Thorax

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CHAPTER 9 Thorax

Heart and great vessels 148

Pleura and lungs 159

Mediastinum 165

Heart and great vessels

Principles of cardiac surgery

Surgery for heart disease has advanced to a point where safe and effective treatment can be offered for most conditions. Assessment of patients has become more refined with the development of special diagnostic techniques, e.g. echocardiography, scintigraphy, cardiac catheterization and cineangiography. Improvements in diagnostic techniques, anaesthesia, surgical techniques and postoperative management have led to better results with lower mortality rates and a reduction in complications.

Postoperative complications

Low cardiac output

This may result from haemorrhage, cardiac failure, tamponade, pulmonary hypertension, or cardiac arrhythmias.

Respiratory failure

This may be due to pulmonary oedema or atelectasis giving rise to hypoxia. Pain from the surgical incision reducing respiratory effort may be contributory.

Renal failure

Due to ATN, resulting from renal hypoperfusion. Haemofiltration/haemodialysis may be required.

Jaundice

Usually a result of transfusions or haemolysis, occurring as a result of cardiopulmonary bypass. Occasionally, liver failure occurs because of low cardiac output.

Cerebral damage

May be due to anoxia, air embolism, thrombus, cerebrovascular disease or fat embolism. Cerebral oedema may occur.

Postoperative treatment

Maintenance of cardiac output

Ensure adequate filling pressure of ventricles (preload). Maintain adequate CVP. Ensure myocardial contractility – inotropes. Maintain heart rate around 90/min. Use isoprenaline or pacing wires inserted at surgery. Reduce peripheral resistance (afterload) with vasodilators, e.g. GTN. Metabolic acidosis may occur and is an indication of poor perfusion. Aortic balloon pumping may be used to reduce cardiac afterload. Haemorrhage and tamponade require urgent re-exploration. Pulmonary hypertension may respond to prostacyclin. Arrhythmias require drugs, cardioversion or pacing.

Prevention of respiratory problems

Optimize cardiac output. Use positive pressure ventilation, diuretics, pain relief, physiotherapy.

Maintenance of urine output

Optimize cardiac output, diuretics, e.g. furosemide, renal dose of dopamine.

Prevention of cerebral problems

Maintain normal BP. Reduce CO₂ by positive pressure ventilation, avoid hyperpyrexia, give dexamethasone.

Congenital heart disease

This occurs with an incidence of 8:1000 live births. Aetiological factors include maternal rubella, Down’s syndrome and maternal drugs, e.g. warfarin and phenytoin.

The following lesions are most commonly encountered (in order of decreasing frequency): VSD, ASD, PDA, pulmonary stenosis, aortic stenosis, tetralogy of Fallot, coarctation of the aorta and transposition of the great vessels. Congenital heart disease may be classified as cyanotic (significant R-to-L shunt) or acyanotic (L-to-R or no shunt). The reader is referred to a textbook of medicine for the symptoms, signs and investigations of these conditions. The treatment and prognosis are indicated below.

Acyanotic

Ventricular septal defect (VSD)

Small defects may close spontaneously but surgery is indicated for large defects, cardiac failure, increased pulmonary vascular resistance and patients with pulmonary blood flow 1.5 times greater than systemic flow. The defect is closed with a prosthetic patch using cardiopulmonary bypass. Mortality and morbidity depend on the preoperative state of the patient and degree of pulmonary vascular resistance. An uncomplicated VSD has an operative mortality of less than 5%.

Atrial septal defect (ASD)

Surgery is indicated if pulmonary flow is 1.5 times systemic. The defect is closed with a patch. Ideally, the operation should be carried out before a child goes to school. Mortality is less than 1% but increases in the presence of pulmonary vascular resistance. Percutaneous device closure is increasingly used.

Patent ductus arteriosus (PDA)

At birth, the pulmonary vascular resistance decreases markedly as the lungs inflate and the ductus arteriosus closes within a few days. Failure of closure may occur in premature babies, hypoxia or maternal rubella. In premature babies a prostaglandin synthetase inhibitor, e.g. indomethacin, may promote closure. All persistent ducts should be closed to prevent infective endocarditis. The ductus is doubly ligated via a left thoracotomy. Endovascular techniques are now in common use. Mortality is less than 0.5%.

Coarctation of the aorta

There are two types: adult and infantile. In the adult form, the aorta is narrow in the region of the ligamentum arteriosum just beyond the origin of the left subclavian artery. Proximal hypertension and LV overload occur. Most adult types can be stented. If surgical correction is required, the ideal age is 7–15 years. Operative procedures include resection with end-to-end anastomosis. If the gap is too large, a woven Dacron graft is inserted. Complications include residual hypertension, spinal cord ischaemia during surgery, recurrent laryngeal nerve palsy, and mesenteric ‘arteritis’ due to increased pulse pressure. Without surgery, the majority of patients are dead before the age of 40. Death occurs from aortic rupture, infective endocarditis, LV failure, cerebral haemorrhage. The operative mortality is about 5%.

The infantile form is rare and usually preductal. It may be associated with other cardiac defects in 60% of infants. Operative mortality is high, reaching 70% for surgery in the first 3 months of life.

Coarctation is commonly now treated by angioplasty in small children.

Congenital valve disease in children

Aortic stenosis or pulmonary stenosis may occur. Treatment is by balloon dilatation during cardiac catheterization or occasionally by open surgery.

Cyanotic

Congenital cyanotic heart disease is uncommon. The two common forms are the tetralogy of Fallot and transposition of the great vessels. Cyanosis may also occur where the L-to-R shunt of a VSD reverses owing to pulmonary hypertension (Eisenmenger complex).

Tetralogy of Fallot

This consists of a VSD, overriding aorta, pulmonary stenosis and RV hypertrophy. Correction involves reconstruction of the RV outflow tract and closure of the VSD. Nearly all children are corrected by a one-stop procedure – early correction in infancy is now the procedure of choice. Very rarely, an aortopulmonary shunt is used for palliative purposes in the first instance. A Blalock–Taussig shunt is the most common. The subclavian artery is divided on one side and anastomosed to the ipsilateral pulmonary artery to improve pulmonary blood flow. The shunt is closed and the defects corrected between the ages of 3 and 5 years. There should be no mortality associated with the shunt operation. However, the quality of cardiopulmonary bypass in children has now improved considerably such that one can expect to get good results with a one-stop procedure.

Transposition of the great vessels

The aorta arises from the RV and the pulmonary artery from the LV. Survival is dependent on co-existing defects, e.g. PDA, VSD, ASD, which permit mixing of the two circulations. Definitive surgical correction involves an ‘arterial switch’ where the aorta and PA are transected and reanastomosed, aorta to LV and PA to RV. This operation has to be done in the first 2 weeks of life before the LV decreases in size. Alternatively interatrial repair can be undertaken at 6 months. A ‘baffle’ made of pericardium is created in the atrium to direct caval blood behind the baffle to the mitral valve and LV and PA, with the pulmonary venous return channelled in front of the baffle to the tricuspid valve, RV and aorta. Operative mortality is about 10%.

Acquired valvular heart disease

This is limited to the aortic, mitral and occasionally tricuspid valves. The pulmonary valve is rarely affected. The valve may be narrowed (stenosis) or rendered incompetent (regurgitation), or both may occur. Except for mitral stenosis and tricuspid incompetence, surgical treatment of acquired valvular disease requires valve replacement. Some types of mitral stenosis may be treated by closed mitral valvotomy while tricuspid incompetence may be treated by valvoplasty.

Types of valve

Mechanical valves

These include: Ball valve – The Starr–Edwards is a metal cage with a silastic ball. It is durable for long periods (up to 25 years). Not used nowadays.

Disc valve. In the past Bjork–Shiley tilting disc valves have been used but these are no longer made.

Bileaflet valve, e.g. St Jude (most commonly implanted in USA), Sulzer-CarboMedics.

All three types require(d) lifelong anticoagulation with its attendant risks. There remains a small risk of thrombosis and embolism. Failure is sudden.

Tissue valves

These are usually porcine xenografts or bovine pericardium. They are mounted on a frame with a sewing ring. The embolic rate is very low and therefore anticoagulants are not required. They lack long-term durability, with up to 75% failure rate at 15 years. They fail gradually.

Free aortic homograft is still a major choice.

Antibiotic-preserved fresh homografts may also be used.

Ischaemic heart disease

This is the commonest cause of death in the UK. Coronary artery disease is four times more common in men than in women although the incidence in women is increasing. It accounts for one-third of all male deaths and one-quarter of all female deaths.

Aetiology

Male sex, smoking, family history, hypertension, hyperlipidaemia, diabetes, obesity, myxoedema.

Symptoms and signs

Angina, MI, CCF. Sudden death. Often nothing to find on examination. Occasionally xanthelasma. Cholesterol nodules. Arcus senilis. Stigmata of diabetes. Peripheral vascular disease.

Treatment

Conservative

Stop smoking. Dietary restrictions. Exercise, correct hyperlipidaemia, control anaemia, control diabetes. Avoid stress. Vasodilators, e.g. nitroglycerine spray; β-blockers, e.g. propranolol. Calcium antagonists, e.g. nifedipine, diltiazem. Aspirin. Graduated exercise programme.

Percutaneous transluminal coronary angioplasty (PTCA)

This is indicated with localized proximal incomplete blocks causing angina unresponsive to medical treatment. A balloon is inserted under radiographic control and the stenosis dilated. There is a 5% risk of infarction and a mortality of less than 1%. Stenting is thought to reduce restenosis rates.

Coronary artery bypass graft (CABG)

Surgery is indicated when there is intractable or unstable angina; triple vessel disease with depressed ventricular function, and left main stem stenosis. A reverse segment of saphenous vein is anastomosed between the aorta and the coronary artery distal to the obstruction. Total arterial revascularization is increasingly common. Both right and left internal mammary arteries are used, as well as the radial artery, as an arterial replacement. The gastroepiploic artery is rarely used to anastomose to the right posterior descending. The results are good when left ventricular function is normal, with a mortality of approximately 1%. At 1 year, 85% of patients have complete freedom from angina. This reduces to 50% at 10 years. About 5% of patients suffer perioperative MI.

Surgery for complications of myocardial infarction (MI)

Ventricular aneurysm

The prognosis without surgery is poor – less than 20% of patients survive 5 years. Death is due to LVF or MI. Rupture is rare but fatal. Surgery is required for excision of the aneurysm. This is carried out on cardiopulmonary bypass with CABG if appropriate.

Mitral regurgitation

Infarct involves the papillary muscles. Treatment is by valve replacement with CABG if appropriate. However, valve repair is increasingly common and has better long-term results.

Ruptured intraventricular septum

This carries a high mortality rate. Early operative repair is advisable but the perioperative mortality rate is high. The defect is repaired with a Dacron patch.

Pericarditis

This is inflammation of the parietal and visceral layers of the pericardium. It may occur as an isolated lesion or as part of a systemic disease. Causes include idiopathic (probably viral), tuberculosis, bacterial (Staphylococcus, Streptococcus or Haemophilus septicaemia), rheumatic fever, collagen diseases, uraemia, traumatic, neoplastic (direct invasion from bronchial carcinoma), post-pericardiotomy syndrome, MI.

Complications of pericarditis

Cardiac tamponade

A pericardial effusion as small as 100 mL may produce symptomatic tamponade if it occurs rapidly, while larger amounts may be well tolerated if it accumulates slowly. Rapid development of an effusion interferes with diastolic filling and results in reduced cardiac output. The fluid may be blood (trauma, ruptured ventricular aneurysm) or inflammatory exudate (any pericarditis).

Symptoms and signs

Tachycardia, hypotension, raised JVP with systolic descent, pulsus paradoxus, reduced heart sounds.

Treatment

Urgent when signs of peripheral circulatory failure. Tamponade is treated by pericardiocentesis with a wide-bore needle inserted under xiphoid process. Samples are sent for bacteriological and cytological examination unless the cause is clearly traumatic. Persistence or recurrence of symptoms is an indication for surgery. The pericardium is opened via a left anterior thoracotomy. A drain is inserted. If the cause is traumatic, a co-existent laceration of the heart may require suture.

Thoracic aorta

Aneurysms

Aneurysms of the thoracic aorta may be true (fusiform, saccular), false or dissecting. Causes include arteriosclerosis, syphilis, previous aortic dissection, trauma and cystic medial necrosis.

Symptoms and signs

Asymptomatic

Found on routine CXR. In ascending aorta it may be associated with valvular incompetence, hoarseness may be due to pressure on the recurrent laryngeal nerve, back pain may be due to vertebral erosion, dysphagia may be due to pressure on the oesophagus and dyspnoea may be due to phrenic nerve involvement. Rarely pain is due to erosion of the sternum.

Investigations

• VDRL: syphilis

• CXR: mediastinal widening

• CT scan.

Treatment

Indications for surgery include rupture, documented enlargement, pain, aortic incompetence. Aneurysms of the ascending aorta and arch require a prosthetic graft replacement on cardiopulmonary bypass. Replacement of the aortic valves and reimplantation of the coronary arteries may be necessary. Aneurysms of the descending aorta are repaired using left heart bypass, replacing the aorta with a prosthetic graft. The most serious complication of repair of descending thoracic aortic aneurysms is paraplegia, occurring in about 5% of patients. Combined surgical and endovascular procedures are increasingly common.

Aortic dissection

In aortic dissection, blood breaks through the intima and creates a false passage through the media. This may rupture back into the main lumen leaving an aorta with a double lumen and the patient may survive. In other cases, rupture with exsanguination may occur, or occlusion of the normal lumen may occur with obstruction to the blood flow through the major branches. As dissection advances, occlusion of side branches may occur, e.g. carotid (hemiplegia), spinal branches (paraplegia), renal arteries (anuria and renal failure), visceral arteries (ischaemic bowel). The aneurysm may rupture back into the pericardium with cardiac tamponade and death. Aetiological factors include arteriosclerosis, hypertension, Marfan’s syndrome and cystic medial necrosis.

Symptoms and signs

Sudden excruciating chest pain radiating to the back. May be difficult to distinguish from MI. Shock. Signs of cardiac tamponade. Hypotension. Disparity of pulses or BP in extremities. MI may occur if disease extends proximally.

Investigations

• ECG may exclude MI

• CXR: mediastinal widening, pleural effusion if rupture

• CT

• MRI

• Thoracic aortogram will show extent of dissection with site of intimal tear.

Treatment

Medical

Control hypertension, e.g. nitrates, alpha blockers. May prevent further dissection. Obtain CT, MRI or angiogram when BP controlled.

Surgical

If the ascending aorta is involved, surgery is undertaken immediately because of the high risk of rupture and fatal cardiac tamponade. The ascending aorta is replaced with a tube graft with or without aortic valve replacement. The principle of the operation is to replace the segment of aorta up to where the blood has entered the false channel and to reapproximate the layers of aorta at the distal suture line. Blood now enters the true lumen, decompressing the false channel and restoring blood flow through the branches. If the dissection is distal to the left subclavian artery, medical or surgical treatment may be undertaken. Surgery is indicated for rupture, failure to control BP, compromise of blood flow to kidneys and other abdominal organs. Paraplegia may occur because of compromise of blood flow to the spinal cord.

Prognosis

Operative mortality is 10–20%. Some patients do not reach hospital alive. If medical therapy is undertaken, patients need regular follow-up with adequate control of BP.

Thoracic trauma

Thoracic trauma accounts for 25% of deaths from trauma. Injuries may be open or closed. Open injuries are the result of penetrating trauma from knives or gunshot wounds. Closed injuries follow blunt trauma and deceleration. The commonest cause of closed injuries is road traffic accidents. Only about 25% of chest injuries require open surgical intervention.

Open injuries

There may be catastrophic bleeding from penetration of the heart or great vessels. Haemothorax, pneumothorax, cardiac tamponade and visceral damage with mediastinitis may occur.

Closed injuries

Rib fractures, pneumothorax, haemothorax, flail chest, aortic injury, myocardial contusion, ruptured diaphragm, ruptured oesophagus, pulmonary contusion and haemorrhage.

Symptoms and signs

Shock, cyanosis, dyspnoea, pain. Hypotension, peripheral vasoconstriction, cyanosis, pulsus paradoxus, diminished heart sound, tracheal deviation, tension pneumothorax. Reduced breath sounds. Altered percussion note. Tenderness over ribs.

Investigations

• FBC: cross-match

• CXR: widened mediastinum, pneumothorax, fractured ribs, fractured sternum, pleural fluid (haemothorax), mediastinal or subcutaneous emphysema, enlarged cardiac outline, ruptured diaphragm

• Aortography

• CT

• Water-soluble contrast swallow

• Peritoneal lavage

• ECG.

Treatment

This may be required before any investigations are carried out:

1. Establish airway, breathing and circulation.

2. If dyspnoea, tracheal deviation and absent breath sounds over lung fields, insert chest drain or wide-bore needle immediately.

3. Examine for other injuries as well as chest injuries.

4. Cover or close sucking chest wounds.

5. Radiographs should be carried out when the patient is stable.

Management of specific complications of thoracic trauma

Pneumothorax (Fig. 9.1)

Open sucking wounds

Air is sucked into the pleural cavity during inspiration. This causes a to-and-fro movement of the mediastinum during respiration and leads to respiratory embarrassment. The open wound must be sealed immediately by application of Vaseline gauze dressings. Surgical closure is carried out as soon as possible. A chest drain should be inserted meanwhile.

Figure 9.1 A pneumothorax is visible on the right side. Note the absence of lung marking at the periphery. The lung edge is visible (arrow).

Closed pneumothorax

This results from an air leak from lung, tracheobronchial tree or oesophagus. It may occur from open or closed trauma.

Simple pneumothorax

May be associated with haemothorax. If the pneumothorax is small (<10%) on CXR, it may be reassessed later by repeat CXR. If larger, a chest drain connected to an underwater seal should be inserted. It is recommended that all traumatic pneumothoraces are drained as there is a risk of tension pneumothorax. Aspiration is appropriate for small spontaneous pneumothoraces.

Tension pneumothorax

This may cause sudden death. Chest pain, dyspnoea, cyanosis occur. Hypotension results from vena cava distortion when the mediastinum is pushed over, decreasing venous return to the heart. There is tracheal deviation to the opposite side and absent ipsilateral breath sounds. Immediate life-saving treatment is by inserting a wide-bore i.v. cannula to decompress the pleural cavity if a chest drain is not immediately available. The wide-bore needle should be replaced by a chest drain connected to an underwater seal.

Flail chest

This is due to blunt chest trauma causing multiple rib fractures, anteriorly and posteriorly, which isolate a segment of the chest wall. The classical description is that the isolated segment moves in and out with respiration in a paradoxical fashion. There is usually associated pulmonary contusion and pneumothorax. If there is no pneumothorax or haemothorax, then the intrapleural pressure remains negative and the flail segment moves inwards as the intrapleural negative pressure increases during inspiration and outwards during expiration. Although paradoxical movement is an important physical sign, it has probably in the past received undue emphasis in the management of flail chest. Often the chest does not move paradoxically because the patient does not allow it to do so because it hurts so much. Usually flail chest is treated with epidural anaesthesia, physiotherapy and oxygen. Endotracheal intubation and intermittent positive pressure ventilation is reserved for those who decompensate. Rib cage fixation has increased in use recently, especially for young patients or those on IPPV.

Simple rib fractures

These may be very painful and inhibit breathing and coughing, leading to chest infection – especially in the elderly. Pain is best relieved by intercostal nerve blocks with a long-acting local anaesthetic. Strapping of the chest wall is a method that affords some comfort but inhibits chest wall movement and may predispose to pulmonary complications. The practice has largely been abandoned.

Cardiac trauma

This may cause damage to the following:

• The myocardium with infarction

• Valves with development of symptoms of valvular incompetence

• Conducting mechanisms with heart block and arrhythmias.

Lacerations will cause cardiac tamponade. Initial treatment is conservative unless there is cardiac tamponade, in which case, needle aspiration or open thoracotomy is required.

Symptoms and signs

Pleuritic chest pain, breathlessness, signs of CCF, peripheral oedema. Ipsilateral reduced expansion, dullness to percussion, absent breath sounds.

Investigations

• CXR: dense shadow over a lung field with concave upper limit (→ Fig. 9.2). If the upper border is horizontal, then a pneumothorax is also present

• Diagnostic aspiration – assess protein content

• Culture and sensitivity

• TB culture

• Cytology for malignant cells

• Pleural biopsy.

Figure 9.2 A right-sided pleural effusion. Note the dense shadow and the concave upper limit of the effusion.

Treatment

It is of the underlying cause. Large effusions need drainage. In malignant effusions, give chemical pleurodesis by instilling a substance into the pleural cavity after drainage. Talc is the most effective, with tetracycline the second most effective. Decortication of the pleura is effective in the control of effusions.

Tumours of the pleura

Primary tumours of the pleura are increasing in incidence. The commonest pleural neoplasm is mesothelioma. Mesothelioma occurs in people with a history of exposure to asbestos. The disease is exceptionally rare in those who have not been exposed. It is most common in males between 40 and 50. Symptoms include malaise, weakness, cough, dyspnoea, weight loss and fever. Radiograph shows pleural fluid and thickening. Diagnosis is established by cytology or pleural biopsy. Radiotherapy or chemotherapy are palliative. Some patients benefit from extrapleural pneumonectomy. Neoplasms of the pleura may also be due to secondary spread from other tumours, e.g. bronchus, breast.

Pulmonary infections

Bronchiectasis

This is a complication of repeated pulmonary infection where the respiratory pathways are permanently damaged and dilated. It usually affects the lower lobes. The dilated bronchi harbour infected sputum, which is expectorated, often in large amounts. Common pathogens include haemophilus and pseudomonas. Causes of bronchiectasis include cystic fibrosis, Kartagener’s syndrome (bronchiectasis, sinusitis, dextrocardia), whooping cough, measles, tuberculosis, inhalation of foreign bodies, pneumonia.

Lung abscess

The causes are bronchial obstruction due to carcinoma, inhalation pneumonitis, inhaled foreign body (especially lung abscess in a child), septic embolus, infected pulmonary infarct, transdiaphragmatic extension of subphrenic abscess. Other causes include: infected cyst; secondary to pneumonia, bronchiectasis or TB; immunosuppression; blood-borne, e.g. staphylococcal septicaemia; fungal.

Tuberculosis

The reader is referred to a textbook of medicine. Surgery is little required in this condition at the present time, since antituberculosis therapy is effective in most cases. However, the incidence of TB is increasing and new cases are being seen associated with AIDS. Surgery is required for some of the complications of TB, e.g. bronchopleural fistula, persistent open cavities with positive sputum, bronchiectasis, haemorrhage and destroyed lung. Of historical interest are the operations of thoracoplasty and phrenic nerve crush. Patients who have had these procedures are occasionally seen (usually in finals!). The procedures are designed to collapse the chest wall and the diaphragm onto the lungs, deflating and ‘resting’ the lungs while healing occurs.

Lung tumours

Bronchial carcinoma

This is the commonest cancer in males in the UK accounting for approximately 50 000 deaths per year. It is the second commonest in females. Of all lung cancers, 75% are related to smoking. Other aetiological factors include chronic exposure to asbestos, nickel, arsenic, petroleum products and radioactive materials. Four histological types are described:

• Adenocarcinoma (30–45%)

• Squamous cell carcinoma (25–40%)

• Small cell (oat cell) carcinoma (15–25%)

• Undifferentiated large cell carcinoma (rarest).

Symptoms and signs

Primary

The tumour may be asymptomatic and seen on routine CXR. Cough, haemoptysis, dyspnoea, chest pain, wheeze, hoarseness, recurrent chest infections, dysphagia.

Complications

• Thoracic: pleural effusion, recurrent laryngeal nerve palsy (hoarseness), SVC obstruction, Horner’s syndrome (ptosis, meiosis, enophthalmos, anhidrosis) especially with Pancoast’s tumour (invasive cancer of apex of lung).

• Metastatic: cachexia, malaise; brain (headaches, fits, personality change); bone (pathological fractures); liver (jaundice); adrenal (Addison’s disease).

• Non-metastatic, extrapulmonary: ADH, ACTH secretion, hypercalcaemia, myasthenic neuropathy, hypertrophic pulmonary osteoarthropathy, thrombophlebitis migrans, gynaecomastia, clubbing.

Treatment

Surgery offers the only hope of cure. Depends on histological type. Non-small cell tumours, if small and localized (especially if occurring peripherally), may be resected. Larger ones may respond to radiotherapy. Small cell tumours are aggressive and are usually beyond surgery, having disseminated at the time of presentation. Combination chemotherapy and radiotherapy prolong survival in small cell tumours. Squamous cell carcinoma is radiosensitive. Most patients are incurable at presentation. Symptomatic relief is the aim. Radiotherapy is appropriate for a bronchial obstruction with lung collapse, SVC obstruction, bone pain and haemoptysis. Endobronchial and SVC stenting procedures may be carried out. SVC obstruction treated by stenting has a success rate of 90% with insertion of a stent via the right femoral vein. Extensive endoluminal disobliteration can be carried out using a cryoprobe/laser and endoluminal brachytherapy.

Surgical treatment involves lobectomy or pneumonectomy and is the only potential cure. Careful selection of patients is required and operability should be assessed by bronchoscopy, CT scan, radioisotope bone scan and ultrasound scan (liver). Contraindications to surgery include distant metastases, SVC obstruction, malignant pleural effusion, recurrent laryngeal nerve and phrenic nerve involvement.

Prognosis

About 35% survive 5 years after lobectomy and 25% after pneumonectomy. Since 75% are not candidates for surgery, the overall survival for 5 years is about 5–10%. Prognosis ultimately depends on the cell type and stage of the disease at the time of diagnosis. Small cell carcinoma has the worst prognosis.

Metastatic lung tumours

Metastatic tumours are common in the lung, which in some cases may be the only site of metastases. Secondaries may be from adenocarcinoma (breast, kidney, bowel), sarcoma (bone) or malignant melanoma. Rarely, single or multiple metastatic lung tumours may be removed as part of the treatment. The primary tumour must be controlled and no metastases should be present elsewhere (CT scan, ultrasound scan, bone scan, PET scan). The best results are obtained with tumours for which there is effective chemotherapy. The best example is the surgical treatment of pulmonary metastases in patients with osteogenic sarcoma. The presence of metastatic colonic tumour in the lung is an increasing indication for ‘metastasectomy’. Results are improving.

Mediastinum

Mediastinal masses may be found incidentally on routine CXR or may be symptomatic. A lateral CXR and CT scan may be required to localize the mass and indicate its aetiology.

Certain lesions are more likely to occur in characteristic mediastinal sites:

• Superior mediastinum: retrosternal goitre

• Anterior mediastinum: dermoid cysts, teratoma, pericardial cysts, bronchogenic cysts, diaphragmatic hernia (foramen of Morgagni), thymoma

• Posterior mediastinum: neurogenic tumours, e.g. dumbbell tumours of neurofibroma, paravertebral mass, e.g. TB abscess, phaeochromocytoma, diaphragmatic hernia, achalasia, hiatus hernia.

In addition to the above, aneurysms and lymph nodes may be apparent in any site. Causes of lymph node enlargement include secondary deposits, sarcoid, lymphoma and TB.

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Thorax

Pneumothorax (Fig. 9.1)

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