CT of the same patient as Fig. 4.14 demonstrates the nodule lies in the SUBASH KC/NMC-15TH/2014 62 CHAPTER 4 Respiratory conditions Lung cancer Lung cancer is the leading cause of cancer-related deaths in men and women worl dwide and strongly associated with cigarette smoking. Clinical presentation Symptoms and signs are often non-speci \201 c, leading to a delay in diagnosis. Common symptoms include persistent cough, weight loss, haemoptysis, and chest p ain. Signs to look for include cachexia, \201 nger clubbing, cervical/supraclavicular lymphadenopathy, reduced lung expansion, reduced breath sounds, or crepitations on ausculta tion. Imaging Plain \201 lm (Fig. Usually the initial imaging investigation. Look for: \200 S igns of a mass. \200 Mediastinal widening. \200 Focal consolidation. \200 Pleural eff usion. \200 Volume loss. \200 Bone destruction. 4.16 ) CT (Fig. \200 Usual method of characterizing and staging disease. \200 Important role i n determining appropriate treatment pathways and 4.17 ) prognosis. Much research currently ongoing into the feasibility of CT screening of at-risk individuals for early-stage lung cancer. Often used to obtain image-guided tissue biopsy. Nuclear medicine PET-CT has rapidly become a mainstay in the staging of potentially treatab le disease and has been shown to detect signi \201 cant numbers of metastases not seen wit h standard CT. More accurate also in assessing mediastinal involvement than CT alone. MRI Used mostly as a problem solver in cases of spinal metastases, invasion of the chest ap ex by Pancoast tumors, and the characterization of adrenal masses. Ultrasound \200 Used for assessment and biopsy of neck nodes or liver metastases. \200 Endoscopic/endobronchial ultrasound involves a small ultrasound probe on an endoscope for characterization and sampling of mediastinal nodes. Information for the radiologist Smoking history. SUBASH KC/NMC-15TH/2014 LUNG CANCER 63 Fig. 4.16 paratracheal stripe in a 55-year-old smoker. CXR revealing a large right upper zone mass with widening of the right Fig. 4.17 lung cancer in the posterior segment of the right upper lobe and pathologically e nlarged right paratracheal lymph nodes. CT of the same patients as Fig. 4.16 con \201 rming the presence of a large SUBASH KC/NMC-15TH/2014 64 CHAPTER 4 Respiratory conditions Lobar collapse Atelectasis and collapse are interchangeable terms meaning diminished lung v olume and deaeration. The most common cause of lobar collapse is bronchial obstruction which may be due to: \200 Mucus plugging. \200 Inhaled foreign body. \200 Endobronchi al tumors. \200 Extrinsic compression of the bronchus by tumor, lymphadenopathy, or aneurysm. Atelectasis does not have to affect an entire lobe may be affected by: \200 Relaxation/pa ssive atelectasis: due to space-occupying effects of \200\224 smaller areas of lung pneumothorax, pleural effusion, or mass. Cicatrization atelectasis: volume loss due to \201 brotic lung disease. \200 Underexpan sion of lung due to many causes including pain, chest wall abnormalities, diaphragmatic weakness. Adhesive atelectasis: complex and due to insuf \201 cient production of surfactant and is seen in respiratory distress syndrome (RDS) of the newborn. Clinical presentation Patients may present with: \200 Dyspnoea: can be sudden if rapid on set of lobar collapse. \200 Cyanosis. \200 Chest pain. Look for: \200 Chest expansion is reduced or absent. \200 The trachea and the heart are deviated toward the affected side. \200 Dullness to percussion over the involved area. \200 Reduced/absent breath sounds. Imaging Plain \201 lm General signs of collapse: \200 Displacement of \201 ssures and opaci \201 cation of the collapsed lobe. \200 Displacement of the hilum (the left hilum is usually at least 1cm higher than right on a normal CXR). Mediastinal shift toward the collapse. \200 Loss of volume. \200 Compensatory hyperluce ncy of the remaining lobes. For speci \201 c examples see Figs. 4.18 \200\223 4.27 . CT \200 This shows the same basic signs as on plain radiograph but to greater effect. \200 Important role in detecting underlying lung tumors or other causes of bronchial obstruction. Nuclear medicine PET-CT is useful in detecting further sites of disease if malignancy has b een con \201 rmed. SUBASH KC/NMC-15TH/2014 LOBAR COLLAPSE 65 Information for the radiologist \200 Smoking history. \200 Duration of symptoms. \200 Suspicion of inhaled foreign body. \200 Presence of haemoptysis. Fig. 4.18 Left upper lobe (LUL) collapse. PA CXR of LUL collapse, showing \200\230veil lik e \200\231 opaci \201 cation of the left chest, obliteration of the heart border, elevatio n of the hilum, and preservation of the arch and descending thoracic aorta. Fig. 4.19 a large tumor surrounding the hilar structures and invading the mediastinum. Note how the lobe collapses forwards to lie against the heart, while the lower lobe continues t o outline the posterior structures such as the aorta. CT scan of a different patient to Fig. 4.18 revealing LUL collapse due to SUBASH KC/NMC-15TH/2014 66 CHAPTER 4 Respiratory conditions Fig. 4.20 left, depression of the left hilum and increased density behind the heart ( \200 \230sail sign \200\231) due to LLL collapse. Left lower lobe (LLL) collapse. PA CXR showing mediastinal shift to the Fig. 4.21 hilum. Note how the lobe collapses medially, to lie against the spine. Axial CT of patient with LLL collapse due to a low density mass at the SUBASH KC/NMC-15TH/2014 LOBAR COLLAPSE 67 Fig. 4.22 cough, showing RUL collapse. The opacity in the right upper chest has a clearly d e \201 ned, curved inferior border, consisting of the elevated horizontal \201 ssure and the inferior border of a right hilar mass (the \200\230Golden S \200\231 sign). Note also mediastinal shift to the right and volume loss in the right chest. Right upper lobe (RUL) collapse. PA CXR of patient with persistent Fig. 4.23 to lie in the anterior chest. Note also enlarged right paratracheal nodes, pleura l effusion, and trace of \202 uid in the pericardium around the ascending aorta. Axial CT of the same patient as Fig. 4.22 . The RUL has collapsed forwards SUBASH KC/NMC-15TH/2014 68 CHAPTER 4 Respiratory conditions Right middle lobe collapse. PA CXR revealing a well de \201 ned soft tissue Fig. 4.24 dens ity extending from the right hilum, associated with loss of clarity to the right heart bord er and minimal signs of volume loss. Fig. 4.25 horizontal and oblique \201 ssures drawn together as the middle lobe collapses between them. Right lateral CXR of the same patient as Fig. 4.24 , demonstrating the SUBASH KC/NMC-15TH/2014 LOBAR COLLAPSE 69 Fig. 4.26 Note volume loss to the right hemi thorax, depression of the right hilum, and the increased density of the collapsed lobe. Right lower lobe (RLL) collapse. PA CXR of patient with RLL collapse. Fig. 4.27 are similar to those on the left with the collapsed lobe lying posteriorly and me dially against the spine. Coronal reformat of CT scan showing collapse of the RLL. Appearances SUBASH KC/NMC-15TH/2014 70 CHAPTER 4 Respiratory conditions Bronchiectasis Irreversible dilatation of those bronchi which contain cartilage in their wa lls, leading to in \202 ammation in the lung and impaired clearance of secretions. Causes include infections (particularly in childhood), cystic \201 brosis, immu- node \201 cien cy, chronic aspiration, ciliary dysfunction, and proximal airway obstruction (e.g. by tumor or foreign body). Clinical presentation Chronic cough and sputum production, dyspnoea, haemoptysis, and recur rent chest infections. On examination there may be clubbing, weight loss, wheeze, and coa rse crepitations in the lungs. Pulmonary function tests are normal or show an obstructive p attern. Imaging Plain \201 lm (Fig. Chest radiographs are the initial investigation but are often normal. \200\230Tubular \200\231 or \200\230cylindrical \200\231 bronchiectasis causes a \200\230streetcar-track \200\231 appearance of parallel lines caused by thick-walled dila ted bronchi. Cystic structures with air- \202 uid levels may be seen in cystic bronchiecta sis. Infection can cause alveolar consolidation. 4.28 ) CT (Fig. HRCT is the most sensitive test, demonstrating both the location and extent of dis ease. Findings include: \200 Dilated bronchi with peribronchial thickening and mucus rete ntion. \200 Bronchi which do not taper peripherally, are larger in diameter than 4.29 ) the accompanying pulmonary artery branch (signet-ring sign), and which reach the lung perip heries. Bronchoceles (bronchi \201 lled with \202 uid). \200 Cystic changes with air \202 u id levels. \200 Crowding of vessels caused by volume loss. \200 Compensatory emphysemat ous changes in non-affected areas. \200 Fibrosis and honeycombing in more severe disease. \200 Expiratory scans reveal areas of air trapping. CT may also provide clues as to the cause of bronchiectasis, e.g. foreign bodies and bronch ial tumors. Bronchography Now very rarely used. Information for the radiologist \200 Duration of symptoms. \200 Any underlying pulmonar y disease (e.g. tumor, cystic \201 brosis, Kartagener \200\231s syndrome). Previous chest infections, particularly childhood infections. \200 Immunode \201 ciency. \200 Previous radiotherapy. SUBASH KC/NMC-15TH/2014 BRONCHIECTASIS 71 Fig. 4.28 multiple ring shadows throughout both lungs in keeping with widespread bronchiect asis. CXR of a middle-aged woman with dyspnoea and cough revealing Fig. 4.29 widespread bronchial dilatation, of both cystic and cylindrical type. Axial CT from the same patient as Fig. 4.28 better demonstrates the SUBASH KC/NMC-15TH/2014 72 CHAPTER 4 Respiratory conditions Cystic \201 brosis De \201 nition Cystic \201 brosis is an autosomal recessive disease of epithelial transportation which affects multiple organs, primarily lung, pancreas, GI t ract, liver, and exocrine glands. Clinical presentation The majority of patients present in the 1 recurrent respiratory infec tions, or meconium ileus at birth. st year of life with failure to thrive, The dominant clinical picture and the major cause of mortality is progressive lung disease. Respiratory Patients have bronchiectasis with chronic cough and recurrent respiratory infec tions. Sinusitis and nasal polyps may be a feature. Clubbing may occur. Gastrointestinal \200 Pancreatic insuf \201 ciency may lead to steatorrhoea and malnutri tion. \200 Thick secretions can cause obstruction due to meconium ileus at birth, meconiu m ileus equivalent in older children, or intussusception. Fibrosing colonopathy is another cause of bowel obstruction. Hepato-biliary In some patients increased biliary viscosity results in cholestasis and even tually cirrhosis. This may present with jaundice or symptoms of portal hypertension such as bleeding from oesophageal varices. Genitourinary tract Male infertility is a frequent complication. Imaging Plain \201 lm This is the mainstay of radiological evaluation in cystic \201 br osis, used in routine screening and to detect complications. Progressive features include h yperin \202 ation, bronchiectasis predominantly in upper zones with areas of mucus pluggin g and atelectasis. Complications include infective consolidation, allergic bronchopulmonary aspergillosis (signs include bronchial dilatation with mucoid plugging \200\230 \201 nger in glove \200\231 sign) and pulmonary arterial hypertension (large central pulmonary arter ies with peripheral pruning). \200\224 CT \200 CT scanning is used as an adjunct to chest radiography and detects more changes of mucoid impaction and bronchiectasis. CT of the abdomen may have a role in the detection of complications such as the varied causes of bowel obstruction. Ultrasound Used in routine review of cystic \201 brosis patients. The primary reason for surveillance is to detect portal hypertension which can occur secondary to biliary \201 b rosis. Other ultrasound features include a small echogenic pancreas and gallstones. SUBASH KC/NMC-15TH/2014 CYSTIC FIBROSIS 73 Information for the radiologist \200 Obviously a known diagnosis of cystic \201 brosis is essential on the request card or any previously documented complications. Previous imaging is essential for comparison of surveillance scans. Fig. 4.30 typical of cystic \201 brosis. Note in dwelling venous access device via the le ft arm. PA CXR showing overexpanded lungs and upper lobe bronchiectasis Same patient as Fig. 4.30 , presenting with acute shortness of breath. Fig. 4.31 CXR now sh ows a large left pneumothorax with depression of the hemidiaphragm implying a tension pneum othorax. Treated with chest drain. SUBASH KC/NMC-15TH/2014 74 CHAPTER 4 Respiratory conditions Pleural effusion Pleural effusions are categorized as either transudates or exudates: \200 Transudate protein level <30g/L. \200 Exudate protein level > 30g/L. Transudates are caused by alterations to hydrostatic, colloid, or oncotic pressures in cond itions such as cardiac failure, nephrotic syndrome, and liver failure. Exudates are associated with in \202 ammation of the pleura or subpleural lung parenchyma and are seen in infection, malignancy, or lung infarction. In general exudative effusions r equire more evaluation and treatment. Clinical presentation \200 15 % of patients will be asymptomatic. When present symptoms i nclude dyspnoea, non-productive cough, and pleuritic chest pain. Signs include dullness to percussion, decreased tactile fremitus, decreased breath sounds, and a pleural friction rub. Imaging Plain \201 lm (Fig. \200 Pleural \202 uid is not visualized on PA radiograph until 4.32 ) > 300ml are present. Lateral radiographs are better at detecting small effusions and can detect as little as 25ml. Hemidiaphragm and costophrenic recesses are obscured. \200 Meniscus-shaped upper surface with the lowest point in mid-axillary line. \200 On supine radiograph, hazy increased opa city on affected side, which does not obscure bronchovascular markings. CT \200 CT chest with contrast should be performed in all patients with undiagnosed effusion, especially if unilateral. Nodular pleural thickening suggests malignancy, smooth pleural thickening is seen in benign conditions such as empyema. In transudative effusions the pleura should not be visible at all. \200 May be other \201 ndings such as cardiomegaly, asbestos plaque, abdominal disease. Ultrasound \200 Ultrasound is used to identify and localize \202 uid prior to aspiratio n or drainage. It also may be used to guide pleural biopsy. NCEPOD (National Con \201 dential Enquiry into Perioperative Deaths) have recently recommended all drainage of pleural effusions be ultrasound-guided. Ultrasound is better than CT at showing loculation and septae within an effusion. Information for the radiologist \200 Relevant medical history. \200 Features of infecti on if present. \200 Asbestos exposure. SUBASH KC/NMC-15TH/2014 PLEURAL EFFUSION 75 Fig. 4.32 Note the shift of the mediastinum away from the opacity and the meniscus extendin g up over the apex of the lung. PA CXR showing a large pleural effusion \201 lling much of the right chest. SUBASH KC/NMC-15TH/2014 76 CHAPTER 4 Respiratory conditions Interstitial lung disease In \202 ammation of the supporting structures (interstitium) of the lung. Frequently results in scarring and \201 brosis. Clinical presentation Common symptoms include dyspnoea and a dry cough. There may be clubbi ng and inspiratory crepitations on auscultation. A large number of causes are described inc luding: \200 Idiopathic, e.g. idiopathic pulmonary \201 brosis (IPF), sarcoidosis. \200 Inhaled substances, e.g. asbestosis, silicosis. \200 Drug induced, e.g. amiodarone, gold. \200 Infective causes, e.g. tuberculosis, atypical pneumonia. \200 Connective ti ssue diseases, e.g. scleroderma, rheumatoid arthritis. \200 Radiotherapy. The diagnosis can often be made by integrating imaging \201 ndings with a detailed histor y, though occasionally bronchoalveloar lavage or lung biopsy is required. Imaging Plain \201 lm Often abnormal with increased reticular ( \200\230linear \200\231) or reticular-nodular ( \200\230linear and nodular \200\231) lung markings. Fibrosis is usua lly associated with volume loss. CT HRCT is the preferred study. Demonstrates the smallest functional unit of the lung, the secondary pulmonary lobule, allowing abnormalities to be accurately localized. Interstitial thickening is seen as either a reticular or reticular-nodular pattern. Additional appearances may include: \200 Honeycombing (small cystic spaces due to \201 brosis). \200 Nodules, e.g. in silicosis. \200 Cysts, e.g. in histiocytosis. \200 Bro nchiectasis secondary to \201 brosis (traction bronchiectasis). \200 Lymphadenopathy, e .g. sarcoidosis, malignancy. \200 Pleural plaques and calci \201 cation, e.g. asbestosis . The distribution of disease is also important in narrowing the differential diagnosis, for example: \200 Upper lobe predominance: TB, sarcoid. \200 Lower lobe predominance: IPF, asbestosis, rheumatoid. \200 Well-de \201 ned localized area: post-radiotherapy. Information for the radiologist \200 Presenting symptoms and duration of illness. \200 History of malignancy/atypical infection/smoking. \200 Potential environmental and drug c auses, e.g. asbestos exposure. \200 Lung function tests. SUBASH KC/NMC-15TH/2014 INTERSTITIAL LUNG DISEASE 77 PA CXR of a 60-year-old patient following a single lung transplant for Fig. 4.33 idiopathic pulmonary \201 brosis. Note the signi \201 cant volume loss in the native \201 brotic lung when compared to the transplanted left lung. SUBASH KC/NMC-15TH/2014 78 CHAPTER 4 Respiratory conditions Connective tissue disease and the lung Most of the connective tissue diseases (CTDs), inclu ding rheumatoid, sys- temic sclerosis, SLE, and dermatomyositis affect the lung in some way . Each condition has a different pattern of common effects, but there is considerable overl ap between them. Clinical presentation Depends on severity of lung involvement and associated features of th e underling disease. In many cases patients will present with lung involve- ment before any other manifestations of CTD. Common symptoms are non-speci \201 c and include progressive exertional dyspnoea and dry c ough. Haemoptysis occurs in patients with diffuse alveolar hemorrhage syndromes and vasculi tis. Chest pain is uncommon but pleuritic chest pain can occur in patients with rheumatoid arthritis or SLE. Signs to look for include \201 nger clubbing, a maculopapular rash, Raynaud \200\231s phenomenon, telangiectasia, peripheral lymphadenopathy, and inspiratory c rackles on auscultation. Imaging Plain \201 lm (Fig. Rheumatoid lung \200 Unilateral pleural effusion is a frequ ent manifestation. \200 Fibrosis. \200 Peripheral necrobiotic nodules. \200 Bronchial wall thickening/bronchiectasis. \200 Cor pulmonale: cardiac enlargement and pulmonary ar tery 4.34 ) enlargement. SLE \200 Pleural and pericardial effusions. \200 Non-resolving consolidation. Systemic sclerosis \200 Fibrosis. \200 Oesophogeal dilatation. CT (Fig. Shows the same features as CXR but in better detail with increased sensitivity and speci \201 city. 4.35 ) Fluoroscopy Barium swallow useful in assessing oesophageal dysmotility often seen in system ic sclerosis. Information for the radiologist \200 Duration of symptoms. \200 Serological results. SUBASH KC/NMC-15TH/2014 CONNECTIVE TISSUE DISEASE AND THE LUNG 79 Fig. 4.34 CXR revealing widespread calci \201 cation within the soft tissues of the chest wall and distortion of the vascular pattern in the lung due to interstitial lung disease. T he patient was proven to have dermatomyositis. Fig. 4.35 pulmonary \201 brosis. Axial CT section from a patient with scleroderma and end-stage SUBASH KC/NMC-15TH/2014 80 CHAPTER 4 Respiratory conditions Pneumoconiosis \200 The term pneumoconiosis refers to the accumulation of inorganic dust in the lungs and the tissue reaction to its presence. Silica, asbestos, coal, and beryllium are the most commonly encountered causes, usually inhaled during occupational exposure. The most important factors in the development of pneumoconiosis are the duration and intensity of exposure to the dust. Clinical presentation \200 Patients with simple coal worker \200\231s pneumoconiosis are usually asymptomatic. They may rarely report cough or sputum production. \200 Complicated coal wo rker \200\231s pneumoconiosis (CWP) produces cough, dyspnoea, and lung function impairment. In advanced disease, cor pulmonale may result. Imaging Plain \201 lm (Fig. Simple CWP \200 Small well-circumscribed nodules between 2 \200\2235mm with a predominant 4.36 ) upper zone distribution. No progression after cessation of dust exposure. Complicated CWP (progressive massive \201 brosis, PMF) \200 Large coalescent opacities > 1cm. \200 Typically peripheral in mid and upper zones: eventual hilar migration. \200 May develop/progress after cessation of dust exposure. \200 Calci \201 ed hilar lymphad enopathy. \200 Loss of volume in upper zones. Cavitation within the upper zone opacities may be seen due to ischaemic necrosis or possibl y to superimposed TB. CT (Fig. \200 Small well-de \201 ned nodules with upper zone predominance. \200 Irregu lar conglomerate masses in both upper zones; may have 4.37 ) cavitated. Focal centrilobular emphysema. \200 Calci \201 ed mediastinal lymphadenopathy (periphera l calci \201 cation described as \200\230eggshell \200\231). Information for the radiologist \200 Respiratory function. \200 Occupational history. \200 Smoking history. \200 Any worrying or unusual symptoms. SUBASH KC/NMC-15TH/2014 PNEUMOCONIOSIS 81 Fig. 4.36 mass-like opacities at both hila, with volume loss in the upper lobes and widespr ead nodularity throughout the lungs, also with an upper lobe predominance. The patient had a long history of coal dust exposure. PA CXR of patient with progressive massive \201 brosis showing bilateral Fig. 4.37 Axial CT of the same patient as in Fig. lesions, nodularity, and architectural di stortion of PMF. 4.36 , showing the bilateral mass-like SUBASH KC/NMC-15TH/2014 82 CHAPTER 4 Respiratory conditions Sarcoidosis Sarcoidosis is a multisystem disorder of unknown cause. The diagnosis is usuall y made on the basis of wide ranging clinical and radiological manifes- tations, and is supp orted histologically by the presence of non-caseating granulomas. There is a worldwide dist ribution, although a geographic pre- dilection for African American, Danish, and Swedish po pulations has been described. It typically affects young to middle-aged adults, with a slig htly higher incidence in women. Morbidity and mortality is usually related to pulmonary disease with a 1 \200\2235 % fatality rate resulting from severe respiratory or cardiac dysfunction. Clinical presentation The clinical course of sarcoidosis varies considerably from self-limi ting illness in up to 2/3 of patients, to chronic progression in 10 \200\22330 Dry cough, d yspnoea, and chest pain occur frequently. % of cases. Lofgren \200\231s syndrome is a form of sarcoidosis that manifests as fever, arthralgia, erythema nodosum, and bilateral hilar lymphadenopathy. Imaging Plain \201 lm (Fig. Findings include intrathoracic lymphadenopathy and parenchyma l abnor- malities often with an upper zone distribution. 4.38 ) A clinical staging system based on the pattern of chest radiographical \201 ndings is used to monitor disease progression and prognosis: \200 Stage 0: normal chest radiograph. \200 Stage 1: lymphadenopathy only. \200 Stage 2: lymphadenopathy wit h parenchymal in \201 ltration. \200 Stage 3: parenchymal disease only. \200 Stage 4: pulmonary \201 brosis. Ultrasound Little routine role but used to assess abdominal involvement and aid biopsy of a ccessible nodes. CT (Fig. Thoracic involvement is more clearly demonstrated than with CXR alone. CT will sho w the pattern of mediastinal involvement and subtle abnor- malities such as pleural nodular ity and bronchovascular thickening. 4.39 ) MRI May be useful in cases of cardiac and neurological involvement. Information for the radiologist \200 Presenting features. \200 Any concerns for alterna tive diagnoses such as TB or lymphoma. \200 Serum ACE. SUBASH KC/NMC-15TH/2014 SARCOIDOSIS 83 Fig. 4.38 CXR showing bilateral hilar adenopathy secondary to sarcoidosis. Fig. 4.39 thickening of the bronchovascular structures, and beading of the \201 ssures. Axial HRCT slice of patient with Sarcoid showing perihilar nodularity, SUBASH KC/NMC-15TH/2014 84 CHAPTER 4 Respiratory conditions Benign asbestos-related disease Asbestos is a naturally occurring, \201 brous silicate an d exposure primarily occurs in occupational settings. The spectrum of asbestos-related thor acic diseases includes benign and malignant pleural disease: \200 Benign pleural effusion s are the earliest sign of disease (with a latency period of 8 \200\22310 years after exposure), and are usually small unilateral exudates. Focal pleural plaques are the radiological hallmark of prior asbestos exposure, and may or may not calcify. Diffuse pleural thickening is smooth and uninterrupted, involving the visceral pleura and extends over at least 25 % of the chest wall. Round atelectasis speci \201 cally refers to an area of atelectatic lung adjacent to pleural thickening. Asbestosis is a term reserved for \201 brosis due to asbestos exposure. Clinical presentation Patients are usually asymptomatic but asbestos effusions can present with episodes of pleuritic chest pain and fever. Diffuse pleural thickening may be suf \201 cient to restrict chest movement and lead to breathlessness. Imaging Plain \201 lm (Fig. \200 En face calci \201 ed plaques are seen as well-de \201 ned opacities with irregular margins, sometimes describes as resembling a \200\230hol ly leaf \200\231. 4.40 ) Diffuse pleural thickening causes blunting of the costophrenic angles, is ill de \201 ned, and more extensive in distribution than focal plaque disease. \200 Asbestosis manifests as pulmonary \201 brosis in the basal, subpleural zones along with calci \201 ed plaque. CT (Fig. Benign pleural plaques are focal, smooth opacities, usually < 1 cm thick, parallel ing the chest wall, often adjacent to ribs. The anterior chest and par- avertebral position s are commonly affected sites. Calci \201 cation is common but not obligatory. The overlyi ng lung is normal as the visceral pleura is unaffected. 4.41 ) Diffuse pleural thickening is more extensive and less well de \201 ned, normally seen in t he paravertebral position. The overlying lung is affected as the viscera pleura contracts. Round atelectasis has a characteristic appearance of a pleurally based mass, with indrawing of adjacent vessels and bronchi. Asbestosis results in similar appearances to idiopathic \201 brosis but with associated pleural disease. Information for the radiologist \200 Length and duration of asbestos exposure. \200 Any features to suggest pleural malignancy, such as chest wall pain? SUBASH KC/NMC-15TH/2014 BENIGN ASBESTOS-RELATED DISEASE 85 Fig. 4.40 asbestos plaque. Note how many plaques follow the line of the ribs, and the heavy diaphragmatic involvement. CXR showing multiple areas of dense pleural calci \201 cation in keeping with Fig. 4.41 anterior chest wall bilaterally. Axial CT slice through typical, well-de \201 ned calci \201 ed pleural plaque on the SUBASH KC/NMC-15TH/2014 86 CHAPTER 4 Respiratory conditions Tuberculosis \200 Tuberculosis (caused by Mycobacterium tuberculosis ) remains the leading cause of death from infectious disease worldwide. Susceptible groups include the immunocompromised, infants, diabetics, and alcoholics. Frequency is increasing, especially amongst those with HIV infection. \200 It is usually transmitted through inhalation. The organisms are deposited in the middle and lower lung zones, spread via the lymphatics to the hilar lymph nodes and then through the bloodstream to more distant sites such as the bone marrow, liver , spleen, kidneys, bones, and brain. After initial infection mycobacteria can remain dormant for many years, only causing clinical infection again when host immunity becomes impaired. Primary TB refers to disease at the site of initial deposition of mycobacteria in lung. Postprimary (or secondary) TB is caused by reactivation of dormant organisms. Clinical presentation \200 Cough. \200 Weight loss/anorexia. \200 Fever. \200 Night sweats. \200 Haemoptysis. \200 Genitourinary symptoms; dysuria, hematuria, prostatitis , orchitis, and epididymitis may be present. \200 Joint pain and swelling. Altered mental status, neck stiffness, decreased level of consciousness, and raised intracr anial pressure can indicate tuberculosis meningitis. Imaging Plain \201 lm (Fig. Primary TB \200 Mediastinal lymphadenopathy: usually unilat eral and more frequent in 4.42 ) children. Consolidation. \200 Ghon focus: calci \201 ed lung lesion. \200 Ranke complex: Ghon fo cus + calci \201 ed lymph node. Post-primary TB \200 Consolidation in apical and posterior segments of upper lobes. \200 Cavitation. \200 Multifocal nodular opacities suggest \200\230miliary \200\231 TB. \200 Occasionally present with unilateral effusion. CT \200 More sensitive and speci \201 c than plain \201 lm. \200 Often shows signs o f upper lobe volume loss, calci \201 cation and \201 brosis in patients with previous (non-active) infection. SUBASH KC/NMC-15TH/2014 TUBERCULOSIS 87 Cavitations in a nodule or consolidation suggests active disease. \200 Involved nodes cla ssically show signs of central necrosis. \200 Linear branching opacities and centrilobula r nodules i.e. \200\230tree in bud \200\231 suggests endobronchial infection. Ultrasound \200 May be used to guide nodal biopsy or pleural aspiration. \200 Useful in cases of renal or bladder involvement. MR Required if CNS involvement suspected. Information for the radiologist \200 Risk factors. \200 Immune status. \200 Bronchosc opy results if available. \200 Treatment history. \200 Vaccination history. Fig. 4.42 peribronchial thickening around the hilum on the left. TB infection was proven fr om sputum cultures. CXR revealing cavitating consolidation in the right upper lobe and SUBASH KC/NMC-15TH/2014 88 CHAPTER 4 Respiratory conditions Malignant pleural disease Most malignant pleural effusions are metastatic. Common primaries to consider include breast, lung, and renal cancer. Mesothelioma is the most common primary neoplasm of the pleura. Around 80 % of cases of mal ignant mesothelioma are associated with previous asbestos exposure. The latency period betw een onset of exposure and development of mesothelioma is between 20 \200\22340 years. Clinical presentation \200 Insidious onset of dyspnoea, fatigue, weight loss. \200 Ches t pain is a worrying symptom. \200 Signs of pleural effusion. Imaging Plain \201 lm \200 Unilateral pleural effusion. \200 Loss of volume in affect ed hemithorax. \200 Rib destruction. CT (Fig. CT chest with contrast should be performed in all patients with suspected pleural malignancy. 4.43 ) Signs on CT which are suggestive of pleural malignancy include: Irregular or nodular pleural thickening. \200 Circumferential pleural disease, involving the mediastinal surface. \200 Pleural thickening of > 1cm. CT can suggest pleural malignancy but is not in itself diagnostic, nor can it differentiate accurately between mesothelioma or metatstic pleural disease. It may be used to perform targeted pleural biopsy. MRI Limited role \200\224 sometimes used if surgical resection being considered but this i s rare. Nuclear medicine \200 PET-CT is not routinely used in mesothelioma unless curative surger y is being considered. Can be useful in cases of metastatic pleural malignancy of unknown primary. Information for the radiologist \200 Asbestos history. \200 Any previous malignancy. SUBASH KC/NMC-15TH/2014 MALIGNANT PLEURAL DISEASE 89 Fig. 4.43 right-chest pain. The scan reveals pleural thickening of encasing the lung. Biops y con \201 rmed mesothelioma. Axial CT slice from a patient who presented with shortness of breath and > 1cm in depth completely SUBASH KC/NMC-15TH/2014 90 CHAPTER 4 Respiratory conditions Mediastinal masses An abnormal soft tissue mass within the mediastinum. Clinical presentation Wide range of presentations depending on location and nature of the m ass. May present with chest pain, stridor, dyspnoea, dysphagia, SVC obstruction, hoarse voi ce, weight loss, back pain, or ruptured aneurysm, for example. May also be an incidental \201 nding. Imaging Plain \201 lm (Fig. PA and lateral chest radiographs may identify and localize th e mass and can help to guide further investigation. 4.44 ) CT (Fig. Usually performed for characterization and occasionally to guide biopsy. Identi \201 es calci \201 cation, cystic areas, and vascular structures better than plain \201 lm. Allows accurate localization of the mass which narrows the dif- ferential diagnosis: \200 Anterior mediastinum 4.45 ) \200\224 anterior to the pericardium, \200\230the 4 T \200\231s \200\231: Thymoma. \200 Thyroid. \200 Teratodermoid (germ cell tumors). \200 \200\230Terrible \200\231 lymphoma. Middle mediastinum \200\224 the heart, aortic root and pulmonary vessels: Bronchogenic cysts and tumors. \200 Ascending aortic aneurysm. \200 Lymphadenopathy. \200 Posterior mediastinum \200\224 posterior to the pericardium: Oesophageal tumor, achalasia, or duplication cysts. \200 Descending aortic aneurysm. \200 Neurogenic tumor. \200 Meningocoele. \200 Extramedullary haematopoiesis. Nuclear medicine Certain tumors show increased uptake on PET, e.g. lymphoma. Scintigraphy c an be used to identify thyroid goiter, ganglioneuromas and phaeochromocytomas. MRI Excellent at depicting neurogenic tumors and spinal abnormalities. Ultrasound Useful to assess the thyroid though will not visualize retrosternal areas adequa tely. Information for the radiologist \200 Age and sex of patient. \200 Presenting symptoms. \200 Previous imaging. \200 Management plan, e.g. biopsy. SUBASH KC/NMC-15TH/2014 MEDIASTINAL MASSES 91 Fig. 4.44 Note the descending aorta is well seen, as are the hilar structures, placing the mass within the anterior mediastinum. PA CXR showing a large soft tissue mass arising from the mediastinum. Fig. 4.45 the anterior mediastinum, enhances with contrast and contains some peripheral nec rosis. CT-guided biopsy con \201 rmed thymoma. CT of the same patient as Fig. 4.44 , con \201 rming the mass lies within SUBASH KC/NMC-15TH/2014 This page intentionally left blank SUBASH KC/NMC-15TH/2014 93 Chapter 5 Vascular differential diagnosis Global cardiomegaly 94 Enlarged left atrium 94 Enlarged left ventricle 94 Enlarged thoracic aorta 94 Enlarged pulmonary arteries 95 SUBASH KC/NMC-15TH/2014 94 CHAPTER 5 Vascular differential diagnosis Global cardiomegaly \200 Ischaemia. \200 Cardiomyopathy. \200 Pericardial effusion. \200 Multiple valvular disease. Enlarged left atrium \200 Increased pressure: \200 Mitral stenosis. \200 Atrial myxom a. \200 Left ventricular failure. Increased \202 ow: Mitral incompetence. \200 Right-to-left shunt. Enlarged left ventricle \200 Increased pressure: \200 Hypertension. \200 Aortic steno sis. \200 Coarctation. \200 Increased \202 ow: Aortic incompetence. \200 Mitral incompetence. \200 Right-to-left shunt. Weakened muscle: Ischaemia. \200 Cardiomyopathy. Enlarged thoracic aorta \200 Aortic stenosis: Post-stenotic dilatation of ascending aorta. Atherosclerosis. \200 Hypertension. \200 Infection: Syphilis. \200 Endocarditis. Coarctation. \200 Marfan \200\231s syndrome. \200 Dissection. \200 Post traumatic. SUBASH KC/NMC-15TH/2014 ENLARGED PULMONARY ARTERIES 95 Enlarged pulmonary arteries Dilated pulmonary trunk only \200 Post-stenotic dilatation (p ulmonary valve stenosis). Dilated central pulmonary arteries/small peripheral vessels \200 Primary pulmonary hypert ension. \200 Chronic pulmonary embolic disease. \200 Chronic lung disease. \200 Eisen menger \200\231s syndrome. Dilated central and peripheral vessels \200 Left-to-right shunt. SUBASH KC/NMC-15TH/2014 This page intentionally left blank SUBASH KC/NMC-15TH/2014 97 Chapter 6 Vascular presenting syndromes Intermittent claudication Rest pain 98 Acutely painful blue leg 99 98 SUBASH KC/NMC-15TH/2014 98 CHAPTER 6 Vascular presenting syndromes Intermittent claudication When atheroma narrows the blood vessels supplying the lower limb, blood \202 ow is reduced and with it the amount of oxygen that can be taken up by the ti ssues. Presentation Muscle ischaemia presents in the same basic way, whether it be cardiac (angina ) or in the lower limb (claudication). Patients suffer pain induced by exercise, relieved b y rest. In claudication the pain is typically felt in the calves, and is brought on by walk ing. Risk factors include: Increased age. \200 Smoking. \200 Hypertension. \200 Family history. Imaging Ultrasound Doppler ultrasound can be used in clinic to assess the patency of periph - eral vessels, and follow up treated areas, but is not accurate enough to be used as a sol e presurgical assessment. CT Can be used to visualize the peripheral vascular tree, but the radiation dose is high, a nd most centers prefer to use MRI. MRI Allows accurate assessment of the peripheral vasculature, identifying stenoses and occl usions in the main lower limb vessels down to the foot. Routinely used in the work-up of pa tients with claudication to plan intervention and follow-up patients after treatment. Angiography Diagnostic angiography has largely been superseded by MRI, but interven- tional radiologists have an ever increasing role in the treatment of these patients. Rest pain Once blood \202 ow to the foot becomes critical, oxygen supply cannot match dem and even at rest and the patient suffers continual pain in the lower limb. Imaging techniques are the same as for claudication. SUBASH KC/NMC-15TH/2014 ACUTELY PAINFUL BLUE LEG 99 Acutely painful blue leg Sudden occlusion of an artery results in acute ischaemia of the st ructures in that vascular territory. The commonest cause is thrombus, but cases can be iatr ogenic, traumatic, or due to other embolic phenomena. Presentation Patients present with an acutely swollen, painful, pulseless leg. Capillary re \201 ll will be reduced and the limb is cold to the touch. Risk factors include: \200 Atrial \201 brillation. \200 Atheroma elsewhere, particula rly the aorta. \200 Smoking. Imaging Plain \201 lm Little acute role but CXR may reveal cardiomegaly as a clue to an u nderlying cardiac cause. Ultrasound Echo should be performed to look for intra-cardiac thrombus, shunts, and valvula r vegetations. Peripheral Doppler ultrasound can be used to con \201 rm the clinical impression of absent \202 ow in the peripheral arteries.