Oxford Handbook of Clinical Surgery (4 edn)
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Basics
(see 
p. 55)
Give 10–20mmol K+ via central line to get serum K+ 4.5–5.0mmol/L.
Give empirical 20mmol Mg+ via central line if none given post-op.
Give of 300mg amiodarone IV over 1h in patients with good left ventricle, followed by 900mg amiodarone IV over 23h.
In patient with poor left ventricular function, give digoxin in 125mcg increments IV every 20min until rate control is obtained, up to a maximum of 1500mcg in 24h.
Synchronized DC cardioversion for unstable patients ( p. 189).
(see p. 180)
Get immediate help if bleeding is >400mL in 30min.
Give gelofusine to get CVP 10–14 and systolic BP 80–100mmHg.
Order further 4U of blood, 2U FFP, and 2 pools platelets.
Send clotting and FBC, request a CXR.
Transfuse to achieve Hb >8.0g/dL, platelets >100 x 109/L, APTT <40.
Give empirical protamine 25mg IV.
Emergency re-exploration is indicated for excessive bleeding.
Get immediate help.
Quickly assess pulse, rhythm, rate, CVP, O2 sats, and bleeding.
Defibrillate VF or pulseless VT, treat AF as above.
Treat bradycardia with atropine 0.3mg IV or pace.
Give gelofusine to raise CVP to 12–16mmHg, place bed head down.
If suspect cardiac tamponade ( p. 480), prepare for re-sternotomy.
If patient warm and vasodilated, draw up 10micrograms of metaraminol into 10mL of saline and give 1mL through a central line, and flush.
If patient still profoundly hypotensive, give 1mL 1:10 000 adrenaline IV.
(see p. 108)
If O2 sats <85% and falling, get immediate help.
Increase the FiO2 to 100% temporarily, check the pulse oximeter.
Look at expansion, auscultate the chest, check PaO2.
If you suspect tension pneumothorax, treat immediately ( p. 480).
Suction the ET tube, check that the patient is not biting on it.
Check that the drain tubing is patent and drains are on suction.
Treat bronchospasm with salbutamol 5mg nebulizer.
Disconnect from the ventilator and hand-ventilate the patient.
Get a CXR: look for pneumothorax, haemothorax, atelectasis, ET tube position, and lobar collapse, and treat (see p. 108).
(see p. 112)
Check that the Foley catheter is patent.
If the patient is hypotensive, treat this first.
Give a fluid challenge of gelofusine to raise the CVP to 14mmHg.
If not hypotensive and CVP >14mmHg, give 20mg furosemide IV.
(see Fig. 17.1)
The left main stem (LMS) arises from the ostium of the left sinus of Valsalva, travels between the pulmonary trunk anteriorly and the left atrial (LA) appendage to the left atrioventricular (AV) groove, dividing after 1–2cm into left anterior descending (LAD) artery, circumflex (Cx), and occasionally a third artery (the intermediate). As it provides almost the entire blood supply to the left ventricle (LV), occlusion can be fatal; severe left main disease is known as ‘the widow maker’.
The LAD runs down the anterior interventricular groove to the apex of the heart, usually extending round the apex to the posterior interventricular groove. A variable number of diagonals are given off over the anterior surface of the LV, small branches supply the anterior surface of the right ventricle (RV), and superior septals are given off perpendicularly to supply the anterior two-thirds of the interventricular septum. Occlusions of the LAD result in anterior MI.
The circumflex originates at 90° from the LMS and runs medially to the LA appendage for 2–3cm, continuing in the posterior left AV groove to the crux of the heart. Occlusions of the Cx result in posterior infarcts. In left dominant hearts (5–10%), the Cx turns 90° into the posterior interventricular groove to form the posterior descending artery (PDA). In 85–90% of hearts, the PDA arises from the right coronary artery (RCA) (right dominant). About 5% of hearts are co-dominant.
A variable number of obtuse marginals (OMs) arise from the Cx to supply the posterior LV. The first branch of the Cx is the AV nodal artery in which 45% course round the LA near the AV groove.
The RCA arises from an ostium in the right sinus of Valsalva, gives off an infundibular branch and then a branch to the sinoatrial (SA) node, and runs immediately into the deep right AV groove where it gives off RV branches to the anterior RV wall. Occlusions of the RCA result in inferior infarcts and bradycardia. The acute marginal is a large branch which crosses the acute margin of the heart. In right dominant hearts, the RCA reaches the crux of the hearts where it turns 90° to form the PDA, which runs in the posterior interventricular groove. Inferior septals, which supply the inferior third of the interventricular septum, arise at 90° from the PDA. The AV node artery is given off by the RCA in 55% at the crux.
Coronary artery anatomy.
Principles of cardiac surgery
Key facts
The majority of procedures are coronary artery bypass graft (CABG) operations, followed by aortic valve replacements, and mitral valve (MV) repair and replacements.
Many patients are elderly with multiple comorbidities, but 90% should be out of ICU within a day or two, and ready to go home in a week.
Preoperative preparation
Careful preoperative work-up is essential. All investigations must be checked; small abnormalities which would not cause a problem in other specialties can have catastrophic results in cardiac surgery.
Full history. Quantify symptoms, previous MI or stroke. Comorbidities (especially COPD, renal failure, peripheral vascular disease), MI <90 days (which increases mortality), drugs (aspirin, clopidogrel, and warfarin normally stopped 5 days preop to reduce bleeding), allergies, recent chest infection. Valve patients must have been cleared by dentist. Ask about previous heart surgery, varicose vein surgery.
Full examination. Look for signs of heart failure. Active infection, e.g. abscess is a relative contraindication to valve replacement. Look at conduit: any evidence of varicose veins?
All patients should have FBC, U&E, LFTs, clotting screen.
Cross-match 2U of blood.
ECG and CXR.
All patients undergoing coronary artery surgery and patients >35y undergoing valve surgery should have coronary angiogram less than 1y-old.
Patients undergoing valve surgery must have had an echo.
Carotid duplex in any patient with history of stroke, TIA, or carotid bruits; some centres perform these routinely in patients >70y old.
Consent by registrar or consultant.
Sliding scale for diabetic patients (see p. 52).
Cardiopulmonary bypass (CBP)
Any operation that involves stopping or opening the heart (valve surgery, surgery on septal defects) or great vessels (ascending and arch aortic dissection and aneurysm surgery, resection of some tumours invading great vessels, e.g. renal cell) requires CPB to maintain blood flow. This involves:
Heparinizing the patient so that blood does not clot in the CPB circuit.
Securing a 24F aortic cannula in the ascending aorta.
Securing a 32F venous cannula in the RA or in the superior vena cava (SVC) and inferior vena cava (IVC).
Connecting both cannulae to the bypass circuit.
The venous return from the body is siphoned into the bypass circuit.
The venous blood is oxygenated, filtered, and can be cooled or warmed, and is pumped back to the patient via the aortic cannula.
At the end of bypass, heparin is reversed with protamine.
Complications of CPB include stroke (atheromatous emboli, hypoperfusion, air, microemboli), SIRS, renal and pulmonary dysfunction (see p. 622).
Pathophysiology of CPB
CPB is unavoidable for many operations. It has a major impact on nearly every organ system and problems associated with bypass include:
Activation of coagulation and complement cascades.
Consumption of platelets and clotting factors, causing coagulopathy.
Microemboli and atherosclerotic emboli from aortic cannulation which can cause stroke and peripheral limb and end-organ ischaemia.
Increased capillary permeability.
Renal, pulmonary, hepatic, and pancreatic dysfunction.
Cardioplegia
CPB does not stop the heart; it just bypasses the beating heart. If the surgeon wants to operate on a still heart, CPB gives the surgeon three options: fibrillate the heart, cool the patient, or use cardioplegia. Cardioplegic arrest is by far the commonest technique.
Cardioplegia is a potassium rich solution.
It can be based on blood or crystalloid (blood delivers O2 better).
It can be warm or cold (cold may reduce ischaemic injury more).
It is delivered into the coronary arteries, either anterogradely by inserting a cannula into the aortic root which is clamped distal to the cardioplegia cannula or retrogradely via the coronary sinus vein.
It can be given continuously or intermittently, every 20min or so.
Cardioplegia arrests the heart and prevents myocardial ischaemia.
Post-operative management
Management of five common post-operative emergencies is outlined on p. 620. Most patients are well enough to be extubated within 6h, leave ITU within 24h, and go home within 5 days. Stable patients should have bloods, CXRs, and ECGs on days 1, 2, 4, and 6.
First 6 hours
Myocardial function deteriorates due to ischaemia-reperfusion injury.
Inotropic support and pacing may be required.
Patient should be fit for extubation by 6h post-op.
Patients should have diuresis >1mL/kg/h.
Mediastinal bleeding should steadily decrease.
Insulin requirements usually increase.
Days 1–2
Inotropes and pacing weaned, invasive monitoring lines removed.
Chest drains removed after 2h of zero drainage.
Catheter and any epidural removed, patient mobilized.
PCA morphine reduced to oral analgesia.
Patient should be on aspirin, low molecular weight heparin, furosemide.
Patient normally eating and drinking.
Days 3–5
Temporary pacing removed if ECG satisfactory.
Valve repair patients should undergo echocardiography.
Physiotherapists assess exercise tolerance.
Back to baseline weight, medications stabilized, ready for discharge.
Coronary artery disease
Definition
Narrowing of the coronary arteries caused by atherosclerosis (see p. 152).
Incidence
Five in 1000 males over 40y have symptomatic ischaemic heart disease (IHD), 5 in 1000 heart attacks per year, 6000 coronary artery operations per year in the UK.
Aetiology
Age, male sex, smoking, ↑ BP, diabetes, hyperlipidaemia, obesity, family history, stress.
Pathology
See p. 152 for description of atherosclerotic disease. Stenoses tend progress in severity and distribution. Rate of progression is variable and regression of lesions has been observed.
Narrowings of 50% of cross-sectional area limit coronary flow reserve (the increase in blood flow that occurs to meet increased O2 demand).
Coronary blood flow at rest is reduced by narrowings of 90%.
LV function may be abnormal. In normal people, global LV systolic function improves with exercise, but in patients with coronary artery disease (CAD), it gets worse in the area supplied by the stenotic arteries.
Acute MI is caused by acute total or subtotal vessel thrombotic occlusion. Patients with proximal LAD lesions are particularly at risk (see p. 54 for description of anatomic territories).
Clinical features
Angina and/or dyspnoea. Severity is classified using the New York Heart Association (NYHA) score. Dyspnoea implies congestive heart failure (CCF).
Class I. Symptoms only with prolonged or strenuous exertion.
Class II. Symptoms causing slight limitation of ordinary activity.
Class III. Symptoms with marked limitation of ordinary activity.
Class IV. Angina occurring even with mild activity or at rest.
Diagnosis
History and examination.
ECG may show evidence of old infarcts.
Exercise treadmill has 97% specificity for exertional angina.
Coronary angiography is diagnostic and obligatory for planning surgery.
Myocardial perfusion studies such as thallium scans are also useful.
CT coronary angiography is increasingly used to screen lower risk patients, but is not helpful in evaluating lesions in high risk patients.
Indications for surgery
The options are medical and percutaneous coronary intervention (angioplasty or stent). Many large trials have been carried out to decide which groups of patients benefit most from surgery. This is currently:
Patients with >70% LMS stenosis.
Symptomatic patients with >70% proximal LAD stenosis.
Symptomatic patients with >70% disease in all three vessels (three-vessel disease).
Patients with less significant coronary disease having cardiac surgery for other reasons, e.g. valve replacement.
Coronary artery bypass surgery
Median sternotomy. A piece of conduit (saphenous vein, left internal thoracic artery (LITA), radial artery) is anastomosed to the coronary artery beyond the lesion and then to the ascending aorta. The LITA is usually anastomosed to the LAD because this combination remains patent for decades and the LAD is the most important stenosis to treat. The LITA is a branch of the left subclavian artery and runs down the inside of the rib cage 2cm lateral to the sternum. The origin from the subclavian is left intact; it does not need to be anastomosed to the aorta.
Coronary artery bypass is mostly performed on-pump (with the use of a CPB machine) on the still heart.
Performing on the beating heart off-pump (without CPB) is more difficult, but gives some advantages (see p. 622).
Complications
Complications (see p. 620) are more likely with advanced age, poor LV function, renal failure, COPD. Risk of mortality is scored, e.g. EUROscore.
Death, 0–1% in low risk patients.
Stroke, 1–2% in low risk patients.
Re-sternotomy for bleeding or tamponade 5%.
Chest infection, AF, wound infection, renal failure.
Prognosis
In untreated patients with symptoms severe enough to warrant coronary angiography, 10% have an acute MI within 1y and 30% have an acute MI within 5y. Hospital mortality of MI is 7–10%.
In three-vessel disease, the 5y survival is 50%, lower if LV function is impaired.
LMS disease has a 2y survival of 50%.
Valvular heart disease
Mitral regurgitation (MR)
Incidence Commonest valvular lesion. Prevalence 2–6%.
Aetiology MV prolapse (congenital or rupture of chordae/papillary muscles), rheumatic disease, endocarditis, connective tissue disorders.
Clinical features Acute MR presents with signs of CCF. Chronic MR causes exertional dyspnoea, orthopnoea. Displaced apex beat, soft S1, pansystolic murmur—loudest at apex, radiating to axilla. AF in 80%.
Diagnosis CXR shows cardiomegaly. Transthoracic echocardiogram (TTE) diagnostic.
Indications for surgery Acute MR, severe chronic MR.
Prognosis Mortality of untreated severe MR is 5% per year. Operative mortality is 2–3% for low risk cases.
Mitral stenosis
Incidence Prevalence <1% in west, commoner in Asia and Africa.
Aetiology Rheumatic heart disease.
Clinical features Dyspnoea, bronchitis, haemoptysis, AF, left parasternal heave, tapping apex beat, loud S1, rumbling mid-diastolic murmur at apex.
Diagnosis CXR shows splaying of carina (enlarged LA). Echo diagnostic.
Indications for surgery MV area <1.0cm2 (normal valve 3–4cm2).
Prognosis Poor once symptoms of heart failure present.
Aortic stenosis
Incidence Prevalence 1–2% in age over 65.
Aetiology Calcific degeneration, bicuspid valve, rheumatic disease.
Clinical features Triad of angina, syncope, dyspnoea. Sudden death. Slow rising and low volume pulse, heaving apex beat, reversed splitting S2, ejection systolic murmur loudest in aortic area radiating to carotids.
Diagnosis ECG shows LV hypertrophy, TTE diagnostic.
Indications for surgery Symptomatic aortic stenosis.
Prognosis Without surgery, 50% of patients with angina are dead in 5y, 50% with syncope are dead in 3y, and 50% with dyspnoea are dead in 2y. UK perioperative mortality is 3–5%.
Aortic regurgitation (AR)
Incidence Less than 1% prevalence.
Aetiology Rheumatoid, endocarditis, aortic dissection, Marfan's and other connective tissue disorders, calcific degeneration, trauma.
Clinical features Acute AR (endocarditis) presents with signs of left ventricular failure (LVF). Chronic AR often asymptomatic. Later, orthopnoea, fatigue, dyspnoea. Signs of wide pulse pressure, collapsing water hammer pulse, Quinke's sign (nail bed pulsation), Corrigan's sign (visible neck pulsation), De Musset's sign (head nodding), Durozier’ sign (femoral diastolic murmur), hyperdynamic displaced apex beat, early diastolic murmur, Austin Flint mid-diastolic murmur due to regurgitant stream hitting anterior MV cusp.
Diagnosis CXR shows cardiomegaly. TTE diagnostic.
Indications for surgery Acute AR is a surgical emergency. Chronic AR is operated on before the ejection fraction <55% or LV dilates >5.5cm.
Prognosis Acute AR has poor prognosis. Chronic AR has good outcome until failure occurs (50% 2y mortality). UK operative mortality is 3–5%.
Options for valve surgery
MV repair (annuloplasty and valvuloplasty)
Results of repair of the aortic valve are unpredictable so it is usually replaced. The MV is often repaired with good results.
Mechanical valves, e.g. St Jude mechanical, Carbomedics
These are made of ceramic. They can be mono- or bileaflet. Ball-and-cage like the Starr Edwards is no longer used.
Advantages. Last forever so patient will not need future surgery.
Disadvantages. Thromboembolic so patient must be warfarinized; patients with bleeding diatheses, women of childbearing age, professional sports players may not be suitable for long-term warfarinization.
Tissue valves (xenografts), e.g. Mosaic, Perimount
These are made of pig valves or cow or horse pericardium, usually suspended on a metal frame covered by a cloth sewing ring.
Advantages. Patient does not need to be warfarinized.
Disadvantages. Tissue valves last for 10–15y in the aortic position and 6–10y in the mitral position, depending on the age of the patient; younger patients (<65–70y) will often need a second operation.
Principles of valve surgery
Median sternotomy incision. MV may be approached via R thoracotomy.
Valve surgery must be carried out with CPB (see p. 626).
Complications
Complications (see p. 620) are more likely with advanced age, poor LV function, renal failure, COPD, pulmonary hypertension, additional CABG.
Death, 0–3% in low risk patients.
Stroke, 5–10% (debris from removing calcified valve, cannulating aorta).
Re-sternotomy for bleeding or tamponade, 5%.
Chest infection, AF, complete heart block requiring permanent pacemaker insertion, wound infection, renal failure.
Prosthetic endocarditis, failure, thrombosis, paravalvular leak.
Aortic valve. Tricuspid valve, sitting within bulb of aortic root. Three dilatations called sinuses of Valsalva. Left coronary sinus gives rise to LMS, right gives rise to right coronary artery. Third known as non-coronary sinus. AV node lies between right and non-coronary cusp. Annulus (where leaflets attach to aorta) is coronal-shaped.
MV. Bileaflet valve, lying between LA and LV. Anterior leaflet smaller than posterior leaflet. Leaflets held in place by chordae which attach to two papillary muscles of LV. Annulus is oval-shaped.
Cardiothoracic ICU
Commonly used terminology (see Table 17.1)
Instead of referring to systolic and diastolic blood pressure, arterial pressure is usually described using single figure: the mean arterial pressure (MAP) which is calculated by adding a third of the difference between diastolic and systolic pressures to the diastolic pressure, e.g. the MAP of a patient with a BP 120/60mmHg is 80mmHg.
The MAP on its own does not adequately describe cardiac function; a number of other parameters are frequently used.
Cardiac output. The volume of blood ejected by the heart per minute.
Stroke volume. The volume of blood ejected by the heart per beat.
Cardiac output equals heart rate x stroke volume.
Cardiac index. Is simply the cardiac output adjusted to take into account the size of the patient and is a more accurate reflection of cardiac function.
Low cardiac ouput
Much of the initial care after cardiac surgery is aimed at preventing, recognizing, and treating low cardiac output states, as these can lead to organ failure, contribute to sepsis, and cause death, even in ‘straightforward’ patients. Low cardiac output can be defined as a cardiac index <2.2mL/min or evidence of end-organ hypoperfusion (e.g. lactic acidosis, oliguria, low mixed venous O2 saturations).
Common causes of low cardiac output include:
Bleeding (occasionally other causes of hypovolaemia, e.g. polyuria).
Tamponade.
Arrhythmias.
Acidosis, hypoxia.
Preoperative cardiomyopathy.
Ischaemia and stunning (myocardial recovery from surgery).
Hypotension can due to low cardiac output, but even a patient with a high cardiac output could be hypotensive if they were very vasodilated (most commonly due to SIRS (see p. 138) or sepsis).
Sometimes a number of problems may be going on at once and it is easy to miss important problems so a systematic approach to assessing post-operative cardiac surgery patients is vital.
General assessment of cardiac surgery patients
Except in emergencies, usually you have time to evaluate every system.
Review the history. What was the ventricular function preop? What other comorbidities? What operation was done—any problems?
Cardiovascular.
Look at the heart rate and rhythm and check the ECG for evidence of ischaemia (ST segment changes), comparing with preop.
Look at the MAP and CVP. A high CVP is always concerning, suggesting tamponade, ventricular failure, or respiratory problems.
Look at the cardiac output, lactate, mixed venous, and feel the patient's extremities; a warm patient with good peripheral pulses cannot have a low cardiac output. What is the SVR?
What inotropes, vasoconstrictors, and antihypertensives are on?
Respiratory. Is the patient breathing spontaneously or ventilated? Look at the O2 saturations and a recent blood gas to check the PaO2, PaCO2, and pH. What does the CXR look like?
Renal. How much urine is the patient making (ideally >1mL/kg/h)? What is the patient's fluid balance (if it is negative or low, the patient may be hypovolaemic; if it is very high, fluid overload is a concern). Check electrolytes; abnormalities can cause arrhythmias.
Bleeding. Should be less than 100cm3/h in the chest tubes, with steady fall in the rate. Look at wound sites (remember groin + leg). Is the haematocrit dropping? Check coagulation.
Assess mental status and focal neurology, analgesia.
Cardiac output = SV x HR | |
Cardiac index = CO/BSA | |
Stroke volume index = SV/BSA | |
Mean arterial pressure = DP + (SP – DP)/3 | |
Systemic vascular resistance = ((MAP – CVP)/CO) x 80 | |
Systemic vascular resistance index = SVR/BSA | |
Pulmonary vascular resistance = ((PAP – PAWP)/CO) x 80 | |
Pulmonary vascular resistance index = PVR/BSA | |
Normal value | |
Cardiac output (CO) | 4.5–8L/min |
Stroke volume (SV) | 60–100mL |
Body surface area (BSA) | 2–2.2m2 |
Cardiac index (CI) | 2.0–4.0L/min/m2 |
Stroke volume index (SVI) | 33–47mL/beat/m2 |
Mean arterial pressure (MAP) | 70–100mmHg |
Diastolic pressure (DP) | 60–80mmHg |
Systolic pressure (SP) | 110–150mmHg |
Systemic vascular resistance (SVR) | 800–1200dyne-s/cm5 |
Central venous pressure (CVP) | 6–12mmHg |
Systemic vascular resistance index (SVRI) | 400–600dyne-s/cm5/m2 |
Pulmonary vascular resistance (PVR) | 50–250dyne-s/cm5 |
Pulmonary artery pressure (PAP) | 20–30mmHg |
Pulmonary artery wedge pressure (PAWP) | 8–14mmHg |
Pulmonary vascular resistance index (PVRI) | 20–125dyne-s/cm5/m2 |
Cardiac output = SV x HR | |
Cardiac index = CO/BSA | |
Stroke volume index = SV/BSA | |
Mean arterial pressure = DP + (SP – DP)/3 | |
Systemic vascular resistance = ((MAP – CVP)/CO) x 80 | |
Systemic vascular resistance index = SVR/BSA | |
Pulmonary vascular resistance = ((PAP – PAWP)/CO) x 80 | |
Pulmonary vascular resistance index = PVR/BSA | |
Normal value | |
Cardiac output (CO) | 4.5–8L/min |
Stroke volume (SV) | 60–100mL |
Body surface area (BSA) | 2–2.2m2 |
Cardiac index (CI) | 2.0–4.0L/min/m2 |
Stroke volume index (SVI) | 33–47mL/beat/m2 |
Mean arterial pressure (MAP) | 70–100mmHg |
Diastolic pressure (DP) | 60–80mmHg |
Systolic pressure (SP) | 110–150mmHg |
Systemic vascular resistance (SVR) | 800–1200dyne-s/cm5 |
Central venous pressure (CVP) | 6–12mmHg |
Systemic vascular resistance index (SVRI) | 400–600dyne-s/cm5/m2 |
Pulmonary vascular resistance (PVR) | 50–250dyne-s/cm5 |
Pulmonary artery pressure (PAP) | 20–30mmHg |
Pulmonary artery wedge pressure (PAWP) | 8–14mmHg |
Pulmonary vascular resistance index (PVRI) | 20–125dyne-s/cm5/m2 |
Lung cancer
Key facts
Commonest cause of death from cancer in the UK.
↑ Incidence in females (25% of cancer-related deaths in women).
Risk factors
Cigarette smoking. Strongly positive association with cigarette smoking (polycyclic aromatic hydrocarbons plus nicotine-related carcinogens).
Radon exposure.
Occupational factors. Asbestos, polycyclic aromatic hydrocarbons, arsenic, nickel, silica, coal tar, aluminium production, coal gassification, exposure to paints, chromium compounds, bischloromethal ether.
Genetic predisposition and male sex.
Pathology
Bronchial carcinoma is classified as non-small cell or small cell.
Non-small cell lung cancer
Squamous cell carcinoma
Twenty to thirty per cent of all lung cancers.
Most common histological type in Europe.
Often arising in large airways as an endobronchial mass (two-thirds).
Slow-growing, late to metastasize.
Adenocarcinomas
Thirty to fifty per cent of lung cancers. Incidence increasing.
Usually peripheral tumours (approximately three-quarters).
Moderate growth with early metastasis.
Large cell undifferentiated carcinoma:
Fifteen per cent of all lung cancers.
Peripheral location more common than central.
Two subtypes. Clear cell carcinoma and giant cell carcinoma. Giant cell tumours are uncommon, <1% of lung cancers. Very poor prognosis.
Histological subtypes
Bronchioloalveolar tumours. Highly differentiated adenocarcinoma; 2.5% all lung cancers.
Adenosquamous carcinomas.
Small cell lung cancer
Neuroendocrine tumours
Approximately 20% of lung cancers. Aggressive tumours, not usually amenable to surgical resection. Three subtypes—pure small cell (90%), mixed small and large cell, combined small cell with areas of squamous or glandular differentiation.
Clinical features
Proximal tumours tend to produce symptoms of major airway obstruction and irritation (haemoptysis, dyspnoea, cough, wheezing,
stridor, hoarseness, Horner's syndrome, SVC obstruction, post-obstructive pneumonia, pleural effusion, Pancoast's syndrome).
Peripheral tumours are often asymptomatic or present with signs and symptoms of pleural or chest wall invasion or pleural effusion (pleuritic chest wall pain, progressive dyspnoea).
May present with symptoms and signs of metastatic spread. Neurological—headache, blurred vision, nausea, diplopia, decreased consciousness, ataxia; bony pain and pathological fracture; liver and abdominal pain, anorexia, jaundice, ascites, liver failure, hepatomegaly; adrenal glands—symptoms of Addison's disease.
Paraneoplastic syndromes.
History and examination
Ask about: history of tobacco smoking (pack years), asbestos exposure, employment history, weight loss of greater than 5% body weight, recent onset of joint pains, change in voice, chest wall pain, back pain.
Look for: lymphadenopathy, evidence of significant weight loss, pleural effusion, localized chest wall pain, clubbing, cutaneous lesions.
Principles of management
Non-small cell lung cancer is relatively resistant to chemotherapy. Curative resection allows best chance of long-term survival. Surgery is normally offered to all patients with stage I and stage II disease, along with specific patients with stage III disease (after chemoradiotherapy). Surgical principles of resection are:
No spillage of cells from primary tumour during resection.
Entire tumour must be resected by lobectomy or pneumonectomy along with intrapulmonary lymph nodes; lesser resections proven to have worse outcome, only considered in high risk patients.
All accessible mediastinal lymph nodes should be excised or biopsied to allow complete staging and plan for any adjuvant therapy.
Frozen section analysis of resection margins to confirm appropriate surgical resection and complete excision of primary tumour.
Survival
Stage I, 5y survival 75%; stage II, 5y survival 40%; stage III, 5y survival <30%.
Post-operative mortality rate. Lobectomy, 2%; pneumonectomy, 6%.
Chemotherapy
To date, no proven benefit from adjuvant therapy in patients with surgically resectable and potentially curative disease.
Radiotherapy
Radical. Used in patients unfit or unwilling to undergo surgery. Also used in those with bulky stage IV disease. Survival benefit in non-surgical patients when combined with concomitant chemotherapy.
Adjuvant. Also used as an adjunct to surgery or as palliation.
Pleural effusion
Key facts
Abnormal amount of fluid within the pleural space. Pleural effusions may be divided into transudate and exudates, according to Light's criteria (see Box 17.1, but the divide is not always clear.
An exudates is characterized by:
Pleural fluid:serum protein >0.5.
Pleural fluid:serum LDH >0.6.
Pleural fluid LDH >200IU.
Causes of transudates
Cirrhosis of the liver.
Nephrotic syndrome.
Glomerulonephritis.
CCF.
Myxoedema.
Sarcoidosis.
Multiple PE.
Causes of exudates
Neoplasms. Mesothelioma, metastatic disease, primary lung cancer.
PE.
Chylothorax.
Haemothorax.
Infectious diseases. Viral and bacterial infections, fungal and parasitic infections, TB.
Gastrointestinal disease. Pancreatitis, subphrenic abscess, intrahepatic abscess, perforated oesophagus.
Collagen vascular disease. Systemic lupus erythematosus, Wegener's granulomatosis, Sjogren's syndrome.
Drug-induced pleural disease.
Mediterranean fever.
Rheumatoid disease, sarcoidosis, yellow nail syndrome.
Asbestos exposure, electrical burns, radiation therapy.
Trapped lung, post-pericardiectomy.
Uraemia, urinary tract obstruction.
Post-myocardial syndrome, Meigs’ syndrome.
Clinical presentation
Small effusions are often asymptomatic. Larger effusions cause cough, chest pain, dyspnoea.
Decreased ipsilateral chest expansion, dullness to percussion, decreased breath sounds over the effusion on auscultation, crepitations may be heard.
Investigations
Chest radiograph. Small effusions are demonstrated by blunting of the costodiaphragmatic angles; larger effusions produce a fluid level with a meniscus.
Ultrasound scan. Useful for loculated effusions, helps to localize optimal site for chest drainage.
CT. Useful when looking at underlying lung and pleural lesions.
Pleural aspiration cytology. May obtain diagnostic information, helpful when planning treatment.
Management
If possible, treat the underlying cause. Simple pleural effusions due to fluid overload may resolve with diuresis.
Tube thoracostomy (see p. 200).
Chemical pleurodesis (tetracycline, blood, talc).
Surgical abrasion pleurodesis.
Surgical pleurectomy (open or thoracoscopic).
Pleuroperitoneal shunt.
Complications
Infection and empyema.
Treatment failure with recurrence of pleural effusion.
Damage to underlying lung parenchyma, leading to prolonged air leak and bronchoalveolar air leak.
Empyema
This is an infected pleural fluid collection, commonly after pneumonia.
Stage I. Acute exudative phase.
Typically occurs 2–5 days after a pneumonia.
Accumulation of fluid with low cellular content and viscosity.
Characterized by low WCC, LDH, and glucose, and a normal pH.
Can be successfully treated with antibiotics only.
Stage II. Fibrinopurulent phase.
Typically occurs 5–14 days after a pneumonia.
Turbid or purulent fluid with heavy fibrin deposits.
Appearance of simple loculations and septations.
May have bacterial invasions and high numbers of PMNs and lymphocytes.
Characterized by low pH and glucose and increased LDH.
Antibiotics and chest tube drainage is required, may need video-assisted thoracoscopic surgery (VATS) decortication.
Stage III. Chronic organizing phase.
Lung trapping by collagen visceral and parietal pleural peel with ingrowth of fibroblast and capillaries.
Antibiotics and aggressive decortications, generally by thoracotomy.
Bacteriology.
Pneumothorax
Key facts
The presence of air in the pleural space with secondary lung collapse.
Primary spontaneous pneumothorax.
Secondary spontaneous pneumothorax.
Post-traumatic and iatrogenic.
Primary spontaneous pneumothorax
Commonly seen in young tall male smokers. More common on the right side. Less than 10% of cases are bilateral. Usually caused by rupture of small subpleural blebs (collections of air <2cm). Usually found at the apex of the upper lobe or the apical segment of the lower lobe. The rest of the lung parenchyma is normal. May also be caused by rupture of bullae (large air-filled spaces).
Presentation
Dyspnoea, chest pain, cough, tachypnoea.
Ipsilateral decreased chest wall movement, hyperresonant hemithorax to percussion, absent breath sounds on auscultation, pleural rub, tachycardia.
Investigations
PA chest radiograph usually diagnostic.
CT scan gives an accurate estimate of size of pneumothorax and is useful for assessment of remaining lung parenchyma and contralateral lung.
Complications
Tension pneumothorax.
Pneumomediastinum.
Haemopneumothorax.
Recurrent pneumothorax.
Conservative management
Observation (small, <20% pneumothorax).
Needle aspiration.
Tube thoracostomy 9 chemical pleurodesis.
Surgery
Surgery is indicated in the following cases.
First episode. Prolonged air leak, tension pneumothorax, haemothorax, bilateral pneumothoraces, residual collapse of lung despite non-surgical treatment, 100% pneumothorax, occupational hazard, pneumothorax secondary to giant bulla, previous contralateral pneumonectomy.
Recurrence of pneumothorax.
The aim is to resect the blebs or bullae and obliterate the pleural space with adhesions, either using chemical or abrasion pleurodesis or parietal pleurectomy (apical or full). It may be performed through a mini-thoracotomy, axillary incision, or thoracoscopically
Recurrence rate
Less than 2% following surgical pleurectomy via mini-thoracotomy.
Five per cent following thoracoscopic procedures.
Five to ten per cent following chemical pleurodesis.
Secondary spontaneous pneumothorax
Causes
Cystic fibrosis, chronic obstructive airways disease (COAD) and other bullous disease, asthma.
Interstitial lung disease.
Infections, including AIDS, mycobacterial, Pneumocystis carinii, bacterial, parasitic, mycotic.
Malignancy. Bronchogenic carcinoma, metastatic lung cancer (sarcoma and lymphoma).
Collagen diseases, catamenial, Ehlers–Danlos syndrome, histiocytosis X, scleroderma, lymphangioleiomyomatosis, Marfan's syndrome.
Rupture of the oesophagus.
Cystic fibrosis
Pneumothorax found in 10% of patients. Remember these patients are possible candidates for future lung transplantation when considering management options. Full parietal pleurectomy is a contraindication to lung transplantation.
COAD
The most common cause of secondary pneumothorax. Age usually >50y. Patients often have very little pulmonary reserve. They may not tolerate surgical management and single lung ventilation. Treatment options are therefore tube thoracoscopy and chemical pleurodesis or long-term tube thoracoscopy.
Infection
Cavitating pulmonary lesions rupture into pleural space.
AIDS
Usually secondary to Pneumocystis carinii and pneumonia. May be presenting feature of AIDS. Most effective treatment is surgical.
Catamenial
Age 20–30y. Incidence 3–6% of women. Occurs 2–3 days following onset of menstruation. Right side more commonly affected. Usually small, presenting with dyspnoea and chest pain. Pathogenesis unclear.
Primary spontaneous pneumomediastinum
Uncommon. Males affected more frequently than females. Occurs following exertion or increased intra-abdominal pressure. Commonly associated with cocaine, marijuana, and crack cocaine usage. It is caused by rupture of alveolar sacs with air tracking along the peribronchial and perivascular spaces into the neck.
Presentation
Sudden onset of chest pain, dyspnoea, dysphagia, cough.
Subcutaneous emphysema over neck and chest wall, Hamman's sign.
Chest radiograph confirms diagnosis.
Management
Non-operative, treat expectantly. Emergency surgical decompression very rare.
Mediastinal disease
Pericardial effusion and cardiac tamponade
Key facts
Pericardial effusion is abnormal fluid in the pericardial space; there is normally about 20mL of plasma ultrafiltrate.
Pericardial effusion may be acute or chronic.
Acute accumulation of fluid can cause cardiac tamponade which is a surgical emergency (see Box 17.2).
Effusions commonly results from pericarditis, CCF, metastatic spread to pericardium commonly from lung or breast malignancy, lymphoma or leukaemia, autoimmune disorders, chronic hepatic and renal failure, infections—specifically HIV.
Suspect cardiac tamponade if the patient has a history of chest trauma.
↓ BP, ↑ JVP, (Beck's triad is ↓ BP, ↑ JVP + muffled heart sounds).
Pulsus paradoxus (exaggeration of the normal ↓ BP with inspiration).
Progressive tachycardia and dysrythmias, including SVT, VF, and EMD.
↓ Urine output.
Excessive widening of the mediastinum on CXR.
Echo may show clot in pericardium and collapse of RV in diastole.
Equilibration of cardiac filling pressures (at cardiac catheterization).
Emergency pericardiocentesis ( p. 204).
Emergency thoracotomy or sternotomy.
Aggressive fluid resuscitation is a temporizing measure.
Clinical features
Very dependent on the time course. Acute accumulation of a small amount of fluid can cause life-threatening cardiac tamponade, whereas slow accumulations of large volumes of fluid may be well tolerated.
Chronic pericardial effusion may present with decreased exercise tolerance, atypical chest pain, orthopnoea, and associated signs of CCF, as well as features of cardiac tamponade.
Management
Medical management includes diuretics and pericardiocentesis.
Creating a hole in the pericardium or pericardial window so that fluid can drain directly into the pleura via:
Thoracotomy or subxiphoid approach.
Left VATS approach.
Thymoma
Key facts
The thymus is a bilobar structure located in the anterior mediastinum which contains lymphoid tissue. It is the location for maturation of T-cells in early life.
Thymoma may be benign or malignant.
Thymectomy is the definitive treatment for myasthenia gravis.
Clinical features
Thymoma is usually asymptomatic in adults, whereas children often present with thoracic outlet obstruction or upper airway compromise.
Clinical features of myasthenia gravis are described on p. 63.
Thymoma appears as a smooth mass in the upper half of the CXR.
CT shows enlarged thymus as well as lymph node involvement.
Treatment
Thymectomy via a median sternotomy.
Mediastinum is the space between the pleural sacs, below the thoracic inlet and above the diaphragm.
Superior mediastinum.
From thoracic inlet to the line from sternal angle to T4–5 space.
Contains great vessels, trachea, oesophagus, phrenic nerves, vagus nerves, thoracic duct.
Anterior mediastinum.
Anterior to pericardium.
Contains sternopericardial ligaments, thymus, lymph nodes.
Middle mediastinum.
Contains pericardial cavity, heart, great vessels, phrenic nerves.
Posterior mediastinum.
Posterior to pericardium.
Contains oesphagus, descending aorta, azygous veins, thoracic duct, lymph nodes.
