CT Persistent cough is sometimes investigated with CT, particularly if there is concern for malignancy, bronchiectasis, or interstitial lung disease. Ultrasound Echocardiography is a reliable method of assessing cardiac function. Fluoroscopy Contrast swallow examinations can demonstrate gastro-oesophageal re \202 ux an d aspiration. SUBASH KC/NMC-15TH/2014 COUGH 35 Information for the radiologist \200 Nature of cough and associated symptoms. \200 Rele vant environmental history e.g. pets, occupational history, smoking. SUBASH KC/NMC-15TH/2014 36 CHAPTER 3 Respiratory presenting syndromes Haemoptysis Haemoptysis is the coughing up of blood from the lungs or tracheobron- chial tr ee (Table 3.2). Massive haemoptysis refers to the coughing up of > 200ml of blood in 24 hou rs. Imaging The cause of haemoptysis may be obvious from the history and investiga- tions shoul d be performed according to the likely diagnosis. Plain \201 lm This should be performed in all patients presenting with haemoptysis. It ma y reveal a mass lesion, mediastinal lymphadenopathy, bronchiectasis, cavitation, consolidat ion, or pulmonary oedema. Ultrasound Ultrasound examination of the heart (echocardiography) can be used to detect car diac causes of haemoptysis including anatomical abnormalities, valvular disease, and ventri cular dysfunction. CT CT of the chest may identify parenchymal or endobronchial lesions, or further characteri ze abnormalities seen on plain chest radiograph. HRCT is performed where generalized lung disease is suspected (e.g. bronchiectasis). Tradit ional intermittent HRCT uses widely spaced, thin sections and is therefore unsuitable for t he assessment of lung cancer or other localized lung diseases. Similarly, IV contrast agent s are not routinely administered making the technique unsuitable for assessment of soft tis sues and blood vessels. CTPA is commonly performed for suspected pulmonary embolism. In this test, iodinated contra st is administered intravenously to opacify the pulmonary arterial tree. Any \201 lling d efects indicate the presence of a pulmonary embolus. In cases of massive haemoptysis contrast enhanced CT can be useful in identifying enlarged bronchial arteries which may be suitable for embolization. Nuclear medicine V/Q imaging should be considered for patients with suspected pulmonary emb olism who have a normal chest radiograph and no known history of respiratory disease. Combi ned perfusion scanning with technetium- 99m-labeled macroaggregates of human albumin and ve ntilation scanning with inhaled radioactive gas or aerosol typically produces a perfusion d efect and not a ventilation defect in pulmonary embolus. MRI The lungs are not well visualized with MR and its use in the assessment of respiratory causes of haemoptysis is limited. SUBASH KC/NMC-15TH/2014 HAEMOPTYSIS 37 Angiography Pulmonary angiography can identify the bleeding source in 90 with massive haemo ptysis and can be combined with embolization of the bleeding vessel. % of patients Other Fibreoptic bronchoscopy may be used in cases of suspected malignancy. It is diagnosti c for central endobronchial lesions and allows direct visualiza- tion of the bleeding site. In cases of more peripheral bleeding the broncho- scopist may be able to identify the affe cted lobe, which is useful information for a vascular radiologist considering embolization. It also permits tissue biopsy, bronchial lavage, or brushings for pathological diagnosis. Table 3.2 Differential diagnosis Pulmonary Cardiac Systemic vasculitis Bronchiectasis Pulmonary embolus Systemic lupus erythematosus (SLE) Bronchogenic carcinoma Left ventricular failure Wegener \200\231s granulomatosis Infection Mitral stenosis Goodpasture \200\231s syndrome TB Pulmonary hypertension Pneumonia Aortic aneurysm (aorto-bronchial \201 stula) Lung abscess Aspergilloma Trauma AV malformation SUBASH KC/NMC-15TH/2014 38 CHAPTER 3 Respiratory presenting syndromes Hypoxia Hypoxia is de \201 ned as reduced oxygen supply to tissues despite adequate blood supply. Possible causes are listed: 1. Reduced oxygen carrying capacity \200 Anemia. \200 Carbon monoxide poisoning. \200 Haemoglobinopathies (e.g. sickle cell, thalassaemia). 2. Reduced blood supply to lungs \200 Pulmonary embolism (thrombus, fat, amniotic). \200 Right-sided heart failure. \200 Pulmonary hypertension. \200 Pulmonary valve stenosis . \200 Congenital heart disease. 3. Reduced diffusion of oxygen across the alveolar membrane \200 Upper airway obstruction (e.g. foreign body). \200 Lower airway pathology (e.g. asthma/COPD/tumor). \200 Materi al within alveoli: In \202 ammatory cells (infection/hypersensitivity). \200 Pulmonary hemorrhage. \200 P ulmonary oedema. \200 Tumor. Interstitial lung disease/ \201 brosis. \200 Bronchiectasis/cystic \201 brosis. \200 Collapse of lung due to pneumothorax or pleural effusion. \200 Neuromuscular disorders ( e.g. Guillain \200\223Barr syndrome). Imaging Plain \201 lm \200 A CXR is likely to be the \201 rst form of imaging used to investigate the hypoxic patient. It is most useful for the 3 earlier. rd category of causes listed Cardiac and mediastinal abnormalities may suggest a cause from the 2 nd category. Remember CXR signs may lag behind the clinical \201 ndings. CT \200 Standard CT thorax \200 CTPA is the investigation of choice for detecting pulmo nary emboli. \200 HRCT acquires 1mm slices to assess the structures of the small airways contrast provides detailed 3D information. and interstitium. Used in the diagnosis of interstitial lung disease and atypical infection . Cardiac CT assesses cardiac structure and function; however is usually performed after an echocardiogram. SUBASH KC/NMC-15TH/2014 HYPOXIA 39 Ultrasound \200 Ultrasound can con \201 rm pleural effusions or pneumothorax prior to guided intervention. Echocardiography evaluates cardiac structure and function. Nuclear medicine V/Q scanning can be used to investigate pulmonary embolism if imme- diatel y available but should only be used in those patients with a normal CXR and no previous car diorespiratory disease. MRI Cardiac MRI assesses structure and function of the heart but is usually a second-line e xamination. Information for the radiologist \200 Relevant history including previous respiratory dise ase, smoking, immunosuppression, malignancy, or previous surgery. A differential diagnosis is vital to choose the most appropriate investigation. SUBASH KC/NMC-15TH/2014 This page intentionally left blank SUBASH KC/NMC-15TH/2014 41 Chapter 4 Respiratory conditions Lung abscess 42 Pneumonia 44 Emphysema/COPD 46 Pulmonary embolus 48 Left ventricular failur e Pneumothorax 54 Wegener \200\231s granulomatosis 56 Pulmonary hypertension Solitary pulmo nary nodule 60 Lung cancer 62 Lobar collapse 64 Bronchiectasis 70 Cystic \201 brosis 72 P leural effusion 74 Interstitial lung disease 76 Connective tissue disease and the lung Pneu moconiosis 80 Sarcoidosis 82 Benign asbestos-related disease Tuberculosis 86 Malignant pleu ral disease Mediastinal masses 52 58 78 84 88 90 SUBASH KC/NMC-15TH/2014 42 CHAPTER 4 Respiratory conditions Lung abscess A lung abscess is a well-de \201 ned collection of pus, usually with a discre te wall and surrounded by in \202 amed lung tissue. They usually develop as a complication of bacterial pneumonia and may be solitary or multiple. Clinical presentation The clinical course is often insidious, with fever, lethargy, and nig ht sweats. Breathlessness and productive cough with haemoptysis may be present. \200 If d ue to aspiration, abscesses often involve the posterior segments of the upper lobes and the apical segments of the lower lobes, as these areas are gravity depe ndent when the patient is supine. Systemic bacteraemia or tricuspid valve endocarditis can cause multiple septic emboli throughout the lungs leading to abscess formation. Secondary abscess formation can occur within pre-existing cavities (bullae or lung cysts), or distal to an obstructed bronchus, e.g. secondary to a carcinoma or inhaled foreign body. Imaging Plain \201 lm Chest radiographs may not be diagnostic in the early stages of absc ess formation, often showing a non-speci \201 c area of consolidation, before pro- gressin g to the classical appearance of a well-de \201 ned mass with an air- \202 uid level (Fi g. 4.1 ). Remember, the air- \202 uid level will only be present on upright \201 lms. Ultrasound Limited role in imaging the abscess itself, but echo is useful if septic emboli from endocarditis considered. CT \200 Identi \201 es cavitation within an area of consolidation. \200 Delineates the position of the abscess with respect to bronchial 4.2 ). anatomy and the chest wall (Fig. Useful for differentiating between intrapulmonary abscess and loculated empyema. Furthermore, CT is invaluable for accurate placement of drainage catheters, if required. Information for the radiologist \200 Is the patient septic? \200 Is the patient at risk of aspiration or is there a history such as an alcoholism, immunosuppression, epilepsy, or dysphagia? Before considering percutaneous drainage appropriate broad-spectrum antibiotics should usually have been given a suitable trial \201 rst. If drainage is being requested lung function and INR will be required. SUBASH KC/NMC-15TH/2014 LUNG ABSCESS 43 Fig. 4.1 thin-walled abscess in the right lung apex containing an air \202 uid level. CXR of a 35-year-old man with fever and purulent cough showing a Fig. 4.2 abscess in the right upper lobe with small amount of surrounding consolidation. No te the thin, smooth wall and air \202 uid level. (Patient grew Staph. aureus from blood c ultures and abscess resolved with antibiotic treatment.) CT of same patient as Fig. 4.1 con \201 rming the position and nature of the SUBASH KC/NMC-15TH/2014 44 CHAPTER 4 Respiratory conditions Pneumonia Bacterial pneumonias are categorized by their infectious agents, which include St reptococcus pneumoniae (the most common cause of bacterial pneumonias), Haemophilus in \202 uenzae species, and Gram-negative organisms. , Klebsiella , Staphylococcus , Legionella Susceptibility to pneumonias increase with very young or old age, COPD, alcoholism, and immunocompromise. Clinical presentation \200 Patients may present with cough productive of sputum (green or rust colored), rigors, malaise, myalgia, dyspnoea, or pleuritic chest pain. \200 Legionella pn eumonia is associated with GI symptoms including anorexia, nausea, vomiting, and diarrhea. Signs are legion, and include fever, wheeze, tachypnoea, tachycardia, dullness on percussio n, decreased breath sounds, rhonchi and rales on auscultation, and a pleural friction rub. Imaging Plain \201 lm (Fig. CXR is the initial investigation in most cases and important in follow-up. \200 Lobar consolidation (ill de \201 ned opacity with air bronchograms). \200 Cavitating pneumonia and bulging of \201 ssures is suggestive of 4.3 ) Klebsiella , (which has a predilection for the upper lobes), TB (see b Tuberculosis, p. 86). Staphylococcus aureus or Pleural effusion. \200 Abscess. \200 Lobar collapse. Ultrasound No role in uncomplicated pneumonia but useful to identify and localize secondary effusions/empyema. CT \200 Not needed in uncomplicated cases which resolve on treatment. \200 Useful in no n-resolving infection to look for an obstructing lesion or atypical features such as cavitation. Information for the radiologist \200 Duration of symptoms. \200 Bronchoscopy results if relevant. \200 Risk factors including immunosuppression. SUBASH KC/NMC-15TH/2014 PNEUMONIA 45 Fig. 4.3 proven streptococcal pneumonia. CXR showing extensive consolidation throughout the left lung, due to SUBASH KC/NMC-15TH/2014 46 CHAPTER 4 Respiratory conditions Emphysema/COPD Emphysema is de \201 ned as irreversible dilatation of the airways distal t o the terminal bronchiole, accompanied by the destruction of alveolar walls and without obv ious \201 brosis. Frequently occurs in association with bronchitis and these entities are referred to with the collective term chronic obstructive pulmonary disease (COPD). Clinical presentation Patients typically present in their 5 productive cough. Smoking is a common factor. th /6 th decade with breathlessness and Clinical signs \200 Hyperin \202 ation, i.e. \200\230barrel chest \200\231. \200 Whee zing. \200 Hyperresonance on percussion. Imaging Plain \201 lm ( Figs. 4.4 and 4.5 ) \200 Increased lung volumes (increased AP d iameter on lateral). \200 Flattened diaphragms. \200 Hyperlucency of lungs. \200 Redu ction in number and caliber of vascular shadows. \200 Bullae (air spaces that measure > 1 cm in diameter). CT Emphysema is usually an incidental \201 nding as CT is not used in the routine care of patients with COPD. CT is indicated in those patients who are undergoing evaluation for surgical intervention, i.e. bullectomy or lung volume reduction surgery. Typical \201 ndings include: \200 Extensive areas of low attenuation without de \201 n able walls. \200 Thin walled avascular areas (bullae). \200 Paucity of vascular marking s in affected areas. \200 Upper lobe predominance in centrilobular and paraseptal emphyse ma. \200 Lower lobe predominance in panacinar emphysema (feature of alpha-1 antitrypsin de \201 ciency). Nuclear medicine V/Q scanning is performed to assess relative lung function and distributio n of disease prior to lung volume reduction surgery. Information for the radiologist \200 Smoking history. \200 Duration of symptoms. \200 Respiratory function tests. SUBASH KC/NMC-15TH/2014 EMPHYSEMA/COPD 47 Fig. 4.4 PA CXR showing bullous emphysema throughout most of the right upper lobe. Note the absence of lung markings in the right upper and mid zones and the depression of the horizo ntal \201 ssure. Fig. 4.5 hemidiaphragms typical of COPD. PA CXR showing overexpanded lungs and \202 attening of the SUBASH KC/NMC-15TH/2014 48 CHAPTER 4 Respiratory conditions Pulmonary embolus A pulmonary embolism (PE) is a blockage of the pulmonary artery, or its b ranches. This may be acute, most commonly a clot from a DVT, or chronic, due to longstandin g thromboembolic disease. Other, less common causes include fat, tumor, air, and amniotic \202 uid emboli. The ideal imaging protocols for diagnosing PE remain a subject of debate amongst radiologists. Clinical presentation Classically, patients present with pleuritic chest pain, breathlessne ss, a swollen leg, and ECG changes but PE may present with symptoms ranging from vague brea thlessness to cardiac arrest. Risk factors include: Recent immobilization. \200 Recent surgery. \200 Previous PE/DVT. \200 Smoking. \200 Pregnancy/oral contraceptive pill. \200 Thrombophilic disorders including malignancy. Imaging features Plain \201 lm \200 Non-speci \201 c and up to 40 % of patients with acute PE have a normal CXR. Will quickly exclude other conditions which may mimic PE, including pneumothorax, pneumonia and aortic dissection, and is important in deciding which imaging m odality will subsequently be used. Ultrasound As the treatment for above-knee DVT and PE is the same, ultrasound scanning and demonstration of a DVT mitigates the need for further investigation. Echocardiography \200 Assessment of right heart strain in acute PE (and may visualize lar ge clot in central pulmonary arteries). Right ventricular hypertrophy in chronic embolic disease. CTPA (Fig. \200 Emboli are seen as intraluminal \201 lling defects within the contrast 4.6 ) enhanced pulmonary arteries. When clot is seen the PPV is high, but these studies can be dif \201 cult to interpret, particularly in the context of respiratory motion artifact and poorly opaci \201 ed pulmonary vessels. CTPA has the advantage of providing additional information not possible with perfusion scan ning, such as the presence of right heart strain and infarcted lung. SUBASH KC/NMC-15TH/2014 PULMONARY EMBOLUS 49 Ventilation/perfusion scanning (Fig. \200 Radioisotope assessment of ventilation (using i nhaled agents such as 4.7 ) Xe-133, Tc-99m aerosol) and lung perfusion (using a venous injection of Tc-99m macroaggrega ted albumin) is the traditional method of PE diagnosis and remains a commonly used test in many departments. A high probability scan is very accurate in con \201 rming the presence of PE, whilst a normal study excludes signi \201 cant PE. However, a signi \201 cant proportion of the studies are indeterminate and further imaging is needed. The chances of an indeterminate scan are much higher in those with an abnormal CXR, hence these patients are normally sent straight to CT. MRI \200 MRI of the pulmonary vasculature is possible; however, spatial and contrast resolution is inferior to CTPA, and MR in acute PE is rarely used. In chronic embolic disease MRA combined with assessment of right ventricular function is commonly used in pre-treatment work-up. Pulmonary angiography Conventional pulmonary angiography is still nominally the gold standa rd for the diagnosis of PE. However, it is an interventional procedure (overall complicatio n rate is 2 \200\2235 centers. % ) and is now rarely performed outside of specialist Information for the radiologist \200 Pretest probability (including D-dimer). \200 Does the patient have asthma or chronic lung disease? Fig. 4.6 arteries in keeping with pulmonary emboli. Axial image from CTPA reveals \201 lling defects in both main pulmonary SUBASH KC/NMC-15TH/2014 50 CHAPTER 4 Respiratory conditions Fig. 4.7 4.6 demonstrating Image from V/Q scan from a different patient than Fig. the norma l appearance bilaterally. This pattern virtually excludes PE. SUBASH KC/NMC-15TH/2014 This page intentionally left blank SUBASH KC/NMC-15TH/2014 52 CHAPTER 4 Respiratory conditions Left ventricular failure Failure of the left ventricle to pump adequately, either as a cons equence of systolic dysfunction (a reduction of myocardial contractility), diastolic dys- f unction (an abnormality of distensibility), or a combination of the two. Clinical presentation Worsening breathlessness, orthopnoea, basal crepitations, wheeze and respiratory failure may all indicate left ventricular failure (LVF). Onset may be acute or insidious. In patients with limited cardiac reserve, a separate episode such as a chest infection may precipitate acute LVF. LVF may develop following acute MI due to the loss of functioning myocardium, arrhythmias, papillary muscle rupture, ventricular septal defect (VSD), or tran smural infarct resulting in haemopericardium. Imaging Plain \201 lm The radiographic changes center on cardiomegaly (cardiothoracic rat io > 55 % ) and pulmonary oedema. As the pulmonary capillary wedge pressure (PCWP) rises, cephalization of the pulmonary vascularity (upper lobar venous diversion) develops. Interstitial oedema is the next sign, as evidenced by peribronchial cuf \201 ng, loss of c larity to vessels, \202 uid in the \201 ssures, and development of interstitial lines: \200 Kerley A lines radiate out from the hila. \200 Kerley B lines: short horizontal li nes in the lung peripheries (Fig. 4.8 ). Further rises in PCWP lead to the development of alveolar pulmonary oedema, seen as bilater al air-space shadowing and pleural effusions. In this phase, it may be radiologically impossible to differentiate heart failure from severe infection. Echocardiogram Features of LVF include poor ejection fraction (EF), poor wall motion and co ntractility, and enlarged left ventricular chamber volumes. Nuclear medicine Very limited role in the imaging in acute LVF. MRI \200 Limited role in the acute setting. \200 MRI is the most accurate modality for assessing LV function as well as myocardial reserve. It is also useful in assessing cardiom yopathy and the underlying cause. CT Limited role in the acute setting but can demonstrate causes such as acute VSD following infarction. SUBASH KC/NMC-15TH/2014 LEFT VENTRICULAR FAILURE 53 Information for the radiologist \200 Any underlying cardiac condition which may be respon sible for acute LVF should be mentioned. One common question is differentiation between LVF and chest infection which can be dif \201 cult purely on plain \201 lms. Clinical story and laboratory results will be needed to complete the picture. Fig. 4.8 PA CXR revealing cardiomegaly, upper lobe venous distension, Kerley B lines, and t hickened interstitial markings in keeping with interstitial oedema secondary to heart failu re. Note also the left pleural effusion. SUBASH KC/NMC-15TH/2014 54 CHAPTER 4 Respiratory conditions Pneumothorax A pneumothorax occurs when air enters the pleural cavity, separating the visce ral from the parietal pleura, with subsequent collapse of the under- lying lung. The air ca n be free within the pleural cavity, loculated, or under tension, causing haemodynamic comp romise and instability. Spontaneous pneumothoraces are more common in asthmatics, patients with emphysema, cystic \201 brosis, and TB. There is also a predisposition to spontaneous pneumothorax in tall thin males (and those with Marfan \200\231s syndrome). Traumatic pneumothorax is often the result of chest wall compression or penetrating injury with lung laceration. Remember iatrogenic causes, such as insertion of central venous lines, lung biopsies, radiotherapy, and positive pressure ventilation. Clinical presentation Pneumothorax can present with sudden onset of chest pain and breath- lessness, or, in the case of tension pneumothorax, with cardiovascular compromise and colla pse. It is an important diagnosis to exclude in the context of trauma, where small pneumothorace s may go undetected on the supine CXR, resulting in rapid decompensation should positive pr essure ventilation be needed. In cases of tension pneumothorax the patient may be tachycardic, hypotensive, and tachypnoeic. Imaging features Plain \201 lm ( Figs. 4.9 and 4.10 ) The visceral pleura is seen as a th in curvilinear line which parallels the chest wall (a skin fold is usually much thicker). The air within the chest cavity will make the hemithorax appear \200\230blacker \200\231, and no lung markings are visible beyond the line of pleura. The presence of rib fractures, subcutaneous emphysema, and bullae should provoke a thorough search for a pneumothorax. Signs of a tension pneumothorax on CXR include: Unilateral hyperlucency. \200 Deviated trachea and mediastinum away from the abnormal sid e. \200 Depression of the ipsilateral hemidiaphragm. The immediate response is needle decompression. Remember \200\224 when the patient is supine a pneumothorax is more dif \201 cult to dete ct, as the air collects superiorly, overlying the lungs, and the pleural edge is often not visible. The heart borders and diaphragms become unusually well de \201 ned. The affected lung base becomes lucent (black) which progresses to the deep sulcus sign, where the costop hrenic angle is depressed, as pressure increases. Ultrasound Ultrasound can be used to diagnose pneumothorax (in specialist hands!) However, it is rarely used in the acute setting. CT CT is the gold standard test for detecting and localizing pneumothorax, and may be neces sary to guide percutaneous drainage. SUBASH KC/NMC-15TH/2014 PNEUMOTHORAX 55 In addition, CT can help clarify the presence of bullae, which may simulate pneumothorax on the plain \201 lm. Information for the radiologist \200 Any history of trauma. \200 Previous history of pn eumothorax. \200 Recent iatrogenic procedure. Fig. 4.9 a pleural edge at the right apex with absent lung markings lateral to it, indicati ng a pneumothorax. Note that the mediastinum remains central and the diaphragms are normall y positioned. CXR of patient with sudden onset of chest pain and dyspnoea, showing CXR of a tension pneumothorax on the right. The collapsed lung is Fig. 4.10 opaci \201 ed, the mediastinum is shifted away from the affected side and the ipsilateral diaphragm is de pressed. This needs urgent decompression. SUBASH KC/NMC-15TH/2014 56 CHAPTER 4 Respiratory conditions Wegener \200\231s granulomatosis Disease of unknown etiology causing granulomatous in \202 ammation of small- and medium-sized blood vessels in the respiratory tract, kidneys, and o ther organs. Clinical presentation \200 Upper respiratory tract symptoms: rhinitis, sinusitis and otit is media. \200 Pulmonary involvement is very common (up to 90 % ) and may cause dyspnoea, cough, haemoptysis, chest pain, or stridor due to airway stenosis. Progressive renal failure secondary to necrotizing glomerulonephritis. \200 Arthralgia an d myalgia. \200 Epistaxis. \200 Scleritis. Imaging Plain \201 lm ( Figs. 4.11 and 4.12 ) \200 Patchy in \201 ltrates and consolid ation due to pulmonary hemorrhage. \200 Cavitating nodules. \200 Pleural effusion. \200 Atelectasis. \200 Pneumothorax (uncommon). Nodules and consolidation may resolve without a trace over a period of months leaving a nor mal radiograph. CT \200 Tracheal/bronchial stenosis (can be life threatening). \200 Nodules which frequ ently cavitate. These may be surrounded by a \200\230halo \200\231 of ground glass opaci \201 cation due to hemorrhage. Peripheral pulmonary infarcts. CT of the sinuses will show any nasal involvement. Ultrasound Renal ultrasound may show small kidneys of increased echogenicity, and guide bio psy. Nuclear medicine Active areas of disease will show increased uptake on gallium scans. MRI Brain/spinal imaging may show neuritis. Information for the radiologist \200 Presenting symptoms. \200 Renal function. \200 V asculitic screen: c-ANCA (centrally accentuated antineutrophil cytoplasmic antibody test): usually but not always positive. Past medical history (e.g. malignancy, PE, rheumatoid disease, immunosuppression) will help to guide differential diagnosis. Consideration of lung/renal biopsy? (Would need current blood tests including coagulation screen.) SUBASH KC/NMC-15TH/2014 WEGENER \200\231S GRANULOMATOSIS 57 Fig. 4.11 lungs. The patient presented with vasculitic rash, haematuria, and dyspnoea. CXR of a young man revealing several cavitating mass lesions in both Fig. 4.12 nosuppressive treatment. The lesions have all regressed, leaving residual scar ti ssue and atelectasis. CXR of the same patient as Fig. 4.11 several months later following immu- SUBASH KC/NMC-15TH/2014 58 CHAPTER 4 Respiratory conditions Pulmonary hypertension De \201 ned as sustained systolic pulmonary artery pressure of at r est or > 30mmHg during exercise with increased pulmonary vascular resistance. > 25mmHg May be primary (idiopathic) or secondary to cardiac, pulmonary or hepatic disease. Causes include: \200 Increased pulmonary blood \202 ow secondary to co ngenital heart disease or high-output cardiac states. Increased pulmonary vascular resistance, e.g. PE, connective tissue diseases, pulmonary \201 brosis, or pulmonary venous hypertension. Clinical presentation Chest pain, dyspnoea, haemoptysis, fatigue, or syncope. There may be signs of right heart failure (raised JVP, hepatomegaly, ascites, oedema). Imaging Plain \201 lm (Fig. CXR may reveal cardiomegaly and enlarged central pulmonary ar teries with peripheral pruning. There may be signs of underlying pulmonary parenchymal dise ase, e.g. COPD. 4.13 ) Echocardiography Demonstrates right ventricular hypertrophy and tricuspid regurgitation and is a non-invasive method of estimating pulmonary arterial pressure. CT May reveal: \200 Right atrial and ventricular hypertrophy. \200 Enlarged central pul monary arteries, occasionally with calci \201 cation. \200 Pruning of peripheral arterie s. \200 Pulmonary emboli. \200 Pulmonary parenchymal disease. MRI Evaluates cardiac chambers, wall motion, stroke volume, and right ven- tricular EF (oft en reduced). Can also be used to depict pulmonary vascu- lature and assess shunts. Pulmonary angiography Allows accurate measurement of arterial pressures. Right heart cathet eri- zation can be performed to assess cardiac function and pulmonary \202 ow dynamics. Information for the radiologist \200 Presenting symptoms. \200 Relevant past medical hi story including risk factors for pulmonary hypertension, e.g. congenital heart disease, sickle cell anemia. Clinical question, e.g. ?PE. ?Interstitial lung disease. SUBASH KC/NMC-15TH/2014 PULMONARY HYPERTENSION 59 Fig. 4.13 enlargement of the pulmonary trunk and main pulmonary arteries with relative oli- gaemia in the lungs themselves, in keeping with primary pulmonary hypertension. CXR of a 54-year-old man with severe breathlessness reveals marked SUBASH KC/NMC-15TH/2014 60 CHAPTER 4 Respiratory conditions Solitary pulmonary nodule A single spherical lesion of 3cm or less in diameter, completely surrounded by lung without any associated atelectasis or lymphadenopathy. Clinical presentation Often an incidental \201 nding on chest radiograph or CT. The main concern is usually to exclude malignancy. Discussion in multidisciplinary meetings is often required to de \201 ne an appropriate management strategy. Imaging Plain \201 lm CXR often identi \201 es the solitary pulmonary nodule (SPN) initi ally. Dual- energy radiography can help determine if the nodule is calci \201 ed and does indeed lie within the lung. CXR may be able to characterize nodules but frequently CT is re quired ( Figs. 4.14 and 4.15 ). CT More sensitive than plain \201 lm for detection of SPNs. May be used for characterizat ion, to guide biopsy, or to monitor indeterminate nodules. To infer benignity, a nodule mus t be stable in volume for a period of at least 2 years. Certain features can help in charac terization: \200 Calci \201 cation: most patterns of calci \201 cation are associated w ith benign conditions such as hamartomas and TB. However, eccentric calci \201 cation is a ssociated with malignancy. Density: e.g. fat indicates hamartoma or lipoma. \200 Margins: speculated or smooth. \200 Cavitation and wall thickness: thick-walled cavities suggest malignancy. \200 Enhan cement pattern: minimal enhancement suggests benignity. \200 Size: unreliable but larger nodules are generally more likely to be malignant. Nuclear medicine Increased uptake on PET suggests malignancy though infection and in \202 am- mation can cause false positive results. PET lacks sensitivity for broncho- alveolar ce ll carcinoma and carcinoid, or if the nodule is <1cm in size. MRI With the advent of rapid acquisition sequences, MRI may have a role in the future. Information for the radiologist \200 Smoking history. \200 Previous malignancy. \200 Family history of lung cancer. \200 Any previous imaging. \200 Risk factors for TB, his toplasmosis. \200 Current symptoms/signs of infection. \200 Management plan if SPN alre ady known. SUBASH KC/NMC-15TH/2014 SOLITARY PULMONARY NODULE 61 Fig. 4.14 CXR of a 60-year-old woman reveals a well-de \201 ned nodule in the right mid zo ne. There are no speci \201 c features to suggest a cause, and further investigation is re quired. Fig. 4.15 right upper lobe, is solid, and has an irregular margin. CT biopsy revealed an ad enocarcinoma and the patient underwent upper lobectomy. 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.