Smaller patches of consolidation, you’re
not going to identify. Percussion note changes
or much change in expansion of the chest when
the patient breathes in and out. And really
it’s the crackles that give the game away
and identify the presence of consolidation
in those circumstances.
Now airways obstruction: COPD is a very common
disease. And therefore we will see patients
frequently with COPD. But one of the subtleties
of that disease is that actually it’s quite
hard to identify a patient with COPD when
you listen to their chest with a stethoscope.
And that, it’s the general observation of
the chest which gives you more clues perhaps
as to what’s going on. So the patient may
be breathless. But that’s not specific for
COPD, of course. They may be using accessory
muscles of respiration. There may be excessive
abdominal movement on inspiration. But again,
that’s not specific for COPD. Pursed-lip
breathing is a sign that does suggest there
is expiratory airflow problems and therefore
airways disease such as COPD.
When you look at the chest though, it is frequently
hyperexpanded. The ribs have come up the horizontal
angle – to a more horizontal angle than
usual, there’s an increased anteroposterior
diameter. And when the patient breathes, there’s
often what we call a tracheal tug where the
cricothyroid cartilage comes down to the sternal
notch on inspiration. And expansion is usually
very obviously reduced bilaterally in patients
with COPD. The trachea remains central because
it’s a bilateral disease. And as I mentioned
earlier, the percussion note, the resonance,
the areas which are resonant might expand
below the vertebral body of T10 posteriorly,
over the liver anteriorly, and over the heart
anteriorly. They may become resonant whereas
previously they should have been – well,
in normal people – they should be dull.
If somebody has severe COPD, they’ll have
central cyanosis and evidence of cor pulmonale
and raised JVP and ankle oedema. When you
listen to the lungs, the commonest sign is
prolonged expiratory phase of the respiration
and quiet breath sounds and, occasionally,
you get a wheeze on expiration as well. But
the absence of a wheeze does not mean they
don’t have COPD.
Pulmonary fibrosis (interstitial lung disease):
so basal pulmonary fibrosis. It’s a disease
that starts – idiopathic disease starts
in the bases and moves up the chest as the
patient get more severely affected. 10 to
15% of patients with fibrosis will have clubbing.
However, that means 85% of patients will not.
Expansion will be reduced bilaterally but
not so obviously perhaps as it would be in
COPD. Percussion note and vocal resonance
will be normal.
Really, the only sign that’s readily identifiable
in patients with early pulmonary fibrosis
are the crackles that you get. These crackles
have a very specific nature which, with experience,
you should be able to recognise as soon as
you listen to them. And they’re called Velcro
crepitations. They’re late inspiratory crackles,
they occur in little bursts and that’s why
they sound like Velcro being pulled apart.
And they tend to occur – they occur over
the areas of fibrosis which, in early disease,
will be both bases. Some patients with pulmonary
fibrosis have underlying rheumatoid arthritis
with systemic sclerosis. And that may be obvious
when you do the general examination that they
have this connective-tissue disease as well.
Obviously, with severe disease, you’d end
up with central cyanosis, the crackles will
have spread throughout both lungs and in fact
the patient can even develop cor pulmonale
just like COPD – end-stage COPD – might
do as well.
Bronchiectasis: that is another cause of clubbing.
Again, it’s relatively uncommon in mild
or moderate disease and really is only present
in patients with a severe disease. You get
bilateral reduced chest expansion if it’s
a bilaterally-affected patient. Most patients
with bronchiectasis are, but not all. But
percussion note and vocal resonance will normal.
And when you listen to the chest, again you’re
going to hear basal crackles but, unlike fibrosis,
these tend to be coarse crackles and can be
associated with squeaks and wheezing as well.
Again, if you’ve got severe disease, the
patient will be breathless at rest, they’ll
have central cyanosis. But, unlike lung fibrosis
where the lungs become smaller as the disease
becomes more severe, the reason why patients
with bronchiectasis develop respiratory failure
is due to associated airways obstruction.
So you may have the signs that you get with
COPD in somebody with severe bronchiectasis.
So that will be hyperexpanded chest, pursed-lip
breathing, prolonged expiratory phase, loss
of dullness over the heart/liver, extent of
the lungs below T10 for example. Occasionally,
there might be evidence of the underlying
cause of the bronchiectasis: rheumatoid hands,
for example, situs inversus if it’s a ciliary
To summarise the main learning points of this
lecture on the clinical examination:
Examination is essential. You need to be able
to identify signs that might confirm the diagnosis
that you suspect after the history. But you
also need to make sure there are no signs
which are incompatible with the diagnosis
that you’re suspecting and that you’re
not going down the wrong route.
Obviously, during acute presentations, you
don’t actually have time to do investigations
and you need to rely on your clinical examination
skills to identify what’s wrong with the
patient and give the appropriate treatment.
And if that is not done effectively, then
you run the risk of, well, essentially allowing
the patient to die needlessly.
To be able to examine a patient properly,
you need a systematic approach to the examination
to make sure you pick up all the abnormalities
that might be present. And you need the knowledge
to be able to interpret those abnormalities.
Most of the major pathologies have distinct
patterns of presentation when you do the examination.
And you need to know these so that you don’t
have to think hard about how to interpret
the signs that you might identify. And therefore
you can rapidly move on to doing the correct
investigations and management and treatment
that is required for the patient.
Thank you for listening.