Cardiovascular examination

The patient was an elderly male. He was propped up in bed, looked breathless and had an oxygen mask on. At this point the trainee was asked what came to mind and she replied that in the context of being asked to examine the cardiovascular system, breathlessness suggested that the patient had heart failure or more precisely left ventricular failure.
He was of average height and weight.
There was no abnormality detected on examination of the head.
On examination of the hands the trainee noted tar staining of the fingers. We asked the trainee what her thoughts were and she replied that this would suggest that the lesion might be related to cigarette smoking (i.e.) ischaemic heart disease.
The pulse rate was 80 beats per minute, regular, normal volume, no variation in character; all pulses were equal and synchronous.
On examination of the neck the JVP was elevated 6 cms above the manubriosternal angle, no dominant wave. This was further evidence in favour of heart failure. The trachea was in the midline.
On examination of the chest, there were no deformities, no visible pulsations.
The apex beat was at the 6th left intercostal space in the anterior axillary line. It was thrusting in nature.
Several points were raised here. First was the importance of documenting that the trachea was in the midline. If this had not been done one could not have said that the heart was dilated, as one had not excluded displacement of the apex due to mediastinal shift.
The heart was dilated with a thrusting apex. This raised several possibilities.
Mitral regurgitation, aortic regurgitation or ventricular septal defect.
Ventricular septal defect was unlikely unless one considered an acquired defect due to myomalacia cordis.
Aortic regurgitation was not likely, as the pulse was not collapsing in nature. Hence the most likely lesion was mitral regurgitation.
There was no parasternal heave, no palpable heart sounds and no thrills
The first heart sound was soft making mitral regurgitation more likely. The second heart sound was normal. There were no added sounds.
There was a blowing pan systolic murmur at the mitral area, radiating to the axilla. This confirmed the diagnosis of mitral regurgitation.
On examination of the back, fine late inspiratory crepitations were heard at both lung bases confirming our initial suspicion of left ventricular failure.
Diagnosis:
Mitral regurgitation
Sinus rhythm
Left ventricular failure
One has to consider the aetiology of mitral regurgitation in this case.
It may be primary valvular disease or it may be secondary to ischaemic cardiomyopathy and stretching of the mitral valve ring (our initial suspicion on seeing the tar staining of his finger)
Learn the causes of mitral regurgitation

Neurology for MRCP PACES

We saw an interesting neurology case yesterday
The patient was a middle-aged Asian male seated propped up in bed. He had an oxygen mask on but this was because he had a chest infection and this had no bearing on his neurological problem. He was obese.
We asked the trainees to examine the lower limbs.
On examination, the size of the lower limbs was definitely small in relation to the patients torso and upper limbs. The shape of the limbs was also of note. The upper part looked reasonably normal but there was progressive wasting from the proximal aspect to the distal aspect of the lower limbs. The trainees described this an inverted champagne glass appearance.
This brought up the possibility of a peripheral neuropathy.
Next, we examined the skin (integument). The trainees noted that there was loss of hair over the distal aspect of the lower limbs, the skin over the distal aspect looked shiny and erythematous, there was scaling of the skin and the nails were dystrophic.
At this point we asked the trainees to think about the diagnosis. They concluded that the trophic changes were most likely a consequence of peripheral neuropathy and in a middle aged obese Asian male the most likely cause was diabetic neuropathy. (The possibility of hereditary motor sensory neuropathy should also be borne in mind)
Examination of the motor system revealed wasting of the quadriceps and the distal
muscles. This was evidence in favour of a lower motor neurone lesion with the distal
aspect being more severely affected, hence most likely to be a peripheral neuropathy.
There were no involuntary movements.
There was no weakness of abduction or adduction of the hips but apart from this all
muscles were weak and ankle movements and movements of the big toe were
completely absent. Further evidence in favour of peripheral neuropathy.
The knee jerk was present although reduced but the ankle jerk was tendon reflexes
was absent even with reinforcement. More evidence in favour of
peripheral neuropathy.
As there was marked weakness of the lower limbs it was not possible to test
coordination.
Sensory examination revealed decreased sensation affecting all modalities with the
distal aspect of the lower limbs being affected maximally (stocking distribution).
Further evidence in favour of a motor sensory neuropathy.
Gait could not be examined, as the patient was unable to walk.
Diagnosis: peripheral neuropathy mixed motor and sensory likely cause diabetes
mellitus but with the other causes of mixed motor and sensory neuropathy also being
considered.