Description
The patient was an elderly man of average height and weight
lying propped up in bed. He appeared breathless. His skin was deeply tanned and
there were small hypopigmented macules on his trunk.
On examination of his head there was no abnormality of size
or shape. On examination of his nose there was flaring of his alae nasi. The
conjunctivae were pale. There was no malar flush.
On examination of his hands, there was no change in size or
shape, his nails were not clubbed and there were no splinter haemorrhages. He
had palmar erythema. Pulse rate was 88 beats per minute, irregular in rhythm and
volume. No collapse. No radio-radial or radio-femoral delay. No tremors were
noted.
There was no abnormality detected on examination of his
forearms or upper arms, the blood pressure was not checked.
On examination of his neck there was no swelling. There was
a visible systolic pulsation reaching up to the ear lobe. This pulsation varied
with respiration; diminishing on inspiration and increasing with expiration. It
was palpable but the pulsation could be reduced by pressure at the root of the
neck and there was hepato-jugular reflux. The carotids were normal and the
trachea was in the midline.
On examination of the chest there was a midline sternotomy
scar and bilateral gynaecomastia. The apex was at the 6th left
intercostal space 2 cms lateral to the mid-clavicular line. The impulse was
diffuse but closure of the first heart sound was palpable. There was no left
parasternal heave and no thrills. No palpable closure of the second heart sound.
On auscultation, the heart rate was 88 beats per minute and
irregular, there was a click coinciding with the first heart sound, a loud
single second heart sound and an opening click in diastole. There was a soft,
blowing pan-systolic murmur at the left sternal edge, no radiation of the
murmur.
On examination of the back there was sacral oedema and
bilateral basal crepitations
On examination of the abdomen the liver was enlarged four
finger breadths and pulsatile.
He had bilateral ankle oedema. There were no scars.
Analysis
♥
On initial approaching the patient one observes a well-nourished
individual who is breathless. Breathlessness in a patient in the cardiovascular
station would most likely suggest heart failure.
(Page 175) The fact that the patient is well nourished suggests that
this is of relatively recent onset, as he has not developed cachexia.
(Page 179) The tanned skin adds weight to
this assumption, as this would indicate that he has been up and about and
probably been on holiday recently. A patient with long standing heart failure
would have been unlikely to undertake this. The hypopigmentation is of doubtful
relevance here.
ª
Flaring of the alae nasi confirms the initial impression of
breathlessness and adds further weight to the impression that he has heart
failure. (Page 250)
ª
The pale conjunctiva suggests that he is anaemic. Now, this brings
in another reason for his breathlessness or it may be the cause of
decompensation of previous cardiac disease.
¨
Palmar erythema suggests liver dysfunction. In the cardiovascular
station this would imply cardiac cirrhosis. (Page
150)
¨
The irregular pulse suggests the patient has atrial fibrillation.
The presence of atrial fibrillation would suggest a lesion in the mitral valve
causing left atrial dilatation. (Page 193)
§
On examining the neck one notices systolic pulsation. Systolic
pulsation could be arterial or venous. Although it is palpable the fact that it
varies with respiration, there is hepato-jugular reflux and it can be
obliterated by pressure at the root of the neck suggests it is the JVP. As it is
a systolic expansile pulsation it is probably a V wave and this suggests
tricuspid regurgitation. The fact that it is palpable suggests high pressure in
the right atrium and this would imply that the patient has pulmonary
hypertension. This lends more support to our impression that the mitral valve is
involved, as mitral valve disease with left atrial dilation would result in both
atrial fibrillation and pulmonary hypertension. (Page
198)
At this stage of the examination the presumptive diagnosis
is:
Mitral valve disease
Atrial fibrillation
Pulmonary hypertension
Tricuspid regurgitation
Anaemia
♥
On examination of the chest one notices the midline sternotomy
scar. A quick glance at the legs shows there are no scars of vein harvesting
this suggests a valve replacement operation and from the evidence we have
gathered so far it is the mitral valve that has been replaced.
(Page 201)
ª
The presence of gynaecomastia suggests treatment with digoxin or
spironolactone. The fact that he has well controlled atrial fibrillation and the
impression of recent onset heart failure would imply that the drug being used is
digoxin rather than spironolactone. (Page 201)
¨
The displaced apex adds weight to the diagnosis of heart failure.
The fact that it is not thrusting makes it less likely to be due to a
regurgitant aortic or mitral valve. (Page 201)
§
The palpable first heart sound adds weight to our impression that
the mitral valve is at the root of the problem (Page
203).
♥
The irregular heart rate confirms our impression of atrial
fibrillation and the fact that there is no significant apex-radial deficit
suggests the fibrillation is well controlled and supports our contention that
the patient is on digoxin.
ª
The click coinciding with the first heart sound supports a
diagnosis of mitral valve replacement (prosthetic valve) and the opening click
further supports this. (Page 205)
¨
The loud single P2 supports our impression that the
patient has pulmonary hypertension. (Page 207)
§
The blowing pan systolic murmur at the left sternal edge supports
our diagnosis of tricuspid regurgitation. (Page
209-214)
♥
Oedema and bibasal crepitations support our diagnosis of heart
failure. (Page 222-223)
ª
The enlarged pulsatile liver supports the diagnosis of tricuspid
regurgitation and also lends support to the suggestion of cardiac cirrhosis.
(Page 223)
Final Diagnosis
The final diagnosis is:
♥
Mitral valve replacement
ª
Atrial fibrillation (well controlled on digoxin)
ª
Pulmonary hypertension
§
Heart failure
♥
Cardiac cirrhosis
ª
Anaemia
(Page 363), which could be due to:
Haemolysis caused by the
prosthetic valve
Or
Bacterial endocarditis (no
stigmata)
GI haemorrhage (the patient is
probably on warfarin for atrial fibrillation)
Chronic heart failure may cause
anaemia but our conclusion was that in this patient heart failure was of recent
onset.
The patient may have renal
failure as a consequence of treatment of heart failure
