Mortality

Risk stratification is important in cardiac surgery and Euroscore is a valuable tool for quantifying operative risk across all types of non-congenital cardiac surgery. Patient, condition, and procedure related factors contribute to a score which predicts 30-day mortality. Predicted operative mortality ranges from < 1% for routine elective procedures to more than 50% for complex emergency operations.

Stroke

Stroke risk varies from 1% to over 10%, and is associated with intracardiac thrombus and severe atheromatous disease of the proximal aorta and carotids. Patients with evidence of peripheral vascular disease have a higher risk of stroke and those with high-grade symptomatic carotid disease may benefit from carotid endarterectomy prior to cardiac surgery (Ch. 21).

Cardiopulmonary bypass (CPB)

Modern cardiac and great vessel surgery became feasible with the development of cardiopulmonary bypass. Venous blood is drained via cannulae inserted into the right atrium or venae cavae and passes to a reservoir. It is then pumped through an oxygenator, which adds O₂ and removes CO₂, through a heat exchanger coil so that its temperature can be varied and finally, the blood is returned to the arterial circulation via a cannula in the ascending aorta or other suitable artery (femoral, axillary) (Figs 22.1, 22.2 and 22.3). Full anticoagulation with intravenous heparin is required to prevent blood clotting in the tubing, oxygenator and pump mechanisms. Roller or centrifugal pumps are used, as these minimize red cell trauma. Semipermeable membranes, or more commonly hollow fibres, form the blood–gas interface within the oxygenator. A trained perfusion technician controls the bypass machine.

Fig. 22.1 Normal cardiac chambers.

(LA = left atrium; LV = left ventricle; RA = right atrium; RV = right ventricle; PA = pulmonary artery).

Fig. 22.2 Schematic of a bypass circuit.

Fig. 22.3 Cannulation for cardiopulmonary bypass.

Upper arrow from right atrium to pump. Lower arrow from pump to aorta.

CPB stimulates a systemic inflammatory response mediated by cytokine release, complement activation and white cell activation. These changes do not generally cause clinical problems but may be implicated in post-bypass pulmonary, renal and cerebral dysfunction. Cerebral damage occurs in about 1% of cases due to intracerebral bleeding, embolization of microbubbles or arterial debris, or inadequate cerebral perfusion. Subtle deterioration in cerebral function, as detected by psychological testing, is more frequent. Coagulopathy and haemolysis are associated with prolonged bypass.

Myocardial preservation

Intensive care

Postoperatively, patients are usually ventilated for a few hours until they are fully rewarmed, and have satisfactory stable haemodynamics, pulmonary gas exchange and acid–base status. Urine output is copious and potassium levels are, therefore, checked frequently so that potassium is administered intravenously to correct urinary losses. Invasive measurement of arterial and central venous pressure is standard. Pulmonary artery catheters may be used to measure pulmonary artery pressure, pulmonary artery capillary wedge pressure and cardiac output.

Complications

Other than death or stroke, established complications include:

Recovery time

Patients undergoing routine elective coronary or valve surgery will usually leave acute hospital care within one week. Those requiring more extensive surgery or emergency procedures may take longer to recover. Most patients will have undergone a median sternotomy (Fig. 22.4). This wound heals quickly and, as the sternal edges are approximated securely by wire or heavy sutures, chest discomfort eases rapidly. Leg vein donor sites may take longer to heal, particularly around the knee. By 2 weeks the patient should be able to walk a few hundred metres, and by 3 months should have returned to full activity, including work.

Fig. 22.4 Surgical approach to the heart.

A Median sternotomy incision. B Right atrium and ascending aorta exposed.

Assessment

Exercise electrocardiography (ECG) is often used as an initial screening test for patients with suspected stable angina. Those with confirmed ischaemia then undergo coronary angiography and assessment of left ventricular function by means of angiography or echocardiography. Contrast medium is injected into the coronary circulation (Fig. 22.5) via a catheter that is usually inserted through the femoral or radial artery (Fig. 22.6). Images are obtained in several different planes so as to minimize the risk of missing eccentric lesions. Intervention is usually only advised for stenoses that exceed a 70% reduction in vessel diameter.

Fig. 22.5 Coronary circulation.

Fig. 22.6 Coronary angiography.

A Left coronary angiogram demonstrating severe left main stem stenosis. B Right coronary angiogram demonstrating multiple stenoses.

Indications

Elective surgery is indicated primarily for the control of angina that is refractory to medical treatment and is unsuitable for percutaneous intervention (PCI) usually with stent insertion. Historically, patients with three-vessel disease or left main stem disease have exhibited a high (c. 8% per year) risk of death from MI with medical therapy alone. Surgery improves long-term survival for such patients, particularly when LV function is also impaired. PCI has an important role in the management of patients with acute coronary syndrome ranging from ST elevation myocardial infarction to unstable angina.

Some patients requiring other cardiac procedures may be shown to have significant coronary disease during cardiological assessment. In these cases, coronary surgery may be added to the primary procedure to improve perioperative survival and prevent future ischaemic problems. Emergency coronary surgery is rare and patients with incipient or established MI fare better with PCI and supportive medical therapy, as the mortality of surgery in this setting is much increased.

Coronary bypass

A coronary artery bypass graft (CABG) delivers blood to the distal coronary artery beyond a stenosis. If the distal artery is obliterated by atheroma, an endarterectomy procedure may be performed to restore the lumen. Originally, nearly all grafts comprised reversed segments of the long saphenous vein anastomosed proximally to the ascending aorta and distally to the coronary artery. Such grafts have patency rates of around 70% at 5 years and 40% at 10 years. Venous graft failure occurs as a result of intimal hyperplasia, which is thought to be, in part at least, a response to arterial pressure. The relatively high rate of vein graft failure stimulated interest in arterial grafts and led to the almost universal use of the internal thoracic artery (ITA). This is usually employed as a pedicled graft when it is left attached to the subclavian artery proximally, but can also be used as a free graft in the same manner as vein. ITA graft patency exceeds 90% at 5 years and 70% at 10 years. A common combination is to use the left ITA for the left anterior descending artery and vein grafts for the other vessels (Fig. 22.7).

Fig. 22.7 Completed coronary bypass procedure with venous and left internal thoracic artery grafts in situ.

The radial artery is a possible option as a free graft for use in people with poor-quality saphenous vein and critical proximal occlusion of more than 70% in the target vessel, and may be used together with ITA grafts to achieve ‘total arterial revascularization’. Occasionally, when there is a shortage of good conduit (e.g. in a ‘redo’ operation), the surgeon may consider using the right gastroepiploic artery, the short saphenous vein and the cephalic vein. Prosthetic grafts occlude early and are not used.

Results

Uncomplicated coronary surgery should carry a 2–3% risk of mortality and a 1–2% risk of stroke. Angina is relieved completely in about 70% of cases, is significantly improved in the remainder, and recurs with a frequency of about 10% per year. Successful revascularization may also improve breathlessness if it is related to myocardial ischaemia, and survival is probably enhanced in patients with left main stem and triple vessel disease. The use of arterial conduits is associated with better graft patency and improved survival. Although there is a trend in that direction for patients with multiple arterial grafts followed up beyond 10 years, the added benefit over one ITA graft placed to the left anterior descending coronary is small. This may reflect the progression of native coronary disease. Secondary prevention is mandatory in all patients with CAD and includes antiplatelet medication (aspirin) and cholesterol reduction (statin) (EBM 22.1).

Mitral valve regurgitation (MR)

Postmyocardial infarction ventricular septal defect

Necrosis of the intraventricular septum due to MI may lead to a ventricular septal defect. Blood flows from the high-pressure left to the low-pressure right ventricle (left-to-right ‘shunt’). This increases right ventricular work and pulmonary blood flow and decreases cardiac output. Typically, the patient complains of sudden, severe breathlessness 3–8 days after an MI and is noted to have developed a pansystolic murmur. The diagnosis is confirmed by echocardiography and coronary angiography is performed. Emergency repair is technically difficult due to the poor quality of the recently infarcted muscle to which the patch is attached. In addition, these patients have impaired cardiac function in the aftermath of an acute MI. Typically, such patients will require mechanical support of their ventricle with an intra-aortic balloon pump. Surgical mortality ranges from 20–50%. Patients with minor shunts are managed medically and may be considered for surgery some weeks later to allow cardiac function to stabilize. The margins of the defect will have healed by fibrosis, making patch repair relatively straightforward with more acceptable operative mortality (< 10%).

Left ventricular aneurysm

LV aneurysm complicates about 8% of MIs and occurs when a large left ventricular free-wall MI scar becomes aneurysmal as a result of intraventricular pressure. A large aneurysm impairs cardiac contraction and increases myocardial work. Complications include clot formation within the aneurysm, which may embolize, and arrhythmias generated within the zone of ischaemic myocardium around the periphery of the aneurysm.

At operation, the aneurysm is excised, the clot removed and the resulting defect usually closed by direct suture, reinforced by buttressing strips of Teflon felt or vascular graft. Occasionally, a small patch repair is performed to preserve the shape of the left ventricle. Surgery performed electively has a mortality of 6–10% and an increased risk of stroke.

Stenosis

Aortic stenosis is the commonest indication for valve surgery in the UK. Although rheumatic disease remains a common problem in underdeveloped countries, the most frequent aetiology in the Western world is calcific aortic stenosis which develops in the older population usually over 70 years. The normal aortic valve has three cusps but a congenital bicuspid valve usually calcifies from the sixth decade onwards (Fig. 22.10). Aortic stenosis causes left ventricular hypertrophy, effort angina, episodes of arrhythmia with syncope or even sudden death, and left ventricular failure.

Fig. 22.10 Calcified aortic valve.

Clinically, the patient has a slow rising pulse, a forceful apex beat and an ejection systolic murmur in the right upper parasternal area that may radiate to the root of the neck. Echocardiography will confirm a valvular gradient, which is considered severe aortic stenosis when this exceeds 60 mmHg. However, measurement of orifice area is independent of cardiac output and may be a more reliable measure. The onset of symptoms should initiate referral for surgery. Patients with cardiac failure have a low cardiac output and consequently a low gradient. In these cases, the decision to operate may be a difficult judgement, based on the absence of any other likely cause of poor left ventricular function and echocardiographic evidence of severe aortic valve disease.

In high risk patients e.g. the very elderly, those with patent ITA grafts or significant other co-morbidities, percutaneous replacement of the aortic valve may be considered (TAVI – transcatheter aortic valve insertion) where a biological valve on a holder is introduced percutaneously via the femoral artery or left ventricular apex.

Regurgitation

Native aortic regurgitation may be due to primary valve pathology (rheumatic fever, endocarditic valve destruction or, rarely, a bicuspid valve) or secondary to aortic root pathology with annular dilatation (see below). Prosthetic valve regurgitation can occur as a result of deterioration of a biological prosthesis, partial obstruction of a mechanical device, or paraprosthetic leakage. Chronic aortic regurgitation causes progressive left ventricular dilatation and hypertrophy.

Clinically, there is a wide pulse pressure – collapsing pulse, lateral displacement of the apex beat and a diastolic murmur in the left parasternal area. Chronic aortic regurgitation is well tolerated and often asymptomatic. In severe cases, the patient may complain of dyspnoea and angina, and may exhibit features of congestive cardiac failure. Surgery is advised to forestall the onset of cardiac failure due to irreversible myocardial damage. The timing of surgery is determined by serial echocardiography measurements demonstrating left ventricular dilatation.

Acute aortic regurgitation produces severe dyspnoea, with rapid onset of left ventricular failure and pulmonary oedema. The patient may require emergency ventilation and urgent surgery.

Surgical outcomes

Elective aortic valve replacement is a relatively straightforward procedure, with a mortality of about 3% and stroke rate of 1%. The risk is increased several-fold in cases that have progressed to cardiac failure, and in emergency cases with acute severe regurgitation.

Stenosis

Although the incidence of rheumatic valvular heart disease is declining, the commonest pathological presentation is mitral stenosis which restricts the flow of blood into the left ventricle, which is consequently small and thin-walled. Cardiac output is also reduced. The left atrium is dilated and left atrial and pulmonary artery pressures are raised. Chronic pulmonary hypertension causes right ventricular hypertrophy and dilatation, and in advanced cases tricuspid incompetence may develop (see below).

Clinically, patients complain of shortness of breath on exertion and may experience palpitations. Chronic atrial fibrillation usually intervenes and the patient may be taking warfarin along with a diuretic therapy for pulmonary congestion. Examination reveals atrial fibrillation, a left parasternal heave due to right ventricular enlargement, and a diastolic murmur best heard at the lower left sternal edge, accompanied by a loud second heart sound. Chest X-ray shows right ventricular and atrial enlargement and the pulmonary artery is prominent. A progressive increase in heart size is often evident on serial annual films and renal function is frequently impaired.

The timing of surgery is a matter of judgement but an echocardiographic calculated mitral valve area below 1 cm² demonstrates severe stenosis and is an indication for surgery. Very occasionally, the patient may have echocardiographic evidence of leaflet fusion only, in which case percutaneous balloon valvuloplasty may be effective. Conservative surgery with separation of the fused leaflets (commissurotomy) and reconstruction of the valve is possible in some younger patients. Usually, however, there is extensive leaflet calcification, with involvement of the subvalvular apparatus. There is shortening and thickening of the papillary muscles and chordae tendinae, tethering the leaflets to the tips of the papillary muscles (Fig. 22.11). Valve replacement is therefore the only practical option.

Fig. 22.11 Excised mitral valve showing the shortening and fusion of the papillary muscles and chordae tendinae in advanced mitral stenosis.

Rarely, patients with a mechanical mitral prosthesis may develop thrombotic occlusion of their valve secondary to inadequate control of anticoagulation or to fibrous tissue (pannus) ingrowth from the sewing ring. This acute emergency causes catastrophic pulmonary oedema and a severe reduction in cardiac output. Emergency salvage valve replacement or debridement is required.

Regurgitation

Chronic mitral regurgitation occurs with rheumatic disease, ischaemic papillary muscle dysfunction, myxomatous degeneration of the mitral valve, a variety of systemic connective tissue disorders and chronic paraprosthetic valvular leakage. Acute regurgitation is much less common and follows acute MI involving a papillary muscle, as noted above, but can also result from spontaneous rupture of a chorda tendina, sudden failure of a bioprosthetic valve leaflet or perforation of an infected native valve. Chronic mitral regurgitation presents a volume load to the left ventricle, which ejects blood preferentially backwards through the incompetent mitral valve to the pulmonary circulation. This situation is often well tolerated for years, with patients typically complaining of shortness of breath on exertion and of occasional episodes of palpitation.

Clinical examination is often relatively unremarkable, apart from a pansystolic murmur radiating from the lower left sternal edge to the axilla and leftward displacement of the apex beat. Surgery is indicated where there is chest X-ray and echocardiographic evidence of left ventricular dilatation, as this process correlates with declining left ventricular function consequent upon the continued volume overload. Acute regurgitation causes pulmonary oedema and emergency surgery is necessary. Regurgitant mitral valves are frequently repaired but often prosthetic replacement is required.

Surgical outcomes

Elective mitral valve surgery for regurgitation is generally a low-risk procedure, with a mortality rate of 4–6% and a stroke rate of about 2%. The risk is much greater (10–15%) for patients with ischaemic regurgitation, owing to the concomitant coronary disease and previous myocardial damage. Valve replacement for mitral stenosis carries a significant mortality (8–12%) due to established pulmonary hypertension, right ventricular failure and poor renal function. The stroke rate is increased to 3–4%.

Emergency valve replacement for acute obstruction or regurgitation carries mortality of the order of 20%.

Cardiac tamponade with penetrating trauma

This is a surgical emergency and the clinical diagnosis is made from an elevated JVP, hypotension and the site of the wound which is commonly the result of an assault with a knife. Prompt anterior thoracotomy, relief of the bloody tamponade and digital control of the penetrating injury to the heart until suitable suture can be achieved may be life-saving. Major injuries to structures may require CPB.

Aetiology, pathology and presentation

This usually presents from the fifth decade onwards and is the leading cause of cancer death in the UK for both men and women. The principal risk factor is smoking; particularly cigarettes, but other rare causes include exposure to various chemicals. The combination of asbestos exposure and cigarette smoking produces a many-fold increase in risk.

With the exception of alveolar cell carcinomas, which arise from cells lining the alveoli, Primary lung cancers arise within the bronchial epithelium and are hence termed bronchogenic carcinoma. They are described as peripheral or central, according to their location within the lung (Figs. 22.17, 22.18 and 22.19). Peripheral lesions may grow to 8 cm or more before causing local symptoms such as chest wall pain. Many are detected as incidental findings on a chest film taken for unrelated reasons, or for non-specific symptoms such as weight loss. Central lesions tend to occlude the airways, causing varying degrees of pulmonary collapse and consolidation (Fig. 22.19). Nodal spread occurs to the intralobar, hilar and mediastinal nodes, and thence to the scalene nodes. Metastases occur in bone, brain, liver, adrenals and lung. Local direct spread may involve the chest wall, vertebrae, trachea, oesophagus and great vessels.

Fig. 22.17 Chest X-ray showing cancer in the right upper lobe.

Fig. 22.18 PET CT images of right upper lobe carcinoma with local nodal and subcarinal disease.

Same patient as Figure 22.17.

Fig. 22.19 Consolidation/collapse of the right middle and lower lobes associated with a central bronchogenic carcinoma.

The approximate frequencies of the various cell types are: squamous 35%, adenocarcinoma 35%, undifferentiated 10%, small cell 15% and rare cancers 5%.

As small cell lung cancer is regarded as a systemic disease at presentation, patients are not usually referred for surgery and are therefore treated with chemotherapy. All other varieties are resected if possible (EBM 22.3). Therefore, for surgical treatment purposes, bronchogenic carcinoma is categorized into small cell and non-small-cell. However, cell type is important as recent advances in pathology have found genetic mutations that identify tumours that may be sensitive to new chemotherapeutic agents.

There may be no clinical features, but haemoptysis, pulmonary infection and weight loss are common presenting symptoms. Paraneoplastic syndromes are infrequent but well described, including ectopic hormone production (adrenocorticotrophic hormone (ACTH), parathyroid hormone (PTH), antidiuretic hormone (ADH)) and a painful periosteal reaction affecting the joints and long bones, termed hypertrophic pulmonary osteoarthropathy. Patients frequently have finger clubbing.

Fitness for resection

Fitness is determined by cardiorespiratory assessment. A history of angina or myocardial infarction does not preclude surgery, provided the symptoms are stable. However, patients with poor left ventricular function and/or unstable angina are not suitable for pulmonary resection. Respiratory investigations including the forced expiratory volume in one second (FEV₁) and carbon monoxide (CO) transfer data, will establish whether pulmonary reserve will be adequate following the intended resection. Patients with an FEV₁ < 50% predicted, prior to resection, are likely to be significantly breathless following surgery and may not be suitable candidates for surgical management. If the CO transfer value is low, implying poor alveolar gas exchange, the minimum FEV₁ figure would have to be revised upwards. However, resection of consolidated or collapsed lung does not affect residual respiratory capability.

Resection

Lung tumours are normally removed en bloc with the surrounding parenchyma and local draining lymphatics. This involves either lobectomy or pneumonectomy. Occasionally, in unfit patients, small cancers are excised within a wedge or segment of lung but the risk of local recurrence is greater in these lung-sparing cases. An area of anterior chest wall directly invaded by tumour can be excised and replaced with synthetic patch, provided it is lateral to the posterior rib angles. Following assessment and surgical resection, the final pathological TNM stage (Table 22.4) is helpful in indicating prognosis and determining whether a patient might benefit from adjuvant therapy usually within the setting of a trial. Patients who are found to have positive mediastinal nodes following resection are routinely referred for adjuvant radiotherapy to the mediastinum in view of the high risk of recurrence in that area. Postoperative chemotherapy may improve 5-year survival across all resected stages by approximately 5%. Although still controversial, this form of adjuvant therapy is likely to become an increasingly common option for suitably fit patients. Operative mortality is about 2% for lobectomy and 6% for pneumonectomy.

Table 22.4 TNM classification of lung cancer

Survival

Reported 5-year survival data are approximately 60% for stage I, 35% for stage II and < 20% for stage IIIa disease. Relatively few patients (< 20%) with non-small-cell bronchogenic carcinoma are suitable for resection at presentation. One strategy to address this problem is the use of neoadjuvant preoperative induction chemotherapy to downstage tumours, although there are as yet no data to support the widespread use of this approach. The other obvious possibility for improving resection rates would be to detect lung cancers at an earlier stage. Previous mass chest X-ray screening studies did not appear to show an improvement in long-term survival, but there is currently renewed interest in screening high-risk individuals (smoking history, > 50 years old) using CT as a more sensitive test.

Mass lesions

Benign and malignant masses may arise in the mediastinum. Some clue to the likely diagnosis is provided by the location of the lesion (Fig. 22.21) within the mediastinum. Where the diagnosis is in doubt, tissue may be obtained by CT-guided needle biopsy. If this is either not feasible or is unsuccessful, a surgical biopsy can be obtained using mediastinotomy, mediastinoscopy or videothoracoscopy. The clinical features vary considerably, with some quite large masses being asymptomatic and identified on routine chest films. Non-specific symptoms include vague chest pain, cough, weight loss, fever and general malaise. Other lesions may cause direct pressure effects, such as tracheal compression by a retrosternal thyroid goitre or oesophageal compression by malignant lymphadenopathy. Thymomas may be identified during the evaluation of patients with myasthenia gravis and resection of these may improve their neurological symptoms.

Fig. 22.21 Topography of mediastinal lesions.

Wherever possible, primary mediastinal tumours are resected, although in many cases this is precluded because the growth involves the great vessels and mediastinal viscera. Benign cysts are usually resected or, less commonly, marsupialized in order to prevent pressure effects or the development of infection. Surgery is generally undertaken via a median sternotomy for anterior lesions or a thoracotomy for mid- and posterior lesions.

Infection

Mediastinal infection is an uncommon but serious condition that is associated with a rapid onset of septicaemia and septic shock. It is almost always a consequence of oesophageal or pharyngeal leakage, which may follow perforation or breakdown of an oesophageal anastomosis (see Ch. 13).

Management

Initial management may involve aspiration or the insertion of a chest drain connected to an underwater seal into the pleural space (Fig. 22.24). This allows the lung to re-expand. In most cases of primary pneumothorax, air leakage stops within 48 hours or so, after which the drain can be removed. If the pneumothorax recurs or the air leakage does not stop, thoracoscopic surgery is indicated. The lung is inspected and any blebs or bullae are stapled. These are usually found at the apices of the upper or lower lobes (Fig. 22.22). Pleurodesis is then performed either by using an abrasion technique to scarify the parietal pleura, or a pleural strip (pleurectomy), or by insufflation of kaolin. Bullectomy and abrasion or pleurectomy carry about an 8% risk of further recurrent pneumothorax. This is reduced to 1–2% with kaolin insufflation, but as this technique involves leaving foreign material in the chest of a young person, it is usually kept in reserve for recurrent pneumothorax or for patients with no obvious culprit bulla or bleb.

Fig. 22.24 Underwater seal drain.

The water acts as a hydraulic valve. This allows air to escape from the pleural cavity with ease but the pressure required to cause reverse air flow is much greater, being increased by the ratio of the surface areas inside and outside the tube that enter the water.

Fig. 22.22 Typical moderate sized apical bulla seen at thoracotomy.

Secondary pneumothorax may not settle rapidly, owing to the poor quality of the underlying lung tissue. It typically occurs in individuals who are poor candidates for general anaesthesia and major thoracic surgery. It is customary, therefore, to wait for 1–2 weeks to see if the air leak will stop spontaneously. If not, videothoracoscopy is undertaken in better-risk patients to inspect the lung for a leaking bulla, which can be closed by stapling. Alternatively, kaolin mixed with local anaesthetic can be inserted as slurry up the drain. This option avoids general anaesthesia but results in significant pain. Either treatment is associated with an appreciable mortality of 5–10%, owing to respiratory and cardiovascular complications.

Empyema

This is a collection of pus within the pleural cavity. It commonly follows pneumonia due to secondary infection of a reactive parapneumonic effusion. In the initial phase, the infected fluid is thin and may be completely evacuated by a low intercostal drain. The empyema quickly becomes thick and loculated as a result of the deposition of fibrin, and at this stage formal surgical drainage is required. The collection is typically placed posteriorly towards the base of the pleural cavity and causes a D-shaped shadow on the chest film (Fig. 22.25). Drainage in this phase may be achieved by videothoracoscopic techniques or by excising a 2 cm segment of rib over the lowest part of the empyema and suctioning and curetting the cavity clean. As dense fibrosis surrounds an empyema, drainage creates a fixed cavity. In elderly or unfit patients, a simple open tube drain is left in situ for many months, during which the cavity gradually shrinks and finally obliterates. In younger patients, open formal thoracotomy with decortication allows the fibrous cavity to be excised and any cortex over the lung removed. This returns more lung function to the patient and avoids prolonged open drainage, so that recovery is more rapid.

Fig. 22.25 Lateral X-ray of empyema.

This film shows the D-shaped outline of a typical empyema with fluid level (arrow).

Other causes of empyema include postsurgical bronchial or oesophageal suture line leakage, oesophageal rupture or perforation, repeat aspiration of pleural effusion, secondary infection of a clotted haemothorax and, rarely, a subphrenic abscess.

Bronchiectasis

Dilatation of bronchi and bronchioles can follow childhood infections e.g. measles or pertussis. The stagnant pools of secretions that collect are subject to continued infection, resulting in episodes of acute pulmonary infection or pneumonia and, more rarely, in haemoptysis. Management is by antibiotic therapy, physiotherapy and daily postural drainage. Evaluation by CT usually demonstrates that the condition is fairly widespread throughout the lungs, but occasionally one lobe may be particularly badly affected. This is more likely when the bronchiectasis is secondary to chronic bronchial obstruction by an inhaled object or, more rarely, from external glandular compression. In this relatively uncommon situation, lobectomy may result in a gratifying decrease in chronic sputum production and in the frequency of recurrent infection. Resection can be technically difficult, as dense vascular adhesions surround the affected lobe.

Pain control

Pain management during the HDU phase is achieved normally by placement of an epidural catheter. It can have disadvantages related to increased fluid requirement, nursing care, and marked pain appreciation when the epidural infusion is stopped. Many units prefer not to place an epidural catheter and to rely instead on a combination of patient-controlled morphine infusion supplemented by parenteral non-steroidal analgesics and local intercostal nerve blocks. These can be conveniently given via a paravertebral catheter inserted at surgery.

Management of secretions

It is vital that patients cough and clear secretions. This requires humidification of oxygen to prevent the secretions becoming excessively viscous, effective pain control, and considerable input from physiotherapy since many patents have pre-existing impaired lung function. Excessive secretions may require to be removed by suction bronchoscopy under light general anaesthesia, and a mini-tracheostomy tube may be inserted via the cricothyroid membrane. In severe cases, ventilation and formal tracheostomy may be required.

Fluid management

Following major thoracic surgery, the pulmonary alveolar- capillary membrane becomes relatively leaky, so that fluid tends to accumulate within the pulmonary interstitial spaces. This decreases lung compliance and increases the work of breathing. A degree of postoperative fluid restriction for the first 48 hours ensures that the left atrial pressure is kept low, thereby decreasing pulmonary venous pressure and the transcapillary gradient.

Late management

All patients receive subcutaneous heparin as prophylaxis for deep venous thrombosis until fully mobile, because the risk of thrombosis is high in thoracic surgery and the consequences of pulmonary embolism are that much worse when lung has been resected. Drains are withdrawn when air leakage stops, and patients are mobilized as rapidly as possible. In an uneventful recovery, discharge home should occur about 6–9 days after major open resection, and after 1–5 days following a video- thoracoscopic minimal-access procedure. The patient’s age, general health and social circumstances will influence these estimates.