Session 8

Question 1

Label This CXR

Answer 1

1. Trachea
2. Hila
3. Lungs
4. Diaphragm
5. Heart
6. Aortic knuckle (Arch of the aorta)
7. Ribs
8. Scapulae
9. Breasts
10. Stomach

(PA film)

Question 2

Where is the costophrenic angle/recess and the carina?

Answer 2

Question 3

Describe the features of a Lobar Collapse on a CXR

Answer 3

[*] Lobar Collapse

• Displacement of the horizontal fissure is an indicator of lobar collapse.
• If there is volume loss of the right upper lobe (e.g. collapse), the horizontal fissure is displaced upwards.
• If there is volume loss of the right lower lobe (e.g. collapse), the horizontal fissure is displaced downwards.

Causes:

• Luminal: aspirated foreign body, mucus plugging, iatrogenic
• Mural (compression of the wall of the bronchial tree): bronchogenic carcinoma
• Extrinsic: compression by adjacent mass (=> decreased volume – diaphragm moves up)

Generic findings

• Elevation of the ipsilateral hemiaphragm
• Crowding of the ipsilateral ribs.
• Shift of the mediastinum towards the side of atelectasis (partial collapse/incomplete inflation of the lung)
• Crowding of pulmonary vessels

Question 4

Describe the features of Consolidation on a CXR

Answer 4

• If alveoli and small airways fill with dense material, the lung is said to be consolidated.
• This may be due to infection (pneumonia, pus), fluid (pulmonary oedema), blood (haemorrhage) or cells (cancer).
• If an area of the lung is consolidated it becomes dense and white opaque). If the larger airways are spared, they are of relatively low density (blacker). This phenomenon is known as air bronchogram and it is a characteristic sign of consolidation.
• Volume may be preserved or increased

Question 5

Describe a Space Occupying Lesion on a CXR

Answer 5

• In this case, a large, round, thick-walled lung cavity, due to squamous cell lung carcinoma.
• A Nodule is <3cm
• Mass >3cm
• Single vs Multiple
• Causes:

Malignant (primary, metastases)
Benign mass lesion
Inflammatory
Congenital
Mimics (bone lesion, cutaneous lesion, nipple shadow)

Question 6

Describe Pleural Effusion on a CXR

Answer 6

• A Pleural effusion is a collection of fluid in the pleural space. Fluid gathers in the lowest part of the chest, according to the patient’s position.
• If the patient is upright when the X-ray is taken, a pleural effusion will obscure the Costophrenic angle/Hemidiaphragm.
• If a patient is supine, a pleural effusion layers along the posterior aspect of the chest cavity, and is difficult to see on a chest X-Ray.
• Pleural effusions appear on X-rays as uniformly white, with a concave area at the top – at the upper border. This is called the Meniscus sign.
• Loss of costophrenic angle.

Question 7

Describe a Pneumothorax on a CXR

Answer 7

• A pneumothorax forms when there is air trapped in the pleural space. This may occur spontaneously, or as a result of underlying lung disease. The most common cause is trauma, with laceration of the visceral pleura by a fractured rib.
• Lung edge measures more than 2cm from the inner chest wall at the level of the hilum, it is said to be ‘large’.
• Signs: visible pleural edge
• Lung markings are not visible beyond this edge.

Question 8

Describe a Tension Pneumothorax on a CXR

Answer 8

• If there is tracheal or mediastinal shift away from the pneumothorax, the pneumothorax is said to be under tension. This is a medical emergency.
• Trachea is pushed away by air in the pleural cavity.

Question 9

Describe Tracheal Displacement on a CXR

Answer 9

• If the trachea is genuinely displaced to one side (the patient is not rotated) try to establish if it has been pushed or pulled by a disease process.
• Anything that increases pressure or volume in one hemithorax will push the trachea and mediastinum away from that side.
• • (E.g. Tension pneumothorax, pleural effusion, tumour)
• Any disease that causes volume loss in one hemithorax will pull the trachea over towards that side (- E.g. collapsed lung, fibrosis

Question 10

Describe Asbestos plaques on a CXR

Answer 10

Calcified asbestos related pleural plaques have a characteristic appearance, and are generally considered to be benign.
They are irregular, well defined and classically said to look like holly leaves.

Question 11

Describe lung hyperinflation on a CXR

Answer 11

COPD can lead to hyperinflation of the lungs. This leads to blunting of both costophrenic angles, and flattened hemidiaphragms.

Question 12

Describe Pneumoperitoneum on a CXR

Answer 12

Lungs are normal, but air is seen under the diaphragm. This is a sign of bowel perforation.

Question 13

Identify cardiac enlargement on CXR and estimate the cardiac index

Answer 13

[*] The widest part of the heart and ribcage are measured laterally. If the heart is over 50% of the width of the thorax, it is enlarged.

[*] Normal ratio <50%

[*] Must be on a PA image

Question 14

Describe a systemic approach to CXR evaluation

Answer 14

[*] Patient demographics

[*] Projection (AP or PA?)

[*] Adequacy (should include 1st rib, lateral margin of ribs, costophrenic angle, vertebrae should be just visible through heart, complete left hemidiaphragm should be visible)

[*] AIRWAY: check rotation, inspiration (lung volumes) and penetration

• Look at trachea – can we see it all the way down? It should be central? We need to look at the carina – if there is a mass under it, the carina splays
• Look at the bronchi – the left hilum should be above the right hilum, are they equal?

[*] BREATHING

• Lungs: are they equal on each side?
• Pleural spaces: check for consolidation, nodules, calcification
• Lung interfaces
• Compare both sides

[*] CIRCULATION

• Mediastinum – aortic arch, pulmonary vessels, hila, right heart border (right atrium, middle lobe interface), left heart border (left ventricle, lingula interface

[*] DIAPHRAGM / DEM Bones

• Diaphragm/Dem bones
• Free gas
• Nodules
• Bone : Fracture/dislocation
• Mass lesion

[*] Review areas

• Apices = Pneumothroax
• Thoracic inlet = Mass
• Paratracheal stripe = Mass / lymph nodes
• AP window = Lymph nodes
• Hila = mass/collapse
• Behind heart = mass
• Below diaphragm = pneumoperitoneum/mass
• Bones – all of them = Fracture/mass/missing
• Edge of films

Question 15

What is meant by interstitial space and interstitial lung disease?

Answer 15

[*] The interstitial space is a potential space between alveolar cells and the capillary basement membrane, which is only apparent in disease states when it may contain fibrous tissue, cells or fluid.

[*] The intersitium provides structural support, is where diffusion takes place and is part of the lung’s abililty to repair itself by providing host defences and repair mechanisms.

[*] Interstitial Lung Disease is a group of diseases, caused by a variety of causes which have similar pathophysiological effects and clinical features.

[*] Interstitial disease doesn’t just affect the interstitium – it affects acini, alveoli lumen, ioclar lumen, bronchioles, epithelial airway cells, vascular endothelial cells, mesenchymal, macraophages and recruited inflammatory cells – in short it affects lung parenchyma diffusely.

Question 16

Give some common causes of Interstitial Lung Diseases

Answer 16

[*] Occupational: Asbestosis (plumbers, pigeon fanciers), Silicosis, Coal Workers pneumoconiosis

[*] Treatment related: radiation, methotrexate (used in treatment for rheumatoid arthritis), nitrofurantoin (used in UTI infections), amiodarone (used to treat arrhythmias especially Atrial Fibrillation), chemotherapy

[*] Connective tissue disease: Rheumatoid arthritis, SLE (Systemic Lupus Erythematosus) Polymyositis, Schleroderma and Sjogren’s

[*] Immunological: Sarcoidosis (abnormal collections inflammatory cells (granulomas) that forms as nodules in multiple organs), Hypersensitivity pneumonitis (aka extrinsic allergic alveolitis)

[*] Idiopathic: fibrosing alveolitis (CFA/IPF – Cryptogenic Fibrosing Alveolitis/Idiopathic Pulmonary Fibrosis); UIP / NSIP (Usual Interstitial Pneumnia / Non-specific Interstitial Pneumonia); DIP (Desquamative Interstitial Pneumonia; LIP (Lymphocytic Interstitial Pneumonia); RB-ILD (Respiratory Bronchiolitis Interstitial Lung Disease); COP (BOOP) (Cryptogenic Organising Pneumonia (Bronchiolitis Obliterans Organising Pneumonia)).

Question 17

What is meant by asbestosis?

Answer 17

[*] Asbestosis (at risk: plumbers, electricians, builders, boiler and pipe laggers, railway engineering workers, old teachers, telephone operators etc) can cause a variety of clinical conditions

• Asbestos plaques
• Diffuse pleural thickenings
• Benign asbestos pleural effusions (BAPE)
• Mesothelioma
• Bronchogenic lung cancer
• Rounded atelectasis
• BUT ONLY ASBESTOSIS refers to interstitial lung disease caused by exposure to asbestos

Question 18

What are the clinical features of Sarcoidosis?

Answer 18

[*] Sarcoidosis: often asymptomatic

• Genetic predisposition
• Restricton / mixed peak flow tests (sarcoidosis can also affect the aiways “obstructive disease”)
• Biopsy – transbronchial, non-caseating granuloma
• Differential diagnosis – lymphoma and TB

Question 19

Describe Idiopathic ILD

Answer 19

• Histological descrptions – high inter and intra observer variability
• Often poor correlation with CT chest and clinician
• Biopsy may not help with management
• Diagnosis based on a combination of histology and X-rays
• Most common type of ILD
• Often no treatment
• Classical symptoms, restrictive spirometry

Question 20

Outline the typical clinical features of interstitial lung disease

Answer 20

[*] Symptoms: shortness of breath, reduced exercise tolerance, dry cough.

• Shortness of breath due to inadequate ventilation (impairing diffusion of O2 and perfusion leading to decreased pO2 and increased pCO2)
• Cough due to inflammation/irritation (no one really knows)

[*] Signs: tachypnoea, tachycardia, reduced chest movement (bilaterally) and coarse, diffuse bilaterall crackles, bilatersal pitting ankle oedema. Cyanosis and signs of right heart failure in severe cases may be present (clubbing, raised IVP, ascites, liver enlargement etc)

• Clubbing is seen in cryptogenic fibrosing alveolitis.

Question 21

Describe the effects of inflammation and fibrosis associated with interstitial diseases, on ventilation and gas exchange

Answer 21

[*] The development of fibrous tissue (in the interstitium), in particular makes lungs less compliant, tending to produce a restrictive ‘ventilatory’ defect.

[*] Airway resistance is not increased. In fact the FEV1/FVC ratio can be >70% due to the increased radial traction on the airway, which keeps airways open.

[*] In addition, lengthening of the diffusion bath between alveolar air and blood will impair gas exchange with oxygen uptake being affected selectively as the resistance to the diffusion of oxygen is much greater than that of CO2.

Question 22

Describe the typical chest x-ray picture of patients presenting with interstitial lung diseases

Answer 22

[*] Fibrosing Alveolitis: small lungs, micro-nodular shadowing (lower lobes), ragged heart borders

[*] Extrinsic Allergic Alveolitis (acute): micro-nodular infiltrate, denser towards the hila

[*] Extrinsic Allergic Alveolitis (chronic): almost normal, progressing to fibrosis in late disease

[*] Sarcoidosis: military and nodular shadowing, diffuse fibrosis

[*] Asbestosis: plaques, fibrosis, mesothelioma

Question 23

List some occupational lung diseases and the environmental factors associated with each.

Answer 23

[*] Whilst a large proportion of respiratory disease is due to the inhalation of harmful substances (tobacco smoke, allergens, microorganisms, etc) found in the general environment, diseases due to the inhalation of substances found in the workplace are considered ‘Occupational Lung Disease’.

[*] Asthma; Lab worker; exposure to rat urine

[*] Diffuse fibrosis; Boiler/Pipe Laggers Railway/ Construction; exposure to asbestos

[*] Nodular Fibrosis (e.g. pneumoconiosis); Coal Miner , Miner, Demolition; exposure to coal dust, silica, asbestos

[*] Alveolitis; Farmer, pigeon fancier; exposure to fungal spores from hay / avian antigens

Question 24

Describe the structure of the visceral and parietal pleura, and the functions of pleural fluid

Answer 24

[*] The pleura is a serous membrane consisting of a single layer of mesothelial cells with a thin layer of underlying connective tissue.

• The Parietal Pleura lines the inside of each hemithorax (the bony thoracic cage, diaphragm and mediastinal surface) and becomes continuous at the hilum of the lung with the Visceral Pleura, which lines the outside of the lung.
• The visceral pleura extend between lobes of the lung into the depths of the oblique and horizontal fissures.

[*] The pleural cavity is a potential space between the two layers of pleura (which are continuous at the hilum).

[*] Both layers are covered with a common film of fluid produced from the parietal surface and absorbed by the parietal (intercostal and internal mammary) lymphatic vessels , not by the visceral (pulmonary) lymphatic vessels. Lymphatic drainage occurs via stomata on parietal pleural surface (mainly mediastinal, diaphragmatic regions)

[*] The pleural fluid allows the two layers to slide on one another, thus in healthy people, the pleura allows movement of the lung against the chest wall while breathing.

[*] The surface tension of the pleural fluid provides the cohesion that keeps the lung surface in contact with the thoracic wall. As a result, when the thorax expands in inspiration, the lung expands along with it and fills with air.

[*] The lungs do not occupy all the available space in the pleural cavity, even in deep inspiration.

Question 25

Describe the blood supply and innervation of the pleura

Answer 25

[*] Blood Supply of the Parietal Pleura

• Costal pleura – intercostals and IMA
• Mediastinal – Bronchial, upper diaphragmatic and IMA
• Pleural dome – subclavian artery
• Venous drainage – peribronchial and venae cavae

[*] Blood Supply of the Visceral Pleura

• Bronchial arteries and pulmonary circulation
• Venous drainage – pulmonary venous circulation

[*] Pleura innervation

• Parietal pleura – somatic, sympathetic and parasympathetic (phrenic and intercostal nerves)
• Visceral pleura – devoid of somatic innervation

Question 26

Describe the factors influencing the formation and re-absorption of pleural fluid

Answer 26

[*] 15ml turnover per day (can increase to 300ml)

[*] Produced by capillary filtration at the parietal pleura only (Starling forces). Pleural fluid volume will increase if:

• Lung interstitial fluid increases
• Increased Hydrostatic (pulmonary intravascular) pressure (e.g. in heart failure)
• Increased Permeability of pleural capillaries (e.g. inflammation, sepsis or malignancy)
• Decreased Oncotic pressure (e.g. liver failure) (fall in plasma osmotic pressure)

[*] Absorbed via lymphatic drainage (by parietal lymphatic vessels). Pleural fluid volume will increase if there is decreased absorption:

• Lymphatic blockage (an obstruction to lymphatic flow in the lungs.
• Systemic venous pressure rises

[*] The intrapleura pressure is normally below atmospheric expect during a forced expiration, because of the elastic recoil of the lungs.

Question 27

Define the term ‘pleural effusion’ and distinguish the terms haemothorax, chylothorax, empyema and simple effusion.

Answer 27

[*] Pleural Effusion: any collection of extra fluid in the pleural space is known as a “Pleural Effusion”

[*] Blood – Haemothorax

[*] Chyle (Lymph with fats in it) – Chylothorax (if thoracic duct is involved)

[*] Pus – Empyema

[*] Serous Fluid – Simple Effusion

Question 28

What are the complications of Empyema?

Answer 28

Early: lung is squashed, can’t expand properly

• Trapped lung
• Fistula

Late:

• Fibrothorax (fibrosis of the pleural space)
• Chronic empyema
• Empyema necessitatis (extension of the pleural infection out of the thorax and into the neighbouring chest wall and surrounding soft tissues)
• Functional restriction

Question 29

State the difference between an exudate and transudate, and the main conditions leading to each in the case of pleural effusion.

Answer 29

[*] Simple pleural effusions (Serous Fluid) is further characterised by protein content:

• Transudates have low protein content - <30g/Litre
• Exudates have high protein content - >30g/Litre

[*] `Transudates

• Increased hydrostatic pressure
• Cardiac Failure
• Decreased capillary oncotic pressure

Hypoalbuminaemia
Nephrotic Syndrome

• Increased capillary permeability

Sepsis

[*] Exudates

• Neoplasma:

Cancer involving pleural surface
Secondary metastases from breast, lung, ovarian, GI, lymphoma
Primary tumour of pleura

• Infection

Pneumonia, TB

• Immune Disease
• Connective tissue diseases: rheumatoid arthritis, lupus
• Abdominal Disease

Pancreatitis (Diaphragmatic inflammation)
Ascites (exudate transverses the diaphragm)
Subphrenic abscess

Question 30

Describe the characteristics of pleurisy

Answer 30

[*] Pleursy, or pleuritis, is an inflammation of the pleura

[*] Sharp pain on inspiration

[*] Pain worse with coughing, sneezing, laughing etc (large breathing moments)

[*] Patients take small breaths and hold affected side of chest

[*] Involvement of diaphragmatic pleura causes pain in the shoulder on the same side (Referred pain)

[*] Characteristic physical sign is Pleural Rub, a creaking nose heard through a stethoscope with respiratory movements

Question 31

What are the causes of pleurisy?

Answer 31

• Infection is the most common cause (TB, pneumonia etc)
• Autoimmune (lupus, rheumatoid arthritis)
• Lung Cancer
• Pneumothorax
• Pulmonary Embolism

Question 32

What is meant by Pleural Fibrosis?

Answer 32

Unabsorbed pleural effusion may lead to fibrosis of the pleura.

A small degree of thickening has no effects, but widespread fibrosis restricts expansion with a measurable reduction in lung volumes and compliance.

Question 33

Describe Pleural Tumours

Answer 33

• Secondary deposits of tumours are not uncommon in the pleura
• The commonest primary tumour is a malignant mesothelioma

Almost all victims exposed to asbestos 20-40 years before
Early symptoms are those of pleural effusion but with a duller pain and more diffuse than that of pleurisy
As the disease progresses pain (due to parietal pleura inflammation) and breathlessness become increasingly severe and there is increasing weight loss. The physical signs are those of a large pleural effusion.
Prognosis is very poor with rare survivors two years after diagnosis

[*]

Question 34

Describe how, in principle congenital abnormalities may affect breathing.

Answer 34

[*] Congenital Abnormalities of the Chest Wall: deformity of the ribs, sternum and thoracic spine

• Sternal abnormalities e.g. pectus carcinatum, pectus excavatum, rarely produce functional impairment though cosmetic impact is considerable.
• Scoliosis and kyphosis may produce significant functional impairment of the thoracic cage and are sometimes congenital.

Question 35

Describe how acquired chest wall abnormalities can lead to problems with breathing

Answer 35

• Trauma: Broken ribs produce pain and possible underlying lung contusion. There may be a pneumothorax. If a large number of ribs are fractured a segment of the thoracic cage may become disengaged mechanically producing a ‘flail’ segment.
• Iatrogenic - Some old patients may have had surgery for TB, designed to collapse underlying lung
• Kyphosis
• Scoliosis
• Ankylosing spondylitis

Question 36

Describe how muscle disease can lead to problems with breathing

Answer 36

• In addition, the muscles involved in breathing may be affected by generalised muscular disease such as muscular dystrophy or by neurological disease such as motor neurone disease or polio.
• The effects of muscle weakness are to produce respiratory failure with a propensity to lower resistance to respiratory tract infections because of poor clearance of secretions.

Question 37

What can chest wall disease lead to?

Answer 37

Inadequate ventilation
Sleep disordered breathing
Poor clearance of secretions
Atelectasis
Pneumonia

Question 38

Describe Fibrosing Alveolitis

Answer 38

[*] Progressive inflammatory condition of the lungs whose cause is unknown

[*] Unclear pathogenesis

[*] Histologically there is increased numbers of activated alveolar macrophages – perhaps triggered by an infection or pollutant.

[*] Activated macrophages attract neutrophils and eosinophils which produce local lung damage by generation of reactive oxidant species and proteases => tissue destruction and fibrosis.

[*] In the early stages, these processes can be restrained by treatment with steroids. Once fibrosis has developed, steroids are less effective.

[*] Condition is relatively rare (3-5 per 100,000). It presents about twice as often in males than in females, most commonly in middle age.

[*] Patients report a progressive shortness of breath on exercise (exertional dyspnoea) often with a non-productive cough. Most patients have finger clubbing. Bilateral inspiratory fine ‘crackles’ can be detected on listening to the chest. The condition progresses at different rates in different patients.

[*] Occasionally the disease progresses rapidly to death in a few months but the more usually progression is slow.

[*] The chest x-ray shows small lungs with micro’nodular shadowing predominating in the lower lobes, with ragged heart borders .

[*] Diagnosis of Fibrosing alveolitis may be confirmed by CT scan, which normally reveals changes predominantly in the lower zones; initially subpleural distribution of fibrosis and may show areas of ‘ground glass’ shadowing indicating alveolitis. The treatment is by high dose oral steroids. The effectiveness of treatment is monitored by repeated lung function tests.

Question 39

Describe Extrinsic Allergic Alveolitis

Answer 39

[*] This is a term for a number of conditions in which the inhalation of organic material triggers a diffuse allergic reaction in the walls of alveoli and bronchioles.

[*] The condition may be acute (sudden onset, rapidly progress) or chronic (develop gradually and persist).

[*] A typical acute form is ‘Farmer’s Lung’, where exposure to an antigen derived from Thermophilic actinomycetes found in mouldy hay produces an influenza-like illness 4-9 hours later with a dry cough and exertional dyspnoea. Sometimes breathless can be severe. On listening to the chest you would expect to hear fine mid and late respiratory crackles. There may also be a wheeze.

[*] A chronic form is ‘Bird Fancier’s Lung’. Here long term exposure to antigens derived from pigeons or budgerigars leads to insidious malaise (feeling persistently unwell), dry cough and breathlessness over months or years. Again you will hear inspiratory crackles.

[*] Finger clubbing odes not occur in either acute or chronic presentation.

[*] In acute disease the chest x-ray shows a diffuse micro-nodular infiltrate denser towards the hila. In the chronic disease, the chest x-ray may be almost normal but the disease may progress to pulmonary fibrosis affecting the upper zones.

[*] In the acute disease: the lung function tests will show small lungs with reduced compliance and reduced gas transfer.

Question 40

Describe Asbestosis

Answer 40

[*] Inhalation of asbestos fibres can lead to a number of conditions which often develop long after the exposure and so still appear today.

[*] Asbestos inhalation is associated with 3 forms of disease:

• Benign pleural plaques
• Asbestosis (pulmonary fibrosis)
• Mesothelioma
• There is also a markedly increased incidence of lung cancer.

[*] Asbestos fibres which penetrate to the alveoli produce an alveolitis with an influx of macrophages coating the fibres to produce characteristic ‘asbestosis bodies’ – this alveolitis progresses to fibrosis.

[*] Clinical features: history of asbestos exposure, exertional dyspnoea and a dry cough. There are inspiratory crackles at the lung bases, which rise as the disease advances.

[*] Pulmonary function tests: shows small lungs, reduced compliance and impaired gas transfer.

[*] There is no treatment for asbestosis per se.

Question 41

Describe Sarcoidosis

Answer 41

[*] This is a condition which affects many systems of the body, most commonly the lungs, skin and eyes.

[*] The characteristic feature is the presence of non-caseating granulomata.

[*] Fluid collected by ‘lavage’ (washing-out) of the airways and alveoli contains lots of cells, including macrophages and lymphocytes.

[*] Clinical features: almost any organ system can be affected but the commonest sites are the hilar glands and the lungs. Incidence varies with ethnic background, being commoner in Afro-Caribbean and Asians than in Whites (17-20/100,000 as opposed to 1.5/100,000). The highest incidence is in the 30’s and 40’s with a female preponderance.

[*] Thoracic sarcoid may be graded by chest x-ray into 4 stages from hilar adenopathy through to irreversible pulmonary fibrosis.

[*] Clinical history: may present acutely with hilar gland enlargement or less acutely, usually with stage II or III disease visible on x-ray but asymptomatic. Generally the chest x-ray is much worse than the condition of the patient. The CXR appearance is variable but commonly includes military and nodular shadowing and diffuse fibrosis.

[*] Lung Function tests: patients have small lungs with reduced compliance and reduced gas transfer. There may be some evidence of air flow obstruction.

[*] In stages I to III steroids are usually effective in suppressing the disease.

Question 42

What should I do next?

Answer 42

• revise radiology lecture
• revise radiology groupwork presentation
• look online at radiologymasterclass.co.uk