Pleural drainage by intercostal tube insertion is a simple, safe, and effective therapeutic manoeuvre which is well within the scope of any physician or emergency medical technician. However, no other simple technique generates more anxiety, technical failure, or iatrogenic morbidity. Chest drain insertion requires detailed knowledge of the relationships between surface landmarks and intrathoracic and abdominal viscera as described in an earlier section (see Section 35.1 272). As for other practical procedures an unsatisfactory outcome usually follows inadequate tuition or misunderstanding of the principles of thoracic drainage.

The surface of the pleura consists of mesothelial cells lying on a basement membrane, beneath which is a connective tissue layer containing elastic and collagen fibres. The pressure in the pleural space is lower than atmospheric pressure because of the elastic recoil forces of lung tissue. Despite the negative pressure, the potential volume of the pleural space is kept to a minimum by constant reabsorption. In a normal, healthy adult the quantity of pleural fluid is about 2 ml; this contains electrolytes and proteins. The protein content is 1.5 per cent providing a colloid osmotic pressure of about 0.8 kPa (8 cmH&sub2;O). The colloid osmotic pressure gradient between blood and pleural fluid is therefore 2.6 kPa (26 cmH&sub2;O). This causes fluid flux from the pleural space into the adjacent blood plasma of both visceral and parietal pleura (Fig. 1) 1979.

Gravity and regional differences in lung deformation cause an apicobasal pressure gradient in the pleural cavity of 0.8 kPa (8 cmH&sub2;O). The hydrostatic pressure in the capillaries of the lung amounts to about 0.9 kPa (9 cmH&sub2;O); and this is considerably lower than the hydrostatic pressure in the capillaries of the systemic circulation of the parietal pleura, which amounts to some 2.9 kPa (about 28 cmH&sub2;O). The hydrostatic pressure in the pleural space is, therefore, lower than atmospheric pressure (due to the retraction forces of the lung) and is lower than the hydrostatic pressure in both pulmonary and systemic capillary systems. The average net pressure gradient resulting from these factors causes transport of fluid from the parietal pleura to the pleural cavity and then to the visceral pleura and the lung parenchyma. The reserves of fluid transport are large since the contact surface formed by the capillaries of the visceral pleura is greater than that in the parietal pleura. Extra fluid in the pleural cavity is absorbed, the rate of transport being determined by the hydrostatic pressure gradient, the colloid osmotic pressure gradient, the elastic recoil pressure of the lung, and, tissue permeability. Absorption of pleural fluid continues until only the minimum quantity required for lubrication of the pleural sheets (about 2 ml) remains. In practice the thickness of the fluid layer is about 5 &mgr;m at the apical area to 10 &mgr;m in the basal area because of gravity.

In practical terms the pleura is a closed collapsible space which can be filled by air or fluid. The pleural space is gas-free because the gas pressure in the tissues is subatmospheric (about 705 mmHg, 94 kPa), roughly the same as that in venous blood. The gas pressure in oxygenated blood differs little from barometric pressure (760 mmHg, 101 kPa). The difference results from cell metabolism and is associated with transport properties of the blood for oxygen and carbon dioxide.

During quiet breathing the pulmonary recoil pressure is about 5 cmH&sub2;O; if air is introduced into the pleural cavity the lung shrinks by an equivalent volume. However, pleural tissue is easily penetrated by most gases and reabsorption of gas from a pneumothorax occurs progressively. The partial pressures of oxygen and carbon dioxide initially rapidly assume the values of the surrounding pleural tissue. However, the total gas pressure in the pleural cavity must remain equal to the barometric pressure minus the pulmonary recoil pressure. This is achieved by an increase in the partial pressure of nitrogen, which produces a nitrogen gradient. Consequently nitrogen diffuses out of the pleural cavity into the pleural tissue, resulting in an increased carbon dioxide and oxygen tension. These gases then also diffuse into the tissues. Excretion of carbon dioxide is rapid, whereas oxygen transport depends on the O&sub2;/N&sub2; ratio. While breathing room air the partial pressure of oxygen is comparatively low and a steady state for O&sub2; is achieved rapidly (Fig. 2) 1980.

Most injuries or diseases which cause accumulation of air or fluid in the pleural cavity impair ventilation. Different pathological states may cause the pleural cavity to fill with air, blood, pleural exudate or transudate, chyle, pus, bile, or gastric contents. Loss of lung volume occurs first by elastic recoil, and then by compression of the lung. Large volumes of intrapleural gas or fluid cause mediastinal shift with volume loss in the contralateral lung. Ventilation of both the collapsed and partially collapsed lung are then seriously compromised. The mechanics of breathing are disturbed and ventilation perfusion imbalance follows (Fig. 3) 1981.

Oxygenation of the blood and elimination of carbon dioxide depends on the balance between ventilation of the lung and its blood supply. Distribution of inspired air is influenced by regional variations in airway resistance and compliance. The latter is governed by gravity-dependent intrapleural pressure gradients. On this account, gas distribution in the lung is uneven, even during normal resting tidal ventilation. Normally in the lower or more dependent pleural space the pressure is closest to atmospheric (least negative). Intrapleural pressure becomes increasingly negative towards the apex or non-dependent region of the lung. When a normal inspiration is taken from end expiration (functional residual capacity), expansion of the initially smaller dependent alveoli is governed by the steep portion of the compliance curve. Consequently they expand more for each unit of pressure change than do those at the apices which are influenced by the upper, flatter portion of the curve. These differences result in preferential distribution of inspired gases to the areas of greater expansion in the dependent portions of the lungs. However, if terminal air spaces have collapsed through pneumothorax or pleural effusion, inspiration results in preferential distribution to already expanded areas because of the influence of the compliance curve. The maldistribution of ventilation is worsened by airflow obstruction in terminal airways from external compression, and elevated intrapleural pressure. When a whole lung or lobe collapses there is perfusion of non-ventilated lung, and a serious veno-arterial shunt effect. Ineffective oxygenation of the venous blood is reflected by widening of the alveolar arterial oxygen tension difference and systemic hypoxia.

Movement of blood through the lungs is also influenced by gravity, and the pressure gradient between the pulmonary arteries and left atrium. Blood flow is normally directed preferentially to the dependent parts of normal lung where ventilation is most efficient. Collapse of these areas of lung causes ventilation-perfusion imbalance and hypoxia. The importance of early evacuation of intrapleural air, blood, or effusion, together with re-expansion of the atelectatic lung is readily apparent.

Pneumothorax is defined as the presence of air between the visceral and parietal pleurae (see Section 35.8 281). It may be induced by trauma or thoracic surgery or occur spontaneously. Simple pneumothorax occurs in association with a great number of underlying lung disease such as asthma, chronic obstructive airways disease, and bullous emphysema. Infective processes, particularly tuberculosis, pyogenic lung abscesses, and fungal disease also cause simple pneumothorax. Pneumothorax occurs in children with cystic fibrosis and in babies with hyaline membrane disease. The most common cause of spontaneous pneumothorax in young adults (16–26 years) is a ruptured congenital bulla, commonly apical in position. In elderly patients bullae develop as consequence of emphysema and chronic obstructive airways disease (Table 1) 545. Mechanical ventilation increases the risk of pneumo-thorax, which occurs commonly in patients requiring long-term support for adult respiratory distress syndrome. Pneumothorax is common in patients with chest injuries, and after needle aspiration of a pleural effusion. Air may enter through the needle, or laceration of the visceral pleura may cause an air leak from the surface of the lung. Cannulation of the subclavian vein and external cardiac compression for cardiopulmonary resuscitation may also cause pneumothorax.

Introduction of air into the potential pleural space allows the lung to collapse by elastic recoil. The effect of the pneumothorax depends on the volume of air. No serious disturbance results unless continuous leakage of air causes intrathoracic pressure to rise above atmospheric pressure. Severe reduction in lung volume or a rise in intrathoracic pressure above atmospheric pressure causes occlusion of intrathoracic airways during expiration and air trapping. Continued ventilation then requires forceful contraction of the inspiratory muscles to overcome the elastic forces of the distended thoracic cage. Tension pneumothorax occurs where an air leak from the lung surface causes progressive rise in intrapleural pressure because of a ball valve mechanism which permits air to enter but not leave the pleural space. This commonly occurs after penetration of the lung parenchyma by a fractured rib or penetrating instrument. Compression of the lung causes atelectasis and reduced pulmonary blood flow. Eventually mediastinal shift distorts the venae cavae, reducing venous return, stroke volume, and cardiac output. Clinically the patient complains of dyspnoea and chest pain.

On examination, the patient is tachypnoeic, agitated, and has hyper-resonance and decreased breath sounds on the affected side. There is decreased motion of the chest wall and mediastinal shift to the opposite side, as shown by the deviated trachea. In severe cases the neck veins are distended and the patient is peripherally cold and clammy.

The diagnosis of pneumothorax is made clinically. Unless the patient is severely compromised by pneumothorax the diagnosis should be confirmed by plain chest radiographs and the need for intervention should be determined from the findings. Patients with tension pneumothorax and respiratory or haemodynamic distress must be treated before confirmation by chest radiography. Uncertainty about pneumothorax in a patient presenting with acute respiratory distress can be resolved by needle aspiration of the pleural cavity and relieved by prompt scalpel incision through the chest wall allowing air under pressure to escape through the track. Having relieved the acute event, the chest drain with underwater seal drainage is inserted secondarily.

Therapeutic needle aspiration of pneumothorax alone is usually inadvisable since the lung may be lacerated by the needle point. When a pneumothorax is large enough to warrant evacuation this is best performed by chest drain insertion, underwater seal drainage and mechanical suction.

The extent of a pneumothorax is determined on the chest radiograph by measuring the distance from the lung border to the inside of the thoracic wall at the level of the anterior bony end of the third rib. Pneumothoraces more than 1.5 cm wide in an adult are defined as significant and drained. Smaller pneumothoraxes are drained if bilateral as a safety measure against simultaneous collapse of both lungs, or if the patient is to undergo intermittent positive pressure ventilation for any reason. This prevents the development of iatrogenic tension pneumothorax. In patients with chronic obstructive airways disease, restrictive or destructive lung disease, or a spinal cord injury, smaller pneumothoraces should be drained.

Pleural effusions may complicate obvious pre-existing inflammatory or malignant disorders, or may arise without evidence of an underlying lung or pleural lesion. A comprehensive list of the causes of pleural effusion is presented in Table 2 546. The fluid may freely fill the pleural space or be loculated between the lobes, against the chest wall or mediastinum, or above the diaphragm. A large volume of fluid may displace the mediastinum. Signs of pleural effusion include diminished chest movement on the affected side, stony dullness to percussion, diminution of breath sounds, and decreased vocal resonance. If the underlying lung is consolidated, bronchial breathing may be heard at the upper level of dullness.

Pleural fluid causes a dense homogeneous opacity on chest radiographs, often seen as a triangular shadow based on the diaphragm with the apex curving up towards the axilla (Fig. 5) 1983,1984. The upper level of the fluid is only seen as horizontal when air is introduced into the pleural space (hydropneumothorax) (Fig. 6) 1985,1986. The chest radiograph cannot differentiate between serous fluid, pus, chyle, or blood: this is only determined by needle aspiration or intercostal drainage. Even then differentiation may require cytological or biochemical analysis. It used to be the practice to differentiate between exudates and transudates by estimation of protein content, though this information is rarely of practical importance. Exudates have a protein content greater than 30 g/l, whereas transudates have a protein level less than 30 g/l. Transudates occur in cardiac failure, where the effusion tends to occur more often on the right. Other transudates occur with hypoproteinaemia from liver disease or from constrictive pericarditis and idiopathic mediastinal fibrosis.

Postpneumonic pleural effusions tend to remain serous if the patient has received antibiotics or to form an empyema if not. When the fluid is serous, the initial cell content is predominantly polymorphic; lymphocytes are present 7 days later. Most pneumonic effusions follow bacterial pneumonia and at an early stage respond to simple needle aspiration. At a later stage chest drain insertion or eventually surgical decortication may be required. Aggressive early treatment reduces the likely need for surgery. Tuberculous effusions are uncommon but may complicate miliary tuberculosis or paravertebral abscess. Active pulmonary tuberculosis sometimes involves the pleura, causing a tuberculous empyema. The pleural fluid is usually straw-coloured and occasionally bloodstained. The predominant cell is the lymphocyte, and tubercle bacilli are cultured though rarely seen on microscopy.

In tuberculosis the value of aspiration is uncertain unless the effusion is causing respiratory distress. Tuberculous empyema can be managed by aspiration or intercostal drainage followed by instillation of streptomycin. Surgical decortication is often required, particularly after rupture of a tuberculous cavity where the hydropyothorax contains both tubercle bacilli and pyogenic organisms.

Bronchial carcinoma in men and carcinoma of the breast in women are the most common causes of malignant pleural effusion (Fig. 7) 1987. Other primary tumours, particularly ovarian, also metastasize to the pleura. Primary pleural tumours may be diffuse, as in malignant mesothelioma commonly with a history of asbestos exposure (Fig. 8) 1988, or localized, as in fibroma of the pleura which almost invariably produces the syndrome of hypertrophic pulmonary osteoarthropathy. Reticuloses such as Hodgkin's disease and lymphosarcoma may present as pleural effusion but almost always involve other organs by this stage.

Malignant tumours cause accumulation of fluid in the pleura in different ways. Visceral pleural deposits may stimulate fluid production and additionally block lymphatics and compromise capillary reabsorption (Fig. 9) 1989. Parietal pleural deposits may also damage lymphatic integrity and increase capillary permeability. Impaired reabsorption of pleural fluid may follow a rise in systemic pressure due to superior vena caval obstruction or cardiac tamponade secondary to pericardial tumour deposits ( Fig. 10 1990,1991 (a, b)). In patients with malignant ascites, overspill of protein-laden lymph through transdiaphragmatic lymphatic anastomoses causes protein-rich pleural effusion.

Clinical presentation is usually with shortness of breath associated with a non-productive cough, or pleuritic chest pain. The diagnosis is made radiologically with a plain chest radiograph and then CT scan for detailed assessment of the pleural surfaces. The nature of the effusion can be confirmed by needle aspiration and cytological examination. Definitive treatment depends on the nature of the tumour. Symptomatic improvement is achieved rapidly by needle aspiration or intercostal drainage. Effusions from metastatic breast carcinoma may resolve after appropriate hormonal or chemotherapeutic treatment. Intrapleural anti-tumour agents have proved disappointing for most lesions. Patients with potential life expectancy of longer than 1 to 2 months should be considered for talc pleurodesis or pleurectomy.

To achieve adhesion of the visceral to the parietal pleura with permanent obliteration of the pleural space various conditions must be met. First, pleural fluid must be completely drained, preferably by insertion of an intercostal drain into the most dependent part of the pleural space. This is followed by continuous application of negative intrapleural pressure by mechanical suction. It is imperative to maintain apposition of the parietal and visceral pleural surfaces continuously during the process to pleurodesis, while fibrinous adhesions bond the two. Intercostal drains should therefore remain in place for at least 4 days whether the patient has undergone pleural sclerosis with blood, tetracycline, a cytotoxic agent, or insufflated talc. Drainage for more than 5 days carries the risk of infection through the drainage track and empyema formation.

Clinical trials have demonstrated talc insufflation to be the most effective of the conservative methods of pleurodesis. This procedure is performed under general anaesthesia with the patient in a lateral position. Pleural fluid is evacuated through a trocar and cannula, and the pleural cavity is inspected with the thoracoscope. This allows biopsies to be taken. Approximately 10 g of talc can then be insufflated by moving the top of the insufflator around the pleural cavity, ensuring uniform distribution. At the end of the procedure, one or two intercostal drains are inserted and attached to an underwater seal. The drains are placed on suction with a high pressure/volume pump (Thompson or Tubbs Barrett) (Fig. 11) 1992. A negative pressure of 15 to 20 cmH&sub2;O applied continuously to the pleural cavity promotes pleurodesis and prevents accumulation of further malignant or inflammatory exudate.

For patients with persistent chylothorax, complete parietal pleurectomy is preferable through a small lateral thoracotomy. This can be reinforced by talc application. Patients with long-standing large pleural effusions are occasionally referred late for pleurodesis, when the lung is already encased in fibrin and will no longer expand. This should be recognized during evacuation of the fluid at thoracoscopy since suction will draw the mediastinum across towards the space evacuated by the fluid.

Pleural effusions also occur in patients with collagen disorders such as acute rheumatic fever, rheumatoid arthritis, systemic lupus erythematosus, and polyarteritis nodosa. These seldom require more than simple needle aspiration. Pleural effusions may follow subphrenic disease, including subphrenic abscess where a reactionary sterile straw-coloured effusion is common. Alternatively, a pyogenic or amoebic hepatic abscess may burst through the diaphragm into the right pleural cavity. Acute pancreatitis may be complicated by a left-sided serous effusion which may be haemorrhagic. This has a high amylase content and is only eradicated by effective treatment of the pancreatitis. Amylase content of the effusion is much higher than that of the serum, and fat necrosis occurs in the pericardial fat. Small bilateral pleural effusions are common in association with ascites, constrictive pericarditis, or cardiac failure.

Chylous pleural effusions may result from abnormalities of the lymphatics. Chylothorax is an unusual condition, classically caused by rupture of the thoracic duct. Occasionally this follows non-penetrating injury where the thoracic duct is stretched over the vertebral bodies by jumping, vomiting, or coughing. There is often a latent interval between injury and chyle filling the pleural cavity. Chyle initially accumulates beneath the mediastinal pleura, then ruptures into the pleural space, causing the patient to become short of breath. Chylous effusion may also occur from rupture of distended lymphatic tributaries which cause multiple small fistulae that weep chyle (Fig. 12) 1993 This difficult problem can be treated successfully with obliteration of the pleural cavity by pleurectomy together with ligation of the thoracic duct at the diaphragm. Injury of the thoracic duct during thoracotomy, particularly for palliation of congenital heart disease, may cause troublesome persistent lymph leak (Fig. 13) 1994. Initial management is by dietary fat restriction, though re-exploration and ligation of the thoracic duct may be required.

There are many causes of empyema including lung abscess, pneumonia, and tuberculosis. Empyema may also follow inadequately treated traumatic haemothorax, bronchopleural fistula formation, lung resection, and subphrenic abscess. Aggressive early treatment by intercostal drainage reduces the need for surgical decortication. In practice, reliance on needle aspiration which fails to clear thick pus and debris often sentences the patient to prolonged antibiotic treatment followed by surgery. If necessary, children should be given a general anaesthetic for intercostal drain insertion. Suction on the drain helps evacuate the pus and obliterate the pleural space.

In patients who present moribund with tension pneumothorax or an extensive haemothorax, a chest drain should be inserted rapidly on the basis of physical findings. Torrential haemorrhage through the drain may demonstrate the need for immediate accident department thoracotomy as a life-saving manoeuvre. In the stable patient a plain chest radiograph is the most important investigation and should be taken before chest drain insertion (Fig. 14) 1995.

Fifteen per cent of patients with fractured ribs, pulmonary contusion, and surgical emphysema in the chest wall will have no pneumothorax. This is because the pleural cavity has been obliterated by previous pneumonic adhesions. In this circumstance insertion of an intercostal drain is extremely dangerous (Fig. 15) 1996.

Evacuation of a haemopneumothorax is carried out with a carefully sited large bore chest drain connected to an underwater seal and placed immediately on high volume suction at a negative pressure of 20 cmH&sub2;O. Indications for thoracotomy based on the results of drainage are discussed in Section 35.12. 273. Thoracic drainage aims to relieve hypoxia and acidosis secondary to hypoventilation and atelectasis. When inserting the drain care must be taken not to confuse the dilated stomach or gut for pneumothorax when the diaphragm is ruptured (Fig. 16) 1997. On the right side herniation of the liver through a lacerated diaphragm may mimic haemothorax.

When the chest radiograph is taken after chest drain insertion further decisions must be made. First, if drainage of blood is inadequate a second large drain may be required. If the lung fails to expand despite technically satisfactory drainage, bronchoscopy may be required to clear the airways of blood, secretions, or teeth in order to promote re-expansion.

With the pleural cavities cleared of blood and air, a better impression of the extent of injuries is obtained. Defects such as ruptured bronchus, lacerated diaphragm, or transected thoracic aorta with a wide mediastinum may then become apparent. Contralateral bleeding or pneumothorax may require chest drain insertion on the opposite side. Failure to evacuate a clotted haemothorax should be followed by thoracotomy. Failure to do so is followed by resolution of the haemothorax with development of a fibrothorax which will progressively reduce the size of the lung and the compliance of the chest wall. Inadequate resolution of haemothorax after early discharge from hospital may require decortication if the vital capacity diminishes to 75 per cent of predicted. This is usually undertaken 5 to 6 weeks after the accident, when organized fibrous tissue can be peeled off the underlying lung. Infection in an inadequately drained haemothorax produces an empyema which again requires thoracotomy. Fibrinolytic agents have been recommended by some to help liquefy haemothorax or empyema. These are seldom effective and are not recommended.

The intercostal drain is simply a conduit used to remove air, blood, pus, or fluid from the pleural cavity, thereby preventing compression of the lung and allowing it to re-expand. Besides draining air and fluid out of the pleural space the drainage system must also prevent their return, encouraged by negative intrapleural pressure created by breathing in. For this dual purpose three basic components are required: an unobstructed chest drain of adequate diameter, a collecting container below chest level, and a one-way mechanism—a water seal or valve to prevent the return of air or fluid.

The patient may have one or two drains in place depending on the extent of pathology. Because air rises and liquid sinks, the tip of a tube to drain air is traditionally placed in the apex of the pleural space and that for liquid at the base posterolaterally in the costophrenic angle. Although these relative positions are used in thoracic surgery where drains are placed accurately with the chest open, percutaneous drain insertion usually results in a single tube sited towards the apex posteriorly (Fig. 17) 1998. In a free pleural cavity blood or air will find the tube, particularly when negative pressure is applied.

The chest drain is joined to about 1.8 m of connecting tubing which leads to a bottle or container placed several feet below the patient's chest level. This tubing allows the patient to turn and move and minimizes the chance that a deep breath could suck liquid back into the chest. The position of the bottle and underwater seal takes advantage of gravity by establishing the patient's pleural space as the area of higher pressure and the collecting bottle as the area of lower pressure. The non-patient end of the tubing is led below the surface of sterile water which serves to create a ‘water seal’ and to establish a closed system by sealing off the open end of the tubing from the atmosphere (Fig. 18) 1999.

The positive pressure in the chest during exhalation can push air and liquid out of the pleural cavity. The air bubbles out through the water and out of the vent tube of the drainage bottle while liquid mixes with the water, raising its level. The length of tube drain below the water surface should be short so that the resistance to air escape is no more than 2 to 3 cmH&sub2;O pressure. If the drainage bottle was full of liquid, such as blood from chest trauma, the resistance to air passage through the underwater part of the tube (say 15–20 cmH&sub2;O) could prevent air escape and produce a pneumothorax even in the presence of a ‘functioning chest drain’. Note that any time the tube is clamped no air or liquid can escape from the pleural space and this puts the patient with a pleural air leak in real danger of developing a tension pneumothorax.

A pneumothorax can take two forms—open and closed. If a chest drain becomes disconnected, opening the pleural cavity to the atmosphere, the lung collapses away from the chest wall by elastic recoil. A relatively small amount of air (about one-fifth of the lung volume) enters the pleural cavity and impairs ventilation since the lung no longer expands sufficiently. As long as the hole in the chest wall is smaller the trachea an open pneumothorax is well tolerated since the other lung continues to function normally. Reconnection of the chest tube with a bout of coughing causes complete re-expansion of the lung. In contrast, if the chest drain is clamped in a patient with an air leak from the surface of the lung, air enters the pleural space, but cannot get out. Each time the patient breathes in more air escapes, builds up in the pleural cavity, and compresses the lung. In tension pneumothorax the pressure may build up rapidly and the lung collapses totally (Fig. 18) 1999. The mediastinum is pushed over to the opposite side and the opposite lung is then also compressed. Compression of the mediastinum by air under pressure also interferes with venous return to the heart, and reduces cardiac output. Eventually impairment of ventilation and reduced cardiac output can cause death.

Traditionally, chest drain clamping has been used on the slight pretext that the drainage bottle may become disconnected or upset and broken. To this end two haemostats with rubber tubing over their tip are commonly kept within easy reach. In practice, complete disconnection of the drain with entry of a small volume of air is a completely trivial and easily reversible event. It is therefore reasonable never to clamp test tubes in patients with pneumothorax, either when the patient gets out of bed, walks, or is taken to some other part of the hospital, or indeed, is transferred from one hospital to another. The drainage bottle should be handled carefully as one would any piece of equipment attached to a patient. It should be kept below chest level, making sure the water seal remains intact. If the drainage tubing comes adrift from the bottle, the end must be cleaned, reconnected and the patient should be asked calmly to cough a few times. This will rid the pleural cavity of the pneumothorax.

For a patient who has never had an air leak, clamping for a short time when changing the drainage bottles does no harm. It is just so much better to be in the ‘no-clamping’ than the ‘clamping’ habit. Drains to the pericardium or mediastinum after cardiac surgery do not usually communicate with the pleural cavity and need not drain to an underwater seal. In practice, however, the underwater seal is usually employed for all thoracic drains and for patients with thoracoabdominal incisions after oesophagectomy.

In all except emergency circumstances, it is important to obtain a posteroanterior and lateral chest radiograph to determine the size, extent, and morphology of the pneumothorax or effusion. Parts of the pleural space may be obliterated, so that precise placement of the drain is required. A CT scan is then useful to define areas of loculation of pus or blood. It is imperative to make certain that either air or fluid is interposed between the chest wall and lung. In about 15 per cent of patients with postpneumonic fibrous intrapleural adhesions, insertion of a trocar through the chest wall will result in penetration of the lung and intrapleural haemorrhage.

Consult the plain chest radiograph unless the drain is to be inserted in an absolute emergency. Loculations of fluid or air may determine the precise site of insertion. It is a fallacy that the drain must be in a basal position to drain blood or an apical position to drain air. Blood, fluid, or air will find the drain in a free pleural cavity particularly when suction is applied.

Choose the site of insertion carefully. For most conditions this will be between the fourth and seventh intercostal spaces between the mid-axillary and anterior axillary lines. The level at which the anterior axillary fold meets the chest wall is a useful guide. Insertion of the drain more posteriorly than the mid-axillary line may cause the patient to compress and obstruct the tube whilst lying on his back. There is no contraindication to inserting the drain through an area of injury, but if there is a possibility of a ruptured diaphragm with viscera in the chest the drain should be inserted higher towards the axilla ( Fig. 19 2000,2001 (a, b)). The anterior approach through the second interspace is best avoided. This route transfixes the two major accessory respiratory muscles, pectoralis major and minor, and in females the scar may be unsightly. If an apical drain is required because of intrapleural adhesions towards the base then the true apical approach above the scapula and into the first interspace posteriorly is preferred (Fig. 20) 2002.

Choose a chest drain of appropriate size. For adult patients with traumatic haemopneumothorax the drain should always be 28 French gauge or larger. Smaller drains will rapidly occlude with blood clot. The same applies to an empyema with thick pus or a chylous effusion. In patients with clotted haemothorax or those with gelatinized pus, drainage will fail and thoracotomy is required. Smaller bore drains are suitable for simple pneumothorax although with time fibrin generated by the inflammatory reaction to the drain will cause blockage. For this reason drains of less than 20 French gauge should not be used in adults. In children drain size depends on age and the distance between the ribs.

In a conscious patient infiltrate 10 to 15 ml of 1 per cent lignocaine through to the periosteum on the upper border of the rib below the chosen interspace. Advancing the needle above the rib should infiltrate the pleura. Passage of the needle into the pleural cavity confirms the presence of free air, fluid, or blood on aspiration. Liberal local anaesthesia facilitates scalpel incision through the full thickness of the chest wall so that the drain can be inserted smoothly without pushing. The needle used for infiltration can be left in situ so that the precise skin area and direction of anaesthetic infiltration is not lost when the skin is cleansed with povidone iodine solution.

Aseptic technique is important since a sterile effusion or haemothorax can easily be turned into an empyema when infection is introduced through the drain. A wide area of skin around the proposed site is cleaned with povidone iodine or chlorhexidine in spirit. The operator should scrub as for a surgical procedure and wear a mask and gloves.

For trauma patients it is wise to cover the procedure with a single dose of prophylactic intravenous antibiotic. In an emergency situation many of these precautions will be over-ruled by the degree of urgency. For life-threatening tension pneumothorax a stab wound through the chest wall without preparation provides immediate relief and should not await aseptic technique or the availability of a drain. An antibiotic should be administered after completing the procedure.

Use a scalpel to incise the chest wall skin and subcutaneous fat 1 to 2 cm beneath the proposed site of pleural incision so that the drain track leads the drain towards the apex of the pleural cavity. The underside of the rib above should be avoided so as to preserve the intercostal nerve and vessels. The scalpel should find the rib below the interspace to be breached; the remainder of the track is then completed by blunt dissection through to the pleural cavity with artery forceps. If there is any question about the adequacy of this incision a gloved finger should be passed through the track. The finger tip should enter the pleural cavity easily without resistance and on removing the finger air, blood, fluid, or pus should exit through the drain site. This precaution should always be taken, when a partially obliterated pleural cavity is expected (Fig. 21) 2003.

The drain should slide easily through the track and into the pleural cavity when blood, fluid, or air will flash fill the tube. When the expected contents of the pleural cavity do not appear in the drain it is important to ascertain why. First there is the possibility that the drain has not passed through the intercostal space but has deflected into the tissues of the chest wall. Second, the radio-opaque contents of the pleural cavity may be solid instead of liquid, as in clotted haemothorax or empyema. Drains have been inserted into mesothelioma and lung tumours. Do not be concerned about allowing air to enter along the drain: this will be evacuated immediately when the lung expands and underwater sealed drainage is established.

When the drain is in good position it is secured with at least zero gauge silk or nylon suture to prevent displacement. Once inserted a drain should never be allowed to fall out. The suture material must therefore be strong enough to ‘bite into’ the plastic tube and grip firmly. A purse string suture is placed around the incision to close the track when the time comes for drain removal.

Attach the intercostal tube to the drainage apparatus and underwater seal. Reusable glass bottles were employed historically but have been replaced by lighter, portable containers with scales permitting accurate measurement of blood or fluid loss (Fig. 22) 2004. This is particularly important in trauma and following cardiac and thoracic surgery since blood replacement in these patients is determined by blood loss. Modern drainage devices combine cylinders for autotransfusion of shed pleural or mediastinal blood. A small isolated underwater seal chamber prevents the fluid drained from reaching a depth which presents significant resistance to free drainage. This can occur in a glass bottle which fills progressively eventually to provide an obstruction of 15 to 20 cm of blood. There is no arbitrary fixed limit to the volume of fluid which may be drained, though rapid evacuation of more than 1 litre of blood or pleural fluid may cause acute mediastinal shift with pain or discomfort. ‘Re-expansion’ pulmonary oedema is rare but occurs unpredictably after drainage of large effusions.

Apply negative pressure suction to the chest drain to ensure evacuation of fluid or air and to assess the rate of continuing haemorrhage or air leak in trauma patients. A Thompson or Tubbs Barrett suction machine is necessary to ensure large volume suction at a negative pressure of 15 to 20 cmH&sub2;O. The Roberts suction pump should not be used in patients with pneumothorax and persistent air leak as it will shift only small volumes of air and may constitute an obstruction in the presence of a rapid air leak. If suction causes pain or increased breathlessness it should be decreased or temporarily stopped. Always disconnect the suction system when not in use. Suction must never be applied to a pneumonectomy space or when a completely collapsed lung will not re-expand. This will cause mediastinal shift and haemodynamic deterioration. Suction is used after partial lung resection.

Check the position and effect of the drain by plain chest radiograph. Is the drain in the expected position or are readjustments necessary? Has the drain cleared the pneumothorax or fluid accumulation? Note the initial volume of blood or fluid evacuated and the continued rate of drainage during suction. The need for thoracotomy following trauma is determined by the continued rate of bleeding. Assess the volume of air leak in patients with pneumothorax in whom drainage of air does not cease in the first few minutes.

When these steps are followed thoracic drainage should be safe and effective.

Loculated apical pneumothoraces occur in patients in whom the pleural space is partially obliterated by inflammatory adhesions, and after thoracotomy and lung resection. In these circumstances the best approach is via the apical posterior intercostal approach. The pleural space to be drained should be clearly defined by plain chest radiographs. The drain is then inserted with the patient in a sitting position preferably on a chair facing and resting on the chair back. Both arms are folded to draw the scapulae away from the midline. The operator stands behind the patient and prepares the skin over the upper posterior thorax. The point of entry is midway between the spinous process of the seventh thoracic vertebra in the midline and the upper medial border of the scapula adjacent to the spine of the scapula. The position is approximately one hand's width away from the thoracic spine ( Fig. 23 2005,2006 (a, b)). The skin and subcutaneous layers in this area are infiltrated with 1 per cent lignocaine.

The number one needle is then changed for a long spinal needle which is aimed downwards towards the posterior aspect of the thoracic inlet. This is roughly perpendicular to the skin and the needle is advanced through the trapezius and rhomboid muscles until the first rib interspace is located. Aspiration of the needle produces air or fluid as the apical thoracic space is entered. The skin to pleural space depth can be estimated by judging the length of needle outside the skin. The needle is left in place as a guide to the direction of the scalpel incision. A 1.5 cm transverse skin incision is then made over the reference point and the track to the pleural space developed by advancing the scalpel vertically through the trapezius muscle for a variable distance. This facilitates passage of the trocar and intercostal drain. During this procedure care must be taken not to allow the trocar to deviate medially towards the structures in the midline. The drain is aimed towards the ipsilateral nipple. The posterior upper ribs tend to overlap each other from above downwards and when the ribs are reached it is sometimes necessary to deviate the trocar tip anteriorly to pass through the intercostal space.

When the drain reaches the pleural cavity it should only be advanced for a further 5 to 7.5 cm (2 to 3 inches). When a suitable position is obtained the drain is sutured into place and attached to the underwater seal. The drain is usually looped anteriorly over the shoulder and fixed to the upper chest. The drain then exits the thoracic cavity in a gentle curve which avoids kinking. This seems to be a particularly comfortable drain for the patient. Its position is verified by chest radiograph.

Once the drain is inserted in the required position and securely fixed no further adjustments should be made. In particular the temptation to advance the drain further into the chest should be avoided since this will introduce infection into the track. The wound should be sealed around the drain with povidone iodine gel or the wound sprayed with clear plastic dressing. Dressings are unnecessary although a thin square of gauze around the drain will absorb exudate. The ill-advised application of large quantities of adhesive tape should be avoided. Many patients suffer blistered skin from sheets of Elastoplast. This practice also hinders expansion of the chest wall and physiotherapy.

The chest drain should never be clamped in the presence of an air leak because of the risk of tension pneumothorax. In contrast, disconnection of the drain from its underwater seal merely allows air to enter the pleural cavity through elastic recoil of the lung. Reconnection of the drain to its underwater seal and resumed suction will immediately clear the pneumothorax.

For patients with simple pleural effusion, chylothorax, or empyema, the drain can be clamped safely prior to changing the underwater seal drainage bottle. During resolution of the acute problem the patient may be taken off continuous suction and allowed to walk around the ward carrying the drainage bottle. For patients with a long-term air leak after pulmonary surgery, the drainage bottle may eventually be replaced with a Heimlich flutter valve. This contains a long, thin-walled rubber tube which allows release of air but collapses when inspiration transmits negative pressure through the drain (Fig. 24) 2007.

When transporting the patient with a chest drain clamps are usually unnecessary and clamps must never be used for patients with a continuous or intermittent air leak. The drainage bottle is carried at a level below the patient's chest to avoid syphon of the water seal back into the chest. It is advisable to clamp the intercostal drain briefly when the bottle must be lifted across the patient during positioning on the operating table, but only in patients with haemothorax or pleural effusion and not those with a brisk air leak. For air leak patients it is safer to disconnect the drain from the underwater seal system and reconnect as soon as possible. The dangerous practice of indiscriminant chest drain clamping has led to the death of air leak patients during inter-hospital transfer for pleurectomy or pleurodesis.

Any surgical drain acts as a conduit for bacterial infection. The chest drain should therefore be removed as soon as its purpose is accomplished. Long-term drainage may be required for chronic air leak in patients with obstructive airways disease or bullous emphysema and in some patients with chylothorax and empyema. Problems which remain unresolved after 2 to 3 weeks should be treated surgically. An intercostal drain should not be left in one site for more than 3 weeks since erosion of the intercostal vessels may cause haemorrhage.

The presence of a drain in the pleural cavity promotes a local inflammatory response and pleural adhesions. This is part of the therapeutic process of chest drainage but is not an indication for prolonged drainage times, which are associated with increased infection rates and morbidity. In patients with simple spontaneous pneumothorax and traumatic haemopneumothorax it takes an average of 12 h to achieve full lung expansion and cessation of air leak. Suction on the drains promotes clearance of the pleural cavity and approximation of the visceral and parietal layers.

In practice many patients are left with a drain in situ for 5 to 7 days, usually without a definite indication. With pressure on hospital beds and resources this duration of intercostal drainage is rarely necessary. In approximately 80 per cent of patients drained for pneumothorax the air leak stops within 12 h. Recent studies have shown that tube removal shortly afterwards does not lead to a higher redrainage rate than for patients whose tubes are kept for longer periods. Mobilization and physiotherapy promotes full re-expansion of the lung. Patients who continue to leak air after re-expansion require drainage until the air leak stops. Suction is applied continuously to keep the parietal and visceral pleura in close apposition, thus promoting the development of inflammatory adhesions. When the lung remains expanded when suction is stopped, suction is suspended for mobility during the day but reconnected at night. After lung resection the drain can usually be removed at 2 weeks, even when bubbling persists. As an interim measure the underwater seal can be replaced with a Heimlich valve to allow free mobility. The drain can eventually be removed 12 h after the last bubble has been observed.

Drains may be retained temporarily to cover anaesthesia for extrathoracic problems or in patients requiring positive pressure ventilation or continuous positive airway pressure management. For patients with pleural effusion, empyema or chylothorax, the drain is kept in situ until the fluid leak stops or blood turns to serous fluid. Failure of resolution within 3 weeks usually leads to surgical intervention.

To avoid pneumothorax through aspiration of air tube removal is performed during a sustained Valsalva manoeuvre which forcibly inflates the lung against the chest wall. Breathing is suspended until the purse string suture is tied. Meanwhile the drain track can be occluded by finger pressure 1 cm above the skin incision.

The skin suture should not be overtightened or rapidly snapped closed since this can cause ischaemia and necrosis within the area of constriction. Sterile technique is not necessary for drain removal but the tip of the drain should be cut off with sterile scissors and sent for culture. The wound is sprayed with clear plastic dressing and covered lightly with a gauze swab or left uncovered. Extensive Elastoplast dressings are not useful and irritate the skin.

Many units ask for a plain chest radiograph after drain removal. Auscultation of breath sounds gives the same information and even in the presence of a small residual pneumothorax redrainage is unnecessary. Chest radiograph is therefore an unnecessary expense and is more useful 24 h later, prior to hospital discharge.

This occurs commonly through poor technique. The chest radiograph may be deceptive when the drain passes forwards or backwards within the soft tissues of the chest wall. The problem is recognized when the expected pleural contents, air, blood, pus, or chyle, do not enter the drain and no clear respiratory swing is obtained on deep inspiration. This may occur with lateral, anterior, or posterior approaches to the pleural cavity. We have seen trocar insertion directly into the mediastinum, brachial plexus, and subclavian vessels during attempted entry of the second intercostal space anteriorly. With the lateral approach the drain may end in the soft tissues of the axilla. When the expected result is not achieved the drain should be removed and the procedure repeated.

Minor lung lacerations are common after trocar drain insertion. When good technique has been used the damage is slight and resolves spontaneously. The most important lung injuries occur when a drain is inserted inappropriately into an obliterated pleural cavity. Postpneumonic adhesions tether the lung to the chest wall in 15 to 20 per cent of patients. This can rarely be recognized from the plain chest radiograph alone but is suspected in patients with a past history of pleurisy, pneumonia, or tuberculosis (Fig. 25) 2008. Major lung laceration usually occurs in trauma patients who present with surgical emphysema in the chest wall. This occurs in the absence of pneumothorax because the lung is unable to collapse and lacerated ribs cause air to leak directly in to the extrathoracic tissues. If the chest radiograph shows no blood or air in the pleural cavity then a drain must not be inserted without digital confirmation of a pleural space. We have seen serious intrapulmonary bleeding after anaesthetists have asked for ‘prophylactic’ pleural drainage prior to positive pressure ventilation in this type of patient.

Liver, spleen, stomach, and bowel have been transfixed by chest drains. This occurs through poor technique when the drain is inserted beneath the sixth intercostal space, and penetrates through the lower part of the pleural cavity and diaphragm into the upper abdomen. This also occurs after traumatic rupture of the diaphragm if siting of the drain has not taken into account the radiological appearance. It is avoided by siting the drain above the sixth interspace, or higher when a large pleural effusion obscures the position of the diaphragm.

When deep liver penetration occurs we advocate leaving the drain in situ for 48 h until resolution of blood clot prevents major haemorrhage. Penetration of the colon requires early laparotomy for peritoneal toilet. Penetration of the spleen or stomach may be managed conservatively, though clinical deterioration will often precipitate laparotomy.

Penetration of the heart is rare but may occur in patients with cardiomegaly, where the left ventricle is in apposition to the chest wall laterally. Exsanguination has occurred through left ventricular penetration followed by removal of the drain. If entry of a cardiac chamber is suspected the drain must be left in situ and the tube clamped pending urgent thoracotomy. Laceration of a major pulmonary vessel occurs particularly when a collapsed lung is deeply penetrated (Fig. 27) 2010. The drain should be left within the pleural cavity and the rate of bleeding determined. When immediate drainage exceeds 1000 ml or the subsequent rate 500 ml/h for three consecutive hours thoracotomy should be performed. Substantial haemorrhage may also occur through penetration of an intercostal or internal mammary vessel. This complication can usually be managed conservatively but occasionally requires exploration.

Large bullae mimic pneumothorax on the plain chest radiograph. Failure to recognize the bulla may result in insertion of a drain and copious air leak. When suction is applied to the drain the air leak increases and results in significant loss of tidal volume with acute exacerbation of breathlessness. The situation is usually recognized because of the continuous large volume air leak. Removal of the drain may result in tension pneumothorax and clamping of the drain causes extensive surgical emphysema. The drain should be withdrawn from the bulla and the patient observed carefully. Tension pneumothorax may require drainage, though frequently the lung already has inflammatory adhesions to the chest wall. Thoracotomy may be undertaken to resolve this situation, although we have successfully passed a Foley catheter through the shortened drain and used the balloon to plug the hole in the bulla and traction to hold the bulla against the chest wall.

Occlusion of a chest drain may lead to recurrent pneumothorax or reaccumulation of blood or fluid. The smaller the chest drain the more likely blockage is to occur. Suction promotes drainage and clearance of the pleural cavity. Clamping of the chest drain promotes occlusion. Even in pneumothorax a fibrinous exudate caused by the inflammatory reaction to the drain will occlude the side holes if suction is interrupted. A great number of pleurectomies for recurrent pneumothorax and decortications for empyema could be avoided if measures were employed to ensure continuous drainage.

Failure to adhere to aseptic technique and unnecessarily prolonged intercostal drainage both promote pleural sepsis. Except for trauma patients, prophylactic antibiotic treatment is not recommended, but a therapeutic course of antibiotics may be required if a patient with a chest drain becomes febrile. The cutaneous drain site may be inflamed or clear serous drainage may become purulent. The drain at fault should be removed and antibiotic treatment continued. Accumulation of pus in the pleural cavity may require needle aspiration or further drainage through a separate site.

Occasionally intercostal drainage produces a surprise. The pleural effusion may be chylous, may contain bile, or contain gastric contents. Chylous effusion may result from trauma or malignant occlusion of the thoracic duct. Continued drainage results in emaciation of the patient. Conservative methods of treatment by fat restriction are seldom successful and surgical pleurodesis is usually required. Bile in the right pleural cavity may follow rupture of a liver abscess through the diaphragm. This situation requires specialized treatment of the underlying pathology. Gastric contents fill the pleural cavity after spontaneous or instrumental perforation of the oesophagus. In the Boerhaave syndrome an acute rise in intragastric pressure splits the lower oesophagus and forces the stomach contents into the left, or more commonly the right chest. The condition is often mistaken for an acute vascular event such as myocardial infarction or aortic dissection, and is seldom diagnosed within 24 h. Early surgical repair and pleural drainage are necessary to avoid mortality or serious morbidity.