Wednesday, February 21, 2007
On examination of his upper limbs there were no abnormalities of size and shape of the limbs and the skin was normal. This excluded a neurological deficit dating back to childhood, (normal size and shape) and significant sensory deficit as there were no skin changes.
No wasting was apparent on routine inspection of the upper limbs and there were no involuntary movements.
Tone was normal at the wrist and the elbow but tone was flaccid at the shoulder. When the patient's arms were raised above the head and let go they fell away without any control. This showed that he had flaccidity at the shoulder and this raised the possibility of either a myopathy or lower motor neurone lesion at the shoulder (see ACES for PACES page 449)
The trainee examined power beginning at the shoulders and working distally and demonstrated weakness of abduction and adduction at the shoulder.
He was asked to re-examine power in the upper limbs beginning distally (starting with the small muscles of the hands) and working proximally (to the shoulders and the muscles around the scapula). This time he noticed that there was wasting of the muscles around the scapula and there was weakness of abduction and adduction at the shoulder and weakness of the muscles around the scapula. This suggested either a myopathy or a lower motor neurone lesion affecting C4, C5.
On examination of his reflexes the biceps jerk and triceps jerk were exaggerated there was an inverted supinator jerk and Hoffman's sign was positive. This indicated a lower motor neurone lesion at C5 with upper motor neurone lesion below that level (see ACES for PACES page 508). This together with the signs found earlier would indicate that he had a lower motor neurone lesion affecting C4, C5 with an upper motor neurone lesion below that level. This would fit in with a cervical myelopathy.
Coordination was poor but this reflected the proximal weakness rather than a cerebellar lesion
On examination of the sensory system there was loss of sensation over C4, C5 on the right hand side and equivocal loss of sensation over C4, C5 on the left hand side
Cervical myelopathy affecting C4, C5 nerve roots
This case was difficult for the trainees. The main reason for missing the diagnosis, in the first instance, was that there was a failure to follow the correct method.
Not examining tone at the shoulder was a crucial mistake. This would have shown evidence of flaccid weakness affecting C5
Examining power by beginning proximally was the most crucial error. The scapular region was not examined and this meant that the wasting and weakness around the scapula was missed and thereby crucial evidence was missed.
The trainee had not seen an inverted supinator jerk before but this is an important sign to look for when performing the tendon reflexes. An additional problem was that the Hoffman reflex was not elicited correctly and hence the positive reflex was missed. Practice performing the Hoffman reflex using the correct method (ACES for PACES page 414)
By the time the reflexes were examined the diagnosis was clear and sensory examination only added further evidence to confirm the earlier suspicions.
Remember the secret of success in neurology is following correct method and analysing at each step. Read up the section on examination of the CNS in chapter 16 of ACES for PACES and practice repeatedly.
Revise the nerve supply of the skin, the muscles and the reflexes ACES for PACES pages 426-428
The patient was an elderly female lying propped up in bed. She was of average height and weight.
There were no abnormalities seen on examination of her head.
On examination of her hands there were no abnormalities found. Her pulse rate was 80 beats per minute, regular in rhythm and volume, normal character, all pulses were equal and synchronous.
On examination of her neck, the JVP was elevated to the angle of the jaw. The dominant wave was an expansile systolic wave. This made the trainee think of tricuspid regurgitation. The venous wave was under high pressure and palpable. This made the trainee think that the cause of the tricuspid regurgitation was right heart failure due to pulmonary hypertension. As the patient did not appear to have significant pulmonary disease the suspicion was that this was due to long standing left ventricular dysfunction.
The trachea was in the midline.
There were no abnormalities seen on inspection of the chest, the apex beat was palpable in the 6th left intercostal space lateral to the midclavicular line. This made the trainee think that either the patient had systolic heart failure or dilatation of the ventricle due to diastolic overload caused by valvular regurgitation. There was no thrust or heave at the apex and there was no parasternal heave.
The 1st heart sound was soft making the trainee think that the mitral valve was not competent. The second sound was also soft.
There was an opening snap heard best at the mitral area this made the trainee think that there was stenosis of the mitral valve.
There was an ejection systolic murmur radiating to the neck suggesting that the patient has aortic stenosis. There was a pan- systolic murmur at the left sternal edge and this increased with inspiration in keeping with tricuspid regurgitation. This had been suspected earlier on the basis of the characteristics of the JVP.
There was also a pan systolic murmur at the mitral area. This increased in expiration and radiated to the axilla in keeping with mitral regurgitation that had been suspected earlier on the basis of the soft 1st heart sound. There was a rumbling mid-diastolic murmur at the mitral area in keeping with mitral stenosis.
There was no sacral oedema and the lung bases were clear.
How would you know whether the mitral stenosis or regurgitation was dominant?
In this case one would suspect that mitral regurgitation was dominant. The pulse was of normal volume, the apex beat was displaced and the first heart sound was soft (see table in ACES for PACES page 221)
How would you tell whether the aortic valve was severely narrowed?
The aortic stenosis was not severe in this patient because she had a normal volume pulse; there was no brachio-radial delay, no thrill, no fourth heart sound (see ACES for PACES page217)
Can a mid-diastolic murmur occur in mitral regurgitation?
Yes, severe mitral regurgitation can cause a flow murmur in mid-diastole (see causes of mid-diastolic murmurs ACES for PACES page211-212)
How do you know that this is not a flow murmur?
The patient has an opening snap, which would suggest stenosis of the mitral valve
Revise auscultation of the heart ACES for PACES pages 204-222
Thursday, February 15, 2007
He was of average height and weight
On examination of the lower limbs the trainee noted that there was no major change in the overall size of the limbs and there were no trophic changes in the skin. These findings indicated that the lesion was not long standing.
The muscles of the lower limb were wasted; there were no involuntary movements. This suggested that the lesion affected the lower motor neurone. The absence of involuntary movement, in particular fasiculations, suggested that the anterior horn cell was not affected.
Tone was flaccid reinforcing the idea that this was a lower motor neurone lesion.
Power was decreased throughout the lower limb with the distal muscles being affected to a greater degree. In keeping with a lower motor neurone lesion. The distribution of the weakness was a paraparesis. What we had now demonstrated was a flaccid paraparesis. This narrowed the possibilities down to just a few (ACES for PACES page 452). Of these options, flaccidity narrowed the possibilities down even further leaving us with the possibility of either a radiculopathy or cauda equina lesion.
Reflexes were absent even with reinforcement, further evidence in favour of a lower motor neurone lesion. Eliciting reinforcement allowed us to see that the upper limbs were functioning normally reinforcing our idea that this was a paraparesis.
It was not possible to test coordination in the lower limbs in view of the weakness.
Sensory examination did not reveal a gross deficit; there was equivocal loss of light touch over the feet. This would be a feature against a cauda equina lesion, as the patient would have had anaesthesia in a saddle distribution.
The most likely diagnosis was a polyradiculoneuropathy.
The candidate was asked whether he would like to ask the patient a question regarding the condition to reinforce the diagnosis. The question was whether the patient’s bladder or bowels were affected. Although autonomic features are common in acute inflammatory demyelinating polyradiculoneuropathy (Guillain-Barre syndrome, AIDP) the bladder is not commonly affected whereas it is commonly affected in cauda equina lesions.
The candidate was also asked whether there was any other physical examination he would like to conduct to exclude a cauda equina lesion. The answer was per rectal examination and testing for anal tone, which would be reduced, and the anal reflex, which would be absent in cauda equina lesions.
Flaccid paraparesis due to a polyradiculoneuropathy possibly acute inflammatory demyelinating (the onset was over a short duration) or Gullain- Barre syndrome
Neurology is a difficult subject and is often considered daunting by most candidates attempting the PACES examination.
It is helpful to know the causes of the types of deficit that occur in neurological practice as this will enable one to localise the site of the lesion
Study the causes of wasting of muscles (ACES for PACES page 443)
Study the causes of flaccidity (ACES for PACES page 449)
Study the different types of distribution of muscle weakness (ACES for PACES page 451-453)
Study the patterns of sensory loss and their causes (ACES for PACES page 455-456)
Saturday, February 03, 2007
On examination of his head he had flaring of his alae nasi, which gave the trainees further evidence of dyspnoea.
On examination of his hands there was clubbing which immediately brought up the suspicion of infective endocarditis.
His pulse rate was 90 beats per minute regular in rhythm. It was a large volume pulse and it was collapsing in nature. Sinus rhythm with a collapsing pulse made the trainee suspect that the patient had aortic regurgitation. Careful examination of the character of the brachial pulse revealed a Bisferiens pulse. This brought up the diagnosis of mixed aortic valve disease.
On examination of the neck the jugular venous pressure was elevated. the predominant wave was a systolic wave causing outward distension of the vein. The trainee though this was a V wave indicating tricuspid regurgitation. The trachea was in the midline.
On examination of the praecordium, the apex was palpable in the 6th intercostal space in the anterior axillary line. It was diffuse in nature. With the trachea in the midline the apex being palpable in the 6th intercostal space in the anterior axillary line indicated dilatation of the heart rather than mediastinal displacement. This would be in keeping with the suspicion of aortic regurgitation although it was not thrusting in nature.
On auscultation the first heart sound was soft suggesting mitral regurgitation.
The second heart sound was soft in keeping with aortic stenosis.
There was an ejection systolic murmur radiating to the neck and a blowing, decrescendo early diastolic murmur at the left sternal edge. Confirming our suspicion of mixed aortic valve disease. There was a blowing pan-systolic murmur at the mitral area that increased in intensity during expiration adding further evidence to the earlier suspicion that the patient had mitral valve disease (tricuspid regurgitation would have made the murmur increase in inspiration)
On auscultation of the ling bases there were fine late inspiratory crepitations in keeping with the earlier suspicion that the patient had left ventricular failure.
The trainee was then asked to listen over the femoral artery.
There was a systolic and diastolic bruit over the femoral artery, which confirmed the suspicion that the patient had aortic regurgitation.
Mixed aortic valve disease (dominant regurgitation)
Possible infective endocarditis
Revise character of the pulse (ACES for PACES page 194)
Revise differentiation of mixed valve disease (ACES for PACES pages 220-221)
Revise abnormalities of the femoral artery (ACES for PACES pages 223-224)
On examination of his head his sclerae were icteric making the trainee immediately suspect that the patient had liver disease. There were multiple telangiectasia over his face in keeping with hepatocellular failure. There was bilateral parotid enlargement which made the trainee suspect that the aetiology of the condition was alcohol abuse.
On examination of the hands there was palmar erythema another feature of hepatocellular failure. He had Dupuytren’s contracture, which was another feature that would suggest the aetiology of the condition was alcohol abuse.
He had multiple spider naevi over his upper chest a further indication of hepatocellular failure. There was no gynaecomastia and the distribution of hair growth over his chest was normal.
The abdomen was distended and the distension was greatest in the flanks this made the trainee suspect that the patient had ascites. There were visible veins on the anterior abdominal wall and the direction of blood flow was from caudal to cranial. This suggested that the patient had portal hypertension.
On palpation of the abdomen no lumps or organomegaly were detected. Percussion demonstrated a horseshoe shaped area of dullness and shifting dullness confirming the trainee’s earlier suspicion that the patient had ascites. Auscultation did not reveal any abnormality.
At this point the trainee was asked to employ the technique of “dipping” and with this technique she was able to note that the liver was enlarged three finger breadths below the costal margin but the enlargement was not detected by routine palpation because of the presence of ascites. This was an important learning point. In the presence of ascites always employ “dipping” to detect organomegaly or masses.
Features of chronic hepatocellular failure
Features of portal hypertension
Hence clinical diagnosis of cirrhosis of the liver
Aetiology probably alcohol abuse
Learn the clinical features of cirrhosis of the liver (the features of hepatocellular failure, features of portal hypertension) the causes of cirrhosis of the liver and clinical clues to the causes of cirrhosis of the liver (ACES for PACES pages 305-306)
Learn the technique of “dipping” (ACES for PACES page 273)
Friday, February 02, 2007
Breathlessness in a patient with a cardiovascular problem was most likely to be due to left ventricular failure.
The patient was of average height but appeared to be thin. The trainee said that this probably indicated that the patient was cachectic on account of chronic illness.
On examination of the head the only physical sign of note was that the patient had flaring of the alae nasi in keeping with the suspicion of left ventricular failure.
On examination of the hands the trainee noted clubbing. In the context of the cardiovascular system there are few causes of clubbing. In the absence of cyanosis and in an elderly patient who was unlikely to have congenital heart disease (even after operative correction) the chances were the patient had infective endocarditis. There were no other peripheral stigmata of infective endocarditis.
The pulse rate was 80 beats per minute irregular in rhythm and volume indicating atrial fibrillation. Atrial fibrillation made the trainee suspect that the patient was likely to have mitral valve disease.
On examination of the neck it was noted that the jugular venous pressure was elevated and it was predominantly a systolic wave, which resulted in outward distension of the vein. This made the trainee think it was a V wave due to tricuspid regurgitation. A V wave in the context of atrial fibrillation and suspected mitral valve disease would raise the suspicion that the patient had right ventricular involvement secondary to the development of pulmonary hypertension as a consequence of mitral valve disease.
On examination of the praecordium it was noted that there was a midline sternotomy scar. This raised the possibility of valve replacement or bypass grafting.
The apex beat was displaced to the 6th intercostal space in the anterior axillary line. It was thrusting in nature. This would indicate that the left ventricle was dilated and there was diastolic overload. With the suspicion of mitral valve disease already raised on account of atrial fibrillation the most likely diagnosis at the moment was mitral regurgitation.
There was left parasternal heave and a palpable pulmonary second sound best felt at the pulmonary area. This was in keeping with the earlier suspicion that the patient had developed pulmonary hypertension as a consequence of mitral valve disease.
On auscultation of the heart the native first heart sound was replaced by a click indicating a prosthetic mitral valve.
The second heart sound was complicated. At the pulmonary area a loud native heart sound was heard in keeping with pulmonary hypertension. At the left sternal edge a click was heard in keeping with a prosthetic aortic valve.
In early diastole an opening click was heard indicating that the mitral valve was a metal valve.
There was a pan-systolic murmur best heard at the mitral area and this radiated to the axilla confirming our earlier suspicion of mitral regurgitation.
On auscultation of the lung bases fine late inspiratory crepitations were heard in keeping with the earlier suspicion of left ventricular failure.
Prosthetic aortic and mitral valves
Atrial fibrillation, pulmonary hypertension, heart failure
Possibly infective endocarditis