectancy.

Tumours of the pleura

The pleura is often secondarily involved as a result of direct or transcoelomic spread of lung or breast malignancy resulting in a malignant pleural effusion. However, there is one malignant tumour of the pleura that deserves mention.

Mesothelioma

Fibrous plaques overlying the pleura are often seen at thoracotomy and are benign in most cases. The most important malignant tumour affecting the pleura is a mesothelioma. This is an aggressive tumour that grows in diffuse layers, encapsulating and compressing the lung substance. It is associated with asbestos exposure and is a notifiable condition because sufferers may be eligible for compensation. There are several different cell types seen within the tumour (adenomatous, squamous or sarcomatous), although there is usually a predominance of one cell type.

Clinical features. The patients often present with large unilateral pleural effusions and dyspnoea and occasionally chest pain. Advanced disease is heralded by weight loss, pyrexia and night sweats.

Investigation. Chest radiography suggests the diagnosis but CT will show marked pleural thickening with compression of the lung. Pleural aspiration may reveal atypical cells but the diagnosis is more certain if thoracoscopic biopsy is performed. This also allows pleurodesis at the same time. Treatment. The disease follows a progressive course over 12—24 months. Cure is rarely possible because the tumour is unresponsive to radiotherapy or chemotherapy, and palliation is difficult. Pain relief and appropriate supportive measures are best arranged at an early stage.

Pneumothorax

Pneumothorax is the presence of air in the thoracic space, outside the lung, that is, between the visceral and parietal layers of pleura which are normally only separated by a thin film of fluid. The lung is collapsed to the extent that it is displaced by the pneumothorax.

Classification of pneumothorax

Spontaneous — primary. The only abnormality is superficial blebs at the apex of one or more lobes, typically the upper lobes, which either leak spontaneously or are triggered by an otherwise unremarkable event such as exertion. It is more common in males, occurs predominantly in the ‘teens or twenties, may be bilateral and may be familial.

Spontaneous — secondary. Any lung disease that breaches the pleura may cause a pneumothorax so probably every possible lung disease will, at one time or another, cause a pneumothorax. The most common causes are obstructive airways disease in any form and bullous emphysema.

Traumatic. See Thoracic trauma section.

Iatrogenic. This is commonly seen in general hospital practice as a result of insertion of central lines for central venous pressure monitoring, intravenous feeding or cardiac pacing.

Open. The air may come from a penetrating injury (stabbing or shooting) and passes in and our of the chest wall with each breath, but no effective ventilation occurs (see Thoracic trauma section).

Closed. Rib fracture — see Thoracic trauma section.

When air in the pleura is under pressure the situation is called ‘tension pneumothorax’ and is a medical emergency. This depends on the non return valve-like mechanism, which is inherent in the structure of the lung. Positive pressure, generated within the airways with coughing or groaning in pain, forces air out which then cannot return through the collapsible peripheral alveoli (Fig. 47.30).

Diagnosis

The first thing is to suspect a pneumothorax and look for it deliberately in patients at risk:

  following needling of central veins;

  sudden deterioration in a ventilated patient;

  any trauma case;

patients with obstructive airways disease.

On examination the affected side is more resonant and the breath sounds, listened for laterally in the axilla, are markedly different and reduced on the affected side. Shifts of the cardiac apex and trachea require severe distortion and are unreliable signs.

Chest radiography should be diagnostic but beware the supine film. Standard films are taken in inspiration. A small pneumothorax is exaggerated by expiration because the pneumothorax occupies proportionally more of the chest cavity.

Management

Tension pneumothorax is relieved by insertion of a large-bore intravenous cannula in a convenient intercostal space (with the usual precaution — see Chest drains) and then the situation can be managed as for a simple pneumothorax.

Spontaneous pneumothorax in a fit individual may cause little in the way of symptoms but in someone with poor respiratory reserve (chronic obstructive airway disease) it may be life threatening.

The natural elastic recoil of the lung is balanced by the negative pressure within the pleural space. Disruption of this equilibrium by air in the pleural space results in collapse of the lung to some extent. If the chest wall remains intact but the lung is punctured by a fractured rib the situation is termed a ‘closed pneumothorax’. The danger is that, if this injury is part of a multiple injury, then positive pressure ventilation may lead to the development of a tension pneumothorax. If the chest wall is breached then this is termed an ‘open pneumothorax’, with the result that air moves in and out of the chest through the wound with each breath and there is no gas exchange across the alveolar surface.

Spontaneous pneumothorax may occur in any individual but is more common in young, slim men. The condition is often associated with apical blebs and there is a 30 per cent chance of recurrence.

Iatrogenic pneumothorax occurs when the lung pamenchyma is breached by a medical procedure such as thoracocentesis, lung biopsy, liver biopsy or central venous cannulation.

Treatment

The initial treatment depends on the nature and severity of the pneumothorax; small pneumothoraces causing little disability may be observed with serial radiographs or may be aspirated. Large symptomatic or traumatic pneumothoraces require the insertion of a chest drain. Repeated spontaneous pneumothoraces are an indication for definitive treatment to prevent recurrence. This depends on the age of the patient, their general condition and the underlying aetiology of the pneumothorax. In older patients, talc pleurodesis has a good chance of success (>60 per cent) but many feel uncom­fortable about this procedure in the young. Procedures such as thoracoscopic abrasion and partial pleurectomy or thoracotomy and pleurectomy (often with stapling of bullae) have a higher success rate. Old patients with severe obstruc­tive airway disease (who may be receiving steroid therapy) present a major management problem.

Pleurectomy. Pleurectomy is the definitive treatment for recurrent pneumothorax. A small posterolateral thoracotomy is performed and as much of the parietal pleura as possible is stripped off the chest wall, particularly at the apex of the hemithorax. There are often apical bullas that may require stapling or over sewing. The parietal surface is abraded with a swab to induce an inflammatory reaction. Large calibre suc­tion drains are inserted to drain the apex and diaphragmatic surfaces of the lung. It is essential that suction is maintained long enough for the lung surface to become firmly adherent to the chest wall (usually 2—3 days). The thoracoscopic method of pleurodesis is becoming commonplace, with comparable results to open pleurodesis.