[SUBJECT]

CHEST CHEST ANATOMY

CHEST PAIN CORONAL CT THORAX
 Determine the likely source of the pain from history
and examination
 Possible sources of pain
o Cardiovascular (heart, vessels)
o Respiratory (lungs)
o Gastrointestinal (oesophagus, stomach)
o Musculoskeletal (ribs, muscles)
Gastrointestinal & Musculoskeletal Chest Pain
 Generally do not require imaging. (including
suspected rib fractures)
Chest pain from a respiratory source
 (e.g. pulmonary embolism, pneumonia) is usually
pleuritic in nature (sharp, worse on inspiration). AXIAL CT THORAX
 Chest X-rays are the first line investigation for
diagnosis in most cases. Exceptions are a suspected
tension pneumothorax (which must be treated
immediately before doing any investigations), and
suspected pulmonary embolism (investigated with
CTPA or VQ scan as first line).
 Dry cough, fine crackles - pulmonary fibrosis
 Pneumonias can be seen on CXR as inflammatory
changes or frank consolidation, there is seldom any
need to do CT for this unless an atypical pneumonia
is suspected.
 HRCT (high resolution CT) thorax is used to
investigate interstitial lung disease and pulmonary
fibrosis.
 Haemoptysis, especially in a smoker, is concerning
for lung cancer and is investigated initially with a CXR.
If the CXR appears normal but the symptoms persist,
a CT thorax may be indicated. Infections (e.g. TB) and
chronic coughing may also cause haemoptysis.

Chest pain from a vascular source

 Rare, but extremely important not to miss. (e,g. aortic

dissection)
 It may be described as tearing pain. Thoracic trauma
and connective tissue disorders predispose to this.
 If the patient is stable enough, they may be
investigated with CT. A widened mediastinum on CXR
is a less reliable sign.
 Cough and breathlessness can have a respiratory or
cardiac cause.
 Productive cough, coarse crackles - pneumonia or
heart failure
 Heart failure is not a radiological diagnosis, i.e. we do
not do CXRs to diagnose heart failure. However, the
signs of heart failure can be seen on CXR.

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PLEURAL EFFUSION
 Transudate: Imbalance of hydrostatic and oncotic
forces. Low protein. Commonly caused by organ
failures (heart, liver, renal, thyroid failures).
 Exudate: Local pathology (infective, inflammatory,
malignant). High protein.
 A pleural tap (thoracocentesis) to obtain a sample of
fluid for laboratory testing can be performed easily
under ultrasound guidance.
 Appearance: Fluid density at the dependent part of
the hemithorax. i.e. at the bases in erect CXR;
posteriorly in supine CT. Causes collapse of adjacent
lung which appears denser (white).

CHEST PATHOLOGY
PNEUMONIA
 Typical: Streptococcus pneumoniae; Haemophilus
influenza
 Atypical: Mycoplasma; Legionella; Pneumocystis
(‘PCP’); Viral; Fungal
 CXR at 6 weeks post-treatment to ensure full
resolution. (and exclude possible underlying lung
mass).
Appearance:
 Typical: Airspace opacity with air bronchograms
(usually one lobe)
 Atypical: Variable; ground glass opacity, nodules with
ground glass “halo”

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PRIMARY LUNG CANCER SECONDARY METASTASES TO LUNG

 Small cell (10%): Located centrally. Poorer prognosis.  The lungs are a common site for metastases, in
Associated paraneoplastic syndromes: ACTH; ADH; particular from breast, bowel and renal primaries.
Lambert-Eaton myasthenic syndrome (LEMS).  Appearance:
 Non-small cell (90%): Adenocarcinoma is located o Soft tissue nodules, usually multiple, located
peripherally. Most common type of lung cancer. anywhere within the lung fields, but
 Squamous cell carcinoma is located centrally. classically more in lower zones.
Associated paraneoplastic syndromes: PTH-like o Can measure anywhere from a few mm to
peptide (Hypercalcaemia - bones, stones, groans, >1 cm in diameter.
moans); Hypertrophic pulmonary osteoarthropathy o Large “cannonball” metastases classically
(HPOA) - expansion of long bones, DIP inflammation, originate from a renal cell carcinoma
finger clubbing. primary.
 Routes of spread: o Metastatic nodules can occasionally be
o Direct - Bronchus, Chest wall, Aorta, cavitating, particularly with squamous cell
Oesophagus lesions, although if cavitation is seen,
o Lymphatic - Hilar, Mediastinal lymph nodes infective causes must be considered.
o Haematogenous - Bone, Brain, Liver,
Adrenal
o Transcoelomic - Malignant pleural effusion
 Appearance: Discrete mass of soft tissue density.
Possibly associated with small lung nodules,
mediastinal & hilar lymphadenopathy, or pleural
effusions.
 Lymphadenopathy is enlargement of lymph node due
to pathology. Definition of enlargement: >1 cm in the
short axis (i.e. width, not length)

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LYMPHOMA
 Malignancy of B or T lymphocytes, with solid lymphoid
tumours. It can involve nodal and extranodal sites.
Subtypes include Hodgkin and Non-Hodgkin.
 Staging is performed with a CT scan or a PET scan,
using the Ann-Arbor classification.
o I: single node group
o II: >1 node groups, same side of diaphragm
o III: >1 node groups, both sides of diaphragm
o IV: extranodal disease (liver, marrow).
 The letter 'B' is added to the stage (e.g. Stage IVB) if
there are 'B symptoms' (fever, weight loss, night
sweats). The absence of ‘B’ symptoms = ‘A’.
 Causes of hilar lymphadenopathy on CXR:
Lymphoma, TB, Sarcoidosis. (Note: Both Lymphoma
and TB can cause the ‘B symptoms’!)
 Appearance: Widespread lymphadenopathy (soft
tissue density), involving one or more groups of lymph
nodes.

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In the coronal CT image below, you can see a massive number

of enlarged lymph nodes in the cervical and axillary areas.

Figure # - Bronchiectasis

PULMONARY FIBROSIS
BRONCHIECTASIS  Pulmonary fibrosis is caused predominantly by
 Bronchiectasis is fixed dilation of part of the bronchial interstitial lung disease.
tree.  Extrinsic (occupational) and Intrinsic (autoimmune)
Causes: causes result in different typical patterns of fibrosis,
 Congenital (cystic fibrosis, primary ciliary dyskinesia where the lung apex or base is more affected.
i.e. Kartagener syn) o Apex > Base: Occupational causes
 Acquired (pneumonia, allergic bronchopulmonary (Exception: Asbestosis)
aspergillosis) o Base > Apex: Autoimmune causes
Appearance: (Exception: Ankylosing spondylitis)
 There is dilatation of bronchi, with or without
thickening of bronchial walls and mucus plugging. Appearance: Reticular shadowing; Honeycombing; Traction
‘Tram-track sign’ can be seen on CT and CXR. bronchiectasis. These are seen best on high-resolution CT but
 The ‘Tree-in-bud sign’ and the ‘Signet ring sign’ can may also be seen on CXR.
be seen on CT.

Figure # - Tram-track sign

Figure # - Tree-in-bud sign

EMPHYSEMA
 Emphysema is one of the two main entities of chronic
obstructive pulmonary disease (COPD), the other
being chronic bronchitis.
o Smoking causes a centriacinar
(peribronchiolar) pattern
o Alpha-1-antitrypsin deficiency causes a
Figure # - Signet ring sign panacinar (diffuse) pattern
 There is destruction of alveolar walls, resulting in
enlargement of airspaces. These become confluent
and eventually form bullae.

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 Bullae can rupture, leading to pneumothorax and PULMONARY EMBOLISM

pneumomediastinum.  Clear guidelines exist regarding the use of imaging in
 CXR findings include hyperinflation, flat diaphragms, the investigation of suspected pulmonary embolism.
and bullae.  In pregnant women, D-dimers are unreliable and
Wells’ score is not validated.
Appearance: Changes of confluent alveoli (hypodense areas of
 Consider performing duplex ultrasound for DVT, and
lung parenchyma) and bullae (small pockets of air) are typical.
CXR to exclude other causes. V/Q scan (or perfusion-
only scan) is generally favoured to minimise radiation
exposure.
 The main concern with CTPA in pregnancy is the
radiation to the mother’s breasts (as the fetus can be
shielded), and the iodine dose to the foetus (needs
thyroid screen when born).

Appearance: Clots are seen as ‘filling defects’. Contrast cannot

fill areas occupied by clots, therefore the contrast (bright)
surrounds the clots (darker).

On V/Q scan, ventilation (inhaled tracer) is normal but

perfusion (IV tracer) is abnormal, indicating a problem with the
blood supply to a particular area.

The images below show the emboli highlighted in red.

The first two images show multiple bilateral emboli, while the
third image shows a saddle embolus. ‘Saddle’ embolus sits in
the bifurcation of the pulmonary trunk where it divides into the
Figure # - Emphysema left and right main pulmonary arteries.

PNEUMOTHORAX
 Pneumothorax can be primary or secondary to
underlying lung pathology.
o Primary: tall, thin, young males who smoke
o Secondary: asthma, emphysema, fibrosis,
Marfan’s, Ehlers-Danlos, cancer
o Other: penetrating injury, blunt injury, rib
fractures, biopsies, line insertions
 It is usually diagnosed on CXR, but may also be
diagnosed on CT if unsuspected previously and a CT
was performed to exclude other causes of chest pain.

Appearance: A pocket or rim of air located outside the lung and

adjacent to the chest wall, most commonly in the apices.
Associated lung collapse. Only visible on lung window.

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AORTIC DISSECTION
 Aortic dissection occurs when blood enters the aortic
wall through a tear in the tunica intima, ‘dissecting’ a
path (false lumen) between intima and media. If the
dissection extends into smaller arteries (e.g. coronary,
carotid, subclavian, mesenteric), it can cause
ischaemia of the supplied area (i.e. MI, stroke, limb
ischaemia, bowel ischaemia).
 Pericardial tamponade can also occur. The main risk
factor is hypertension.
 Classification systems are Stanford and DeBakey,
both based on involvement of the ascending aorta
(poorer prognosis).

CXR may show widened mediastinum. CT chest (pre and post

contrast, arterial phase) is the ideal investigation, to determine
presence of aortic intramural haematoma, true lumen and
extent of dissection.

Appearance: There is a true lumen and a false lumen,

separated by an intimal flap (tunica intima which has been
detached from tunica media). The false lumen is usually larger
(higher pressure) and hypodense (darker as contrast delayed)
compared to the true lumen, although this is not reliable. To
differentiate them with more certainty, a normal part of the
aorta should be found and followed as this will join into the true
lumen.

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