Investigation \200 Full blood count, D-dimer (negative result will help exclude pulmonary emboli), renal, live r and thyroid function. CXR, HRCT (to look for early diffuse parenchymal lung disease if th e transfer factor is low (see below). An ECG and an echocardiogram are useful as exclusion criteria as well as diagnostic tools. Other therapies \200 Physiotherapists can teach patients with dysfunctional breathing to slow and regularize the ir breathing rhythm. Pulmonary rehabilitation is effective in reducing the breathlessness o f COPD and other chronic lung diseases. Non-invasive ventilation will help patients with ne u- romuscular problems who are struggling to maintain adequate ventilation. Many other non- drug therapies have been tried in patients who are breathless, but here is little evidence to support their use. AUTHOR \200\231S TIP In hyperventilation, the ECG can be abnormal with wide- spread T-wave inversion and ST segment depression. Spirometry, lung volumes , carbon monoxide transfer factor. If these are also normal it is useful to proceed to a \200\230respira- tory \200\231 exerc ise test, where gas exchange is measured whilst the patient exercises on a treadmill or cyc le ergometer. A simpler exercise test such as a shuttle or six minute walk may be undertake n \201 rst, just to con \201 rm that exercise capacity is impaired. Check the oxygen sat uration on air, and proceed to arterial blood gas analysis if it is less than 94%. Further reading Jennings AL, Davies AN, Higgins JPT, et al. Opioids for the palliation of b reathlessness in terminal illness. Cochrane Database of Systematic Reviews 2001; 4. The adult clinical component for the home oxygen service in England and Wales.http://www.br it-thoracic.org.uk/ page294.html C DAVIES 40 3.3 Haemoptysis This is a common presentation of respiratory disease de- \201 ned as the expectoration of blood from hemorrhage into the respiratory tract. It can vary from streaks of blood within sputum to massive, life-threatening hemorrhage. All patients with unexplained haemoptysis require further investigation to identify one of the many causes. The ur- gency of investig ation and treatment will depend on the rate of bleeding and source, and the severity of und erlying lung disease. Most patients do not require admission for investigation or managemen t. AUTHOR \200\231S TIP Always examine the mouth and nasal cavities for possi- ble causes of b leeding and consider the possibility of GI hemorrhage. NB In up to 20% patients a source wi ll not be identi \201 ed \200\223 cryptogenic haemoptysis. Investigations Chest radiograph The chest radiograph may be normal or show signs of the lik ely origin of the bleeding, e.g. a mass, consolidation, bronchiectactic changes. Causes of haemoptysis Laboratory investigations \200 \200 \200 Most common causes Bronchiectasis Tuberculosis * Pneumonia especially Streptococ- cal pneumoniae * Bronchial c arcinoma * Pulmonary embolism * FBC and clotting. Group and save/cross match if massive bleeding. ANCA, autoantibodies and anti-GBM antibodies if vas- culitis is suspected. CT scan \200 Other rarer causes Pulmonary infections A CT scan should be performed in most subjects unless the cause is already known (e.g. a pa tient with recurrent bleeding from bronchiectasis or a tumor). CT scanning may show the cau se of bleeding or may direct the clinician to the likely site of bleeding at subse- quent i nvestigations such as bronchoscopy. Patients suspected of bronchiectasis will also require high resolution CT imaging or image reconstruction to identify parenchymal disease. When pu lmonary embolic disease is considered within the differential diagnosis, CT pulmonary angio graphy should be performed. For some diagnoses further diagnostic investigations may be unn ecessary after the CT scan, e.g. bronchiecta- sis, pulmonary embolism, AV malformation, pul monary \201 brosis. Acute bronchitis Lung abscess Aspergilloma or invasive fungal disease Tumors Carcinoid tumo r Endobronchial metastasis, e.g. breast, melanoma, colon Pulmonary parenchymal diseases Pul monary vasculitis/alveolar hemorrhage syndromes Pulmonary \201 brosis Pulmonary vascular disease Severe pulmonary hypertension AV malformation Mitral stenosis (rare nowadays) Conge nital malformation Aortic aneurysm Miscellaneous causes Endometriosis Anticoagulant therapy or coagulopathy, e.g. DIC Iatrogenic, e.g. Swan \200\223Ganz catheter, bronchial biopsy Dr ugs, e.g. cocaine, thrombolytics Bronchoscopy Bronchoscopy and CT scanning should be considered complementary investigations in patients with haemopty- sis. The timing of bronchoscopy has not been shown to affect th e outcome of investigating the cause of haemopty- sis and it is usual for CT scanning to be performed prior to bronchoscopy. AUTHOR \200\231S TIP Bronchoscopy should be considered in patients with massive haemoptysis , to identify possible source of bleeding when CT is normal, and when CT scan has identi \201 ed a likely abnormality responsible for the bleed- ing. Bronchoscopy may help obtain t issue or microbio- logical samples to con \201 rm the diagnosis, e.g. bronchial tumor, TB, parenchymal lung disease (by transbronchial biopsy) and can help locate anatomical origin of bleeding when considering bronchial arterial embolisation Evaluation of a patient with haemoptysis History: key points \200 \200 Identify time course and likely volume of blood. Identify symptoms suggestive of malignancy , infection, bronchiectasis or embolism. Smoking history. Ask about risk factors for aspira tion. Medications including illicit drugs. \200 \200 Other investigations Where the clinical picture indicates an alternative cause for bleeding further investigations may include: \200 Examination: key points \200 \200 \200 The examination may be normal. Look for signs of bronchiectasis or malignancy. In patients with massive haemoptysis, assessment of air- way and circulation are essential (see Investi gations). Echocardiography, e.g. to identify pulmonary hyperten- sion or mitral valve disease. Bronch ial arterial angiography and embolisation (see below). CHAPTER 3.3 Haemoptysis 41 Massive haemoptysis Massive haemoptysis is fortunately rare (about 5% of epi- sodes of haem optysis) and is often de \201 ned as expectora- tion of blood exceeding between 100 \200 \223600 ml in 24 hours. This de \201 nition is rather arbitrary as the outcome will depend on the volume, rate and cause of the bleeding, and the underlying respiratory reserve and ability of the patient and medical staff to maintain a clear airway. Drugs \200 Tranexamic acid is a drug that inhibits \201 brinolysis, is useful to reduce bleeding. Us ual dose is 15 \200\22325 mg/kg 2 \200\2233 times daily oral or 0.5 \200\2231g 3 times dail y IV. Antibiotics \200\223 when infection is a likely trigger (e.g. in bronchiectasis). Ne bulised adrenaline \200\223 5 \200\22310 ml of 1 in 10,000. Bronchoscopy Bronchoscopy is useful in massive haemoptysis. Rigid bron- choscopy may allow a clearer view of the airway but re- quires expertise and anesthesia. In practice most clin icians will have access to \201 breoptic bronchoscopy in the \201 rst in- stance. Gener al anesthesia and intubation may still be re- quired. Bronchoscopy may allow: \200 \200 Commonest causes \200 Bronchiectasis \200\223 due to dilated, ectatic and tortuous ves- sels around the abnormal airways. Bleeding may be trig- gered by inter-current infection. TB \200\223 either due t o active infection or damaged airways from previous infection. Aspergilloma. Bronchial tumo rs \200\223 usually large, centrally located. More common with squamous cell carcinoma. Lu ng abscess. Identi \201 cation of the likely origin of the bleeding. Introduction of topical adrenalin e (5 \200\22310 ml of 1:10000 or 1:20000) directly to the source of bleeding or blindly int o the main bronchi. Lavage with iced 0.9% saline to induce vasoconstriction and reduce blee ding. Introduction of a balloon catheter (e.g. 14Fr Foley 100 cm long) to tamponade the mai n bronchus leading to the bleeding site or introduction of a smaller catheter (e.g. 4 \200 \2237 Fr Foley 200 cm long) can be passed through the scope into a segemental bronchus. Las er or electrocautery to the visualized bleeding lesion. \200 \200 \200 Early involvement of a respiratory specialist is recom- mended. In some cases, e.g. patient s with cancer, the main approach to management may be entirely palliative. Management of massive haemoptysis Initial resuscitation and investigations \200 \200 \200 Airway protection. Administer oxygen. Assess cardiovascular status and resuscitate with IV \202 u- ids as necessary. Move patient to a higher monitoring area or intensive care sett ing. Early anesthetic input may be required. Check FBC and coagulation and take measures to cor- rect any coagulopathy. Discussion with a hematologist may be needed. Cross match bloo d. Assess arterial blood gasses. Chest radiograph \200\223 may reveal likely cause. Chest CT (and/or CT angiography). Pulmonary angiography and embolisation Once the patient has been resuscitated and stabilize d a de \201 nitive procedure to prevent further bleeding may be necessary depending on cli nical circumstances. As bleeding is usually from a bronchial artery, abnormal vessels may b e identi \201 ed at angiography and then occluded using either non-absorbable glue or stee l coils. This technique is usually only available in a few specialist centers but has succe ss rates of up to 85%. Bronchial wall necrosis may occur after embolisation and there is a risk of spinal cord paralysis due to inadvertent embolisation of a spinal artery. Rebleedin g may occur in 10 \200\22320% of patients, and de \201 nitive treatment of the cause shoul d be initiated afterwards to reduce risk. \200 \200 \200 Protection of the non-bleeding lung Surgery In selected cases surgical resection of the affected bleeding site, e.g. by lobecto my, can be successful, but surgery in setting of acute massive haemoptysis has reported mor tal- ity between 20 \200\22330%. Surgery may still be indicated after successful embolisati on of a bleeding site or for selected patients with bleeding from resectable lesions such a s AV malformations, bronchial adenoma, aspergilloma. AUTHOR \200\231S TIP \200 Protection of the non-bleeding lung is a major priority as spillage of blood into the other lung can cause air- way obstruction and lead to respiratory failure or asphyxia. To achiev e this requires identi \201 cation of the likely site of bleeding. If known: Position the patient onto their side, either \202 at or at about 30 , so that the bleeding lung is in the dependent position. Further reading Lordan JK, Gascoigne A, Corris PA. The pulmonary physician in critical care . Illustrative case 7: assessment and management of massive haemoptysis. Thorax 2003; 58: 8 14 \200\223819. Introduce a single lumen endotracheal tube into either main stem bronchus so that the tube protects the non- bleeding lung. This is easier to achieve when bleeding is from the left s ide as the tube is more likely to enter the right main bronchus. Intubation of the left mai n bronchus is more dif \201 cult. An alternative is to use a double lumen endotracheal tub e, although experience of insertion and subsequent care may be lacking in some centers. The y tend to have a smaller lumen too, which may block with blood. N WARD & N WITHERS 42 3.4 Chest pain Chest pain is a frequently encountered symptom in all areas of medical practice, being the most common site of pain that prompts the sufferer to seek medical attention. It may signal the onset of a severe or life-threatening condition but more commonly will have a less ser ious cause. A focused history with a careful clinical examination may be suf \201 cient to decide the cause of the chest pain but further investiga- tion is often required. Knowledg e of disease prevalence and awareness of risk factors can help formulate an appropriate dif ferential diagnosis and guide further investigation. Initial assessment of chest pain may i nclude questions about character of the pain, onset, location, radiation, severity, duratio n, exacerbating or relieving factors and its relationship to breathing, coughing and moveme nt. Read- ers should be aware that cardiac chest pain can present with atypical symptoms su ch as pleuritic pain and chest wall tenderness in a small proportion of patients. The prese nce of associated symptoms such as breathlessness, cough, sputum or haemoptysis may help po int to a respira- tory cause of the chest pain. An algorithm for the initial approach to a patient with chest pain is suggested in Fig. 3.4.1. When considering respiratory causes of chest pain, knowl- edge of the thoracic neuro-anatom y will help understand- ing of how certain pathologies present. The lung paren- chyma and v isceral pleura have no pain innervation. Parietal pleura is supplied by the intercostal ner ves giving rise to pleuritic chest pain. Central diaphragmatic pleurisy can present with re ferred shoulder tip pain as it is supplied by pain \201 bres which run in the phrenic ner ve. The outer dia- phragm is innervated by the lower 6 intercostal nerves and can give rise to referred upper abdominal pain. Chest wall pain can be of differing character depending on the cause and tissue affected. It may be pleuritic type pain (e.g. with rib pathology), it may be localized or diffuse dull pain and can be associated with chest wall tenderness. Pain in a der- matomal distribution, particularly with hyperaesthesia can occur with herpes zoster infection and with lesions affect- ing the intercostal nerve or nerve root. The tra chea and large bronchi have pain \201 bres running in the vagus nerve and can give rise t o retrosternal or anterior chest pain which is often raw or burning in character and worse on inspiration. Rarely, massive mediastinal adenopathy can give rise to anterior chest pain although more commonly inva- sive adenopathy will present with ipsilateral chest pain. A l imited list of differential diagnoses for respiratory causes of chest pain is shown in the box. Patient with chest pain Differential diagnosis of respiratory causes of chest pain Pleuritic pain Patient unwell, cardiovascular instability or low GCS* Brief assessment or triage Sudden onset Pulmonary embolus Spontaneous pneumothorax Onset over hours Pneumonia Pleurisy Pericarditis Onset over days Patient stable Connective tissue associated pleurisy Empyema History, Examination ECG, CXR, initial investigations Commence ABC approach to resuscitation Onset over weeks Malignancy Tuberculosis Chest wall pain Sudden onset Life threatening illness immediately identified e.g. STEMI** Commence definitive treatment Trauma e.g. assault, violent coughing Developed over days Costochondritis Vertebral body collapse Developed over weeks Malignancy e.g. mesothelioma Nerve root irritation Attempt to identify origin of chest pain Tracheobronchial pain Infection Irritant inhalation Mediastinal pain Invasive adenopathy Other e.g Referred pain Panic attack Non organic Cardiac e.g acute coronary syndrome Pericarditits Aortic dissection Respiratory See box Gastrointestinal e.g gastro oesophageal reflux, oesophagitis Fig. 3.4.1 Algorithm for initial approach to a patient with chest pain. *GCS = Glasgow coma score **STEMI = ST elevation myocardial infarction CHAPTER 3.4 Chest pain 43 An approach to investigation of the patient with chest pain due to a suspected respiratory cause is suggested in Fig. 3.4.2. Suspected respiratory cause for chest pain Tracheo- bronchial pain Pleuritic chest pain Chest wall pain Mediastinal pain Consider: Consider: Consider: Consider: CT thorax Clinical probability score +/ \210\222 D dimer \200 V/Q scan or Fig. 3.4.4 CT pulmonary angiogram showing bilateral proximal pulmonary artery thromboemboli c disease with a saddle embolus. Sputum culture Thoracic spine X ray CTPA Fibreoptic bronchoscopy CT thorax In recent years several biomarkers such as D-dimer and cardiac troponins have become readil y available to aid the diagnosis of chest pain. It is important, however, to be aware that these tests have low speci \201 city and should not be used in isolation of other clinical \201 ndings. In a proportion of people the cause of the chest pain can not be conclusive ly identi \201 ed. The authors feel that it is important to avoid the temptation to attach a diagnostic label that is not proven. It is generally best to explain diagnostic uncertai nty to the patient and the refer- ring physician. Bone scan \200 MRI CTPA Autoantibodies Pleural fluid aspiration Echocardiogram CT thorax Fig. 3.4.2 V/Q scan = ventilation perfusion scan; CTPA = Computed tomography pulmonary angi ogram AUTHOR \200\231S TIPS \200 Biomarkers such as D-dimer and cardiac troponin have a large number of false positive cause s. When considering the diagnosis of pulmonary embo- lism the clinical probability score mu st be calculated \201 rst to assess if a D-dimer assay will be helpful. Only a normal res ult (which excludes PE) is of any clinical value; an abnormal result (however high) does no t imply a signi \201 cantly increased probability of PE. Patients with airways diseases su ch as asthma and COPD can complain of chest wall pain particularly worsened by breathlessne ss. Pleuritic pain may ease or become duller in character as a pleural effusion develops. Further reading BTS Guidelines for the Management of Suspected Acute Pulmonary Embolism. Th e British Thoracic Society Standards of Care Committee, Pulmonary Embolism Guideline Develo pment Group. Thorax 2003; 48: 470 \200\223484. D-Dimer in Suspected Pulmonary Embolism. A statement from the British Thoracic Society Stan dards of Care Committee, Dec 2006. www.brit-thoracic.org.uk/c2/uploads/ ddimerstatement.pdf Fig. 3.4.3 CXR of former dockyard worker presenting with chest wall pain and weight loss, s howing volume loss in the right hemithorax with diffuse right pleural thickening and right pleural effusion typical of mesothelioma. Mahajan N, Mehta Y, Rose M, et al. Elevated troponin level is not synonymous with myocardia l infarction. Int J Cardiol 2006; 111: 442 \200\223449. Swap C J, Nagurney J T. Value and limitations of chest pain history in the evaluation of pa tients with suspected acute coronary syn- dromes. JAMA 2005; 294: 2623 \200\2232629. Von Korff M, Dworkin SF, Le Resche L, et al. An epidemiologic com- parison of pain complaints. Pain 1988; 32(2): 173 \200\223183. P DENNISON & G PHILLIPS 44 3.5 Pre-operative assessment Respiratory physicians are not infrequently asked by surgi- cal colleagues to assess \201 tness for surgery, either in a patient with known respiratory disease or where respira- to ry disease has been suggested by pre-operative tests. This chapter will deal with the pre-o perative assessment of the respiratory patient and ways of assessing speci \201 c risks po sed to such patients by particular operations, together with strategies for \200\230optimi zing \200\231 a patient preoperatively. Table 3.5.1 ASA Physical Status classi \201 cation system A normal healthy patient I. A patient with mild systemic disease II. A patient with severe systemic disease III. A patient with severe systemic disease that is a threat to life IV. A moribund patient who is not suspected to live without the operation V. Pre-operative assessment \200 Should be undertaken before the operation in a time- frame that allows any essential preope rative investiga- tions to be performed and optimization strategies to be implemented. Shou ld include full history and examination to clarify the respiratory diagnosis. Should includ e targeted investigations and a plan for optimization of the patient \200\231s pre- and pos t-operative well-being. Should consider that surgery may exacerbate the under- lying respir atory disease and/or that the respiratory disease itself may lead to peri-operative and/or post- operative complications which may be pulmonary and/ or non-pulmonary. A declared brain-dead patient whose organs are being removed for donation purposes VI. The investigations that are commonly considered pre- operatively include: Blood tests (FBC, renal function, coagulation) There is no evidence from randomized control led trials that testing will alter the health outcomes in patients. However there is an inc reasing prevalence of abnormality with age. Pre-operative CXR \200 The proportion of pre-operative abnormal CXR results increases with age and severity of res piratory disease. Many of these changes will be chronic, however, and may not lead to chang es in clinical management. The CXR may be useful for clari \201 cation of the respira- tor y diagnosis and for comparison if peri-operative pul- monary complications arise. When no C XR is available, consider performing one if ASA status is \211 3, in major operations or o perations for malignant neoplasm. If symptoms have changed since the previous CXR con- side r repeating it. History and examination: key points \200 \200 \200 Clarify the respiratory diagnosis. Assess disease severity. Determine whether or not there are any reversible factors. Establish what treatment has already been tried, whether or not this can be escalated, and what treatment has not yet been tried. Preoperative investigations Electrocardiogram (ECG) \200 Preoperative tests can be useful in several ways: \200 Consideration should be given to obtaining a preopera- tive ECG unless pulmonary disease is mild and the oper- ation is minor. There is an increasing prevalence of ECG abnormalities with age and severity of disease. Abnormalities on the preoperative ECG have been associate d with increased risk of in-hospital cardiovascular death in major operations. Assessing risks and potential complications of a particu- lar operation in a particular pat ient. Changing the clinical management of the patient to reduce morbidity/mortality: (a) Pr eoperatively Optimizing the patient \200\231s condition. Avoiding last-minute cancelations or delays. Arterial blood gas analysis (ABG)/oxygen saturations \200 (b) Intra-operatively There is a lack of data suggesting that measuring preop- erative ABGs can independently pre dict post-operative complications or affect clinical management in extra- thoracic or non-r esective lung surgery, and they should therefore not be considered to be a routine test. In resective lung surgery, earlier studies suggested increased complications with hypercapnoe a (PaCO2 > 6 KPa) and it was initially considered a strong relative con- traindication to s uch surgery (ATS/ERS guidelines). However, later studies did not show a predictive effect o n complications. Whilst such patients may be excluded sur- gery on other grounds e.g. FEV1, preoperative assessment of ABGs is not routinely recommended in current BTS guidelines for lung resection. Low arterial oxygen saturations (<90% at rest) are asso- ciated with incre ased complications and are incorpo- rated in lung resection assessment (see Chapter 13.4: p p. 292 \200\223297). Anesthetic technique e.g. general versus local an- esthetic/sedation. Operative type e.g. s taged operations. (c) Post-operatively Timing of operation. Level of care post-operatively e.g. HDU/ICU/ward. Incidental \201 nd ings, e.g. lung mass noted on shoulder X-ray, interstitial markings on a CXR. Care must be taken, however, not to unnecessarily delay surgery by carrying out further investigations b ased on false positive or insigni \201 cant results. Recent guidelines have been published by NICE on preop- erative testing in all patients. Th ey take into account physical status as judged using the ASA (American Society of Anaesthes iologists) classi \201 cation (Table 3.5.1) and the extent of the operation. CHAPTER 3.5 Pre-operative assessment 45 Pulmonary function tests. \200 Table 3.5.2 Lee index for estimating perioperative cardiac risk in noncardiac surgery Post-operative pulmonary complications in extratho- racic/non-resective lung surgery seem t o be associated with lower FEV1 and TLCO values. Particular risk is asso- ciated with FEV1 <1L or <60% predicted. Spirometry is helpful in clarifying the respiratory diagno- sis and objectively assessing response to optimization strategies. In resective lung surgery, spiro metry is mandatory to assess \201 tness for operation. If the post-bronchodilator FEV1 >1 .5L (for lobectomy) or >2L (for pneumonec- tomy), no further tests are required. If FEV1 is below these values, predictive postoperative FEV1 cardiopul- monary exercise testing sh ould be undertaken (see Chapter 13.4, pp. 292 \200\223297). No. of risk factors Risk of major postoperative cardiac event (death or non-fatal myorcardial infarction or car diac arrest) % (95% CI) 0 0.4 (0.1 \200\2230.8) 1 1.0 (0.5 \200\2231.4) 2 2.4 (1.3 \200\2233.5) \211 3 5.4 (2.8 \200\2237.9) Score 1 for each of the following: (a) High-risk surgery (intrathoracic, intraperitoneal, s uprainguinal vascular surgery) (b) History of ischaemic heart disease (history of myocardial infarction, positive exercise test result, current ischaemic chest pain or nitrate use, Q waves on ECG, or any of the ab ove after CABG/angioplasty procedure) Cardiopulmonary exercise testing \200 This is not widely available in the UK, but can be useful in high risk patients undergoing extra-thoracic/non- resective lung surgery. Patients with anaerobic thresholds <11 ml/kg/mi n are at high risk for major surgery, particularly if this occurs in combination with evide nce of myocardial ischaemia. They should be considered for either aggressive pre- and post- operative optimization in a critical care setting or recon- sideration of the need, if the procedure is not life saving. In resective lung surgery, cardiopulmonary exercise test- in g is helpful in predicting risk. VO2 max <15ml/kg/min predicts that the patient is at incre ased risk (see Chapter 13.4, pp. 292 \200\223297). (c) History of congestive heart failure (history of heart failure, pulmonary oedema, or paroxysmal nocturnal dyspnoea, S3 gallop rhythm or bilateral rales on examination, or CXR showing increased pulm vasc resistance) (d) History of cerebrovascular disease (stroke/TIA) (e) Insulin dependent diabetes (f) Preo perative serum creatinine >175 mol/L technique. Close liaison with surgical and anesthetic colleagues is essential, and sometime s the operative risks cannot be altered. Some general points apply, however: Smoking cessation Cigarette smokers are at increased risk of cardiovascular and pulmonary c omplications. Smoking increases carboxy- hemoglobin levels, decreasing oxygen delivery, whi lst nic- otine increases blood pressure, heart rate and causes systemic vasoconstriction. S mokers have increased mucus production, decreased ciliary activity and impaired pulmo- nary immune function, together with impaired wound heal- ing and increased incidence of wound i nfections. Clear benefit is seen from periods of abstinence of >6 \200\2238 weeks before su rgery and, even if this is not possible, abstinence of 24 \200\22348 hours pre-surgery also has important bene \201 cial physiological effects. Risk assessment Risk from a particular operation can be assessed by looking at patient fact ors, operative factors and anesthetic factors. Patient factors Risk factors for postoperative pulmonary complications include cigarette sm oking (2 \200\2235 fold increase in risk), and COPD (2 \200\2233 fold increase in risk). To a lesser extent age, functional dependence, alcohol use, impaired sensorium and weight los s are also risk factors. Severity of asthma does not predict complications in elective proc edures. Other patient risk factors are useful in assessing preopera- tive risk. The most im portant of these are the cardiac risk factors, as postoperative cardiac complications are c om- mon. Several indices are available for predicting cardiac risk, one of which is the Lee risk index (Table 3.5.2). Postoperative care Recognizing patients at increased risk for postoperative complications a llows appropriate decisions to be made ahead of time to try to minimize those risks. These include determining the site of post-operative or even pre- operative care e.g. HDU/ITU, to gether with (if appropriate) postoperative aggressive physiotherapy with lung expan- sion e xercises, or selective nasal decompression after abdom- inal surgery. Patients may bene \201 t from \200\230shared care \200\231 post- operatively from both respiratory physician s and surgeons. Operative characteristics Thoracoscopic and upper abdominal procedures in par- ticular have a deleterious affect on respiratory function through pain, reduction of diaphragmatic func tion and sometimes pleural effusion. Decreased ability to breathe deeply or cough due to pa in leads to atelectasis, mucus retention, increased incidence of pulmonary infection and re duced gas exchange. Video assisted thoracoscopic surgi- cal (VATS) procedures with smaller thoracotomy ports result in fewer such complications. Duration of operation may also contri bute to the risk of pulmonary complica- tions, especially in operations lasting >3 \200\223 4 hours. Further reading Guidelines on the selection of patients with lung cancer for surgery. British Thoracic Society. Thorax 2001; 56; 89 \200\223108. Joo HS, Wong J, Naik VN, et al. The value of screening preoperative chest X-rays: a systema tic review. Can J Anesth 2005; 52: 568 \200\223574. Noordzij PG, Boersma E, Bax JJ, et al. Prognostic value of routine preoperative electrocardiography. Am J Cardiol 2006; 97(7): 110 3 \200\2231106. Anesthetic characteristics Intubation can cause intra-operative bronchospasm, although most induction agents are bronchodilators. In gen- eral, regional anesthesia is safer than gene ral anesthesia. Pre-operative tests, National Institute of Clinical Evidence. Pretreatment evaluation of no n small cell lung cancer, ATS/ERS guidelines. AJRCCM 1997; 156: 320 \200\223332. Smetana GW, Lawrence VA, Cornell JE, et al. Preoperative pulmo- nary risk strati \201 cati on for non-cardiothoracic surgery: system- atic review for the American College of Physicia ns. Ann Int Med 2006; 144(8): 581 \200\223595. Optimizing the respiratory patient Optimization of the patient may involve escalation/addit ion of therapy, or modi \201 cation of current therapy, e.g. inhaler R RAJENDRAM 46 3.6 Solitary pulmonary nodule De \201 nition A solitary pulmonary nodule (SPN) is a single lesion \211 3cm in diameter surrounded by normal lung without lymphade- nopathy or atelectasis. Lesions >3cm are almost always malignant and are called masses. assess with CXR (e.g. lung apices, perihilar, costophrenic angles) are seen well on CT. CT can also stage malignancy and help guide needle biopsy. Table 3.6.2 Common causes of benign and malignant nodules Epidemiology A nodule is seen on 0.1-0.2% of CXRs. It is usually > 8mm in diameter before i t is clearly visible. CT is more sensitive and \201 nding nodules as small as 2mm is comm on. The reported prevalence of malignancy varies widely be- tween studies but the risk of m alignancy in nodules de- tected on CXR is probably 30 \200\22340%. Small nodules (<8mm) are dif \201 cult to investigate but fortunately are much more likely to be benign. Malignant nodules Percentage Benig Percentage nodules 25% Adenocarcinoma 47% Healed/ non-speci \201 c granulomas Squamous cell carcinoma 22% Solitary metastasis Undifferentiated 8% Granulomatous infections 15% NSCLC 7% Hamartomas 5% Etiology There are several possible causes for a SPN (Table 3.6.1), but > 95% are neoplasms (usually primary), granulomas (usually infection) or hamartoma (Table 3.6.2). SCLC 4% Bronchioloalveolar cell 4% Table 3.6.1 Causes of solitary pulmonary nodules CT densitometry measures the attenuation of a lesion and aids detection of calci \201 cati on. Enhancement with IV contrast also suggests malignancy. However, the sensitivity and spe ci \201 city of these measurements are low and combi- nation with other clinical and radio logical features in- creases their usefulness. Low-dose techniques should be used to reduce the dose of radiation if multiple follow-up CT scans are required. Neoplastic (malignant or benign) Bronchogenic carcinoma Single metastasis Lymphoma Carcinoi d Connective tissue & neural tumors \200\223 \201 broma, neuro \201 broma, blastoma, sa rcoma Hamartoma Lipoma Nodule characteristics Size: Table 3.6.3 shows the relationship between size and risk of ma lignancy. Lesions >3cm in diameter are very likely to be malignant, but other possible caus es include lung ab- scess, Wegener \200\231s granulomatosis, round pneumonia, rounded atele ctasis, and hydatid cyst. Nodules <8mm are too small to biopsy or assess with positron emis sion tomography (PET) so the most sensible option is follow-up CT. Shape: generally unhelpf ul but, a very irregular edge, co- rona radiata (spiculation), lobulation, or notching sugg est bronchogenic carcinoma. A well-de \201 ned, smooth edge suggests a benign lesion or me tastasis. In \202 ammatory (infectious) Granuloma \200\223 TB, histoplasma, coccidioidomycosis, bla stomycosis, Cryptococcus, Nocardia Lung abscess Round pneumonia Hydatid cyst In \202 ammatory (non-infectious) Rheumatoid arthritis Wegener \200\231s granulomatosis Sa rcoidosis Lipoid pneumonia Congenital Arteriovenous malformation Sequestration Lung cyst Table 3.6.3 Method of detection, size of nodule and risk of malignancy Method of detection Size (mm) Approximate risk of Others Pulmonary infarct Round atelectasis Mucoid impaction malignancy CT only \211 4 <1% CT, Rarely CXR >4 \200\2238 6% CXR or CT >8 \200\22330 50% Initial detection of a SPN: CXR and CT Chest radiography: provides information on size, sha pe, cavitation, growth rate, and calci \201 cation. These features can help suggest whethe r the lesion is benign or malignant. However, none are speci \201 c (see below). CT has ma ny advantages over CXR e.g. better resolution and detection of small nodules. Regions that are dif \201 cult to Attenuation: nodules may be solid, non-solid (ground glass; underlying lung parenchyma pres erved and visible through nodule) part solid (mixed solid and ground glass). Table 3.6.4 sh ows how the risk and growth rate of malig- nancies vary between these types of nodule. CHAPTER 3.6 Solitary pulmonary nodule 47 Rate of growth: serial CXR or CT can assess growth (dou- bling time; Td i.e. doubling of no dule volume). A 26% in- crease in diameter (e.g. 11mm to 14mm) on CXR re \202 ects a doubl ing of volume as nodules are seen in 2-D rather than 3-D and the volume of a sphere is 4/3i r3. However, a 3mm change is dif \201 cult to detect using CXR. The Td of bronchogenic ca rcinoma is generally 1 \200\22318 months (mean 4 \200\2238). Outside this range bronchogeni c car- cinoma is unlikely but not impossible; <1 month suggests infections; >18 suggests be nign processes (e.g. granuloma, hamartoma, carcinoid, rounded atelectasis). If there is no change over 2 years, the SPN is probably benign. Further follow-up (up to 5 years), may be indicated particularly for non-solid nodules as indolent malignancies with Td >730 days may be missed (see Table 3.6.4). Most studies have focused on investigation and very few outcome studies have been performed . The suggestions in this review are therefore based on evidence that is graded 1B-2C at be st. The mortality associated with lung cancer is generally high (5-year survival rate 14%), but early lung cancer, (stage 1A; T1N0M0; primary tumor <3cm), may have a 5-year survival rate of 70-80%. Metastastectomy also offers the potential of cure to some patients with tre ated extra-pulmonary malignancy. Thus, the patient with cancer who presents with a SPN coul d be cured. It is impossible to ignore the emotional and medicolegal implications of missin g a potentially curable cancer. Most recommendations (and current practice) at least partly re \202 ect this anxiety. This must be balanced against the substantial radiation exposur e this group of patients may receive and which may itself induce malignancy. Table 3.6.4 Nodule characteristics, doubling time and risk of malignancy Further investigations Lab studies: the role of lab studies is limited. Anemia or elevated in \202 ammatory markers may suggest malignancy or infection. Deranged liver function test s or bone pro \201 le may suggest metastases. Histoplasma or coccidioidomyco- sis serology may identify infections with these fungi. A gamma interferon blood test (e.g. Elispot) can be used to detect tuberculosis. Sputum cytology: is generally only indicated for investiga - tion of patients with central nodules who are unable to tolerate or unwilling to undergo other invasive tests. PET: the metabolic rate and glucose uptake of malignant nodules is gr eater than normal lung. Thus enhancement on 18-F-2 \202 uorodeoxyglucose (FDG) PET makes it likely to be malignant. The sensitivity and speci \201 city are >90% and me- diastinal metastases can be detected, improving the staging of non-invasive lung cancer. Furthermore, the yield from biopsy may be increased if the metabolically active regions of nodules are sampled. However, false-positives occur in infectious or in \202 amma- tory nodules which are metabolically active. Tumors with low metabolic rates (e.g. carcinoid and bronchoalveol ar carcinoma) may be dif \201 cult to distinguish from background activity. Furthermore, F DG-PET is less sensitive for nod- ules <20mm in diameter and may miss lesions <10mm. Single -photon emission computed tomography (SPECT): cheaper than PET but the sensitivity, speci \201 city and diag- nostic accuracy (89%, 67%, and 81%, respectively) are simi- lar. It is performed using a radiolabeled somatostatin-type receptor binder, technetium Tc P829. SPECT has not been assessed in large studies; in a smaller series, the sensitivity fell signi \201 cantly for nodules <20mm. Bronchoscopy and transbronchial needle aspiration (TBNA): ma y be helpful if the SPN is endobronchial, near a large airway or mediastinal nodes need to be sampled. Because the diagnostic yield from bronchoscopy is gener- ally <20% if the SPN i s <2cm, bronchoscopy has a limited role in the investigation of SPN. Transthoracic aspirati on biopsy (TTAB): the accuracy is high (90 \200\22395%) when the SPN is \211 2cm, but is l ess (60 \200\22380%) in lesions <2cm. Sensitivity for speci \201 c benign diagnosis is low er (11 \200\22368%); so most specimens are non-diagnostic. Complications include pneumothor ax which occurs in up to 30% (of these 5% require a chest drain) and haemoptysis which occu rs in 5 \200\22310% (usually minor and resolves sponta- neously). HRCT characteristics Risk Mean Td of malignancy (days) Non-solid (ground glass) 34% 813 Partly solid (<15mm) 40 \200\22350% 457 Solid (<10mm) 15% 149