Sunday, October 14, 2007
He started off as usual with a general examination and noted that the patient was seated up in bed, appeared breathless and had an oxygen mask on.
I asked him what he thought at this point, keeping in mind it was a patient with a known cardiovascular problem. He replied that he would say the patient had heart failure. (ACES for PACES page 177)
We asked him to carry on and he said he thought the patient was of average height and weight.
He next examined the patient’s hands. He went though in order and noted that the nails were normal, there were a few bruises on the skin, the bones, joints and tendons were normal but there was generalised wasting of the small muscles of both hands. I asked him why he thought the muscles were wasted and then he took a further look at the patient and said that he thought this was due to generalised wasting of muscles and that the patient looked emaciated. I asked him why the patient was emaciated reminding him that this was a patient with known cardiovascular disease. He replied that the most likely condition in the context of cardiovascular disease and heart failure was cardiac cachexia. (ACES for PACES page 179)
He next examined the pulse and said that the patient had a low volume pulse with several ectopic beats. I asked him what he thought the diagnosis was in a male patient in sinus rhythm (few ectopics) and a small volume pulse in a PACES simulation. (ACES for PACES page 190-195) He replied that the most likely diagnosis would be aortic stenosis. I reminded him that a diagnosis had more than one component and he then replied that the patient had aortic stenosis, was in heart failure and had cardiac cachexia.
On examination of the head the only abnormalities were flaring of the alae nasi in keeping with heart failure and a high arched palate.
On examination of the neck the JVP was not elevated and there were no other abnormalities.
On examination of the chest he noted a diffuse apex, soft 2nd heart sound and an ejection systolic murmur at the aortic area with radiation to the neck (ACES for PACES page 216-217)
There were basal crepitations.
We went through the findings again and reiterated how the diagnosis was made by the time he had finished examining the hands and that the remainder of the examination merely confirmed the suspicions that had been raised.
Sunday, September 30, 2007
The patient was an elderly man. He was seated up in bed and had an oxygen mask on. He was of average height but he looked thin. His skin was pigmented.
We paused there and analysed the findings up to that point. We thought that at this point we could think that the patient had a problem involving the respiratory system because of the breathlessness and it was probably a chronic illness because of the emaciation (ACES for PACES page 248).
We thought about the causes of skin pigmentation and thought of Addison’s disease in association with tuberculosis and we also thought about non-metastatic manifestations of bronchial carcinoma (ACES for PACES page 249)
On examination of the head we noticed that the head was thin and almost skeletal reinforcing our impression of emaciation and chronic illness.
The alae nasi were flaring reinforcing our impression that the patient was in respiratory distress.
There was no specific abnormality noted on examination of the hands.
On examination of the neck we noted that the neck was quite thin in keeping with the emaciation that we had noted.
The trachea was deviated to the left hand side.
The medical students went through the causes of tracheal deviation (ACES for PACES page 257)
Next, we examined the patient’s chest.
We noted that the patient’s chest wall was thin and almost skeletal. We also noted gynaecomastia. The medical students were asked why the patient was likely to have gynaecomastia in the context of the other findings so far. Non-metastatic manifestations of bronchial cancer came to mind (ACES for PACES page 259)
The respiratory rate was 28 per minute
Respiratory movements were decreased on the right hand side. We stopped there and asked the students what the causes of decreased respiratory movements were (ACES for PACES page 261)
We then asked in the context of the findings so far what the diagnosis could be
Tracheal deviation to the left and reduced movements on the right would suggest either pleura effusion or pneumothorax on the right side. However we had already thought that the illness was a chronic process and this made us think that the diagnosis was pleural effusion
Taking into account the emaciation, pigmentation and gynaecomastia the cause of the effusion was most likely a bronchial cancer.
Vocal fremitus was decreased on the right hand side in keeping with our suspicion of pleural effusion on that side. (ACES for PACES page 262)
Percussion note was stony dull on that side in keeping with pleural effusion (ACES for PACES page 262)
Breath sounds were decreased on the right hand side vocal resonance was reduced and there was aegophony at the upper level of the effusion (ACES for PACES page 263-264)
Right sided pleural effusion underlying bronchial cancer
Wednesday, August 08, 2007
The trainee examined the patient and presented the findings and following this we went through the technique of cardiovascular examination in detail and analysed the findings.
We started off by having a general look at the patient and her surroundings. There was a yellow booklet by the bedside, which indicated that the patient was on warfarin. This immediately made us think of either an arrhythmia such as atrial fibrillation or a metallic heart valve.
The patient was a young female who was seated comfortably in bed. She was of average height but slim. Her skin was deeply tanned. I asked the trainee what the tan would mean and we concluded that this meant the patient was not unduly unwell and had been fit enough to go on holiday.
There was no marked abnormality on examination of the head although her palate seemed high arched.
There was no abnormality of her hands; her pulse rate was 80 beats per minute and regular, normal volume and character, no radio-radial or radio-femoral delay.
The fact that she was in sinus rhythm made us think she was on warfarin for a prosthetic valve.
There was no abnormality of her neck. In particular the JVP was not raised and the trachea was in the midline.
On examination of her chest a midline sternotomy scar was noted. The presence of the scar together with the fact that we had already noted the anticoagulation booklet made us think the patient had a prosthetic heart valve reinforcing the impression we had made by noting that she was in sinus rhythm.
The apex beat was in the 5th intercostal space just medial to the midclavicular line and the character was normal.
The heart rate was also 80 beats per minute and regular, dual rhythm.
The first heart sound was normal.
The second heart sound was replaced by a closing click of a prosthetic valve. This made us think that she had a prosthetic aortic valve. We listened carefully in systole and heard an opening click at the left sternal edge. Further evidence that she had a prosthetic aortic valve.
There was a soft systolic murmur at the aortic area, which was not conducted to the neck. Probably a flow murmur. No diastolic murmur was heard. No extra-cardiac sounds were heard.
There was no oedema and the lung bases were clear. However when we examined the patient’s back we noted a left sided thoracotomy scar
The trainee concluded that the patient had a prosthetic aortic valve, she was in sinus rhythm and that there was no evidence o heart failure. There was no valvular leak.
I asked him what the thoracotomy scar could be due to. One of our previous trainees who is now a registrar had a similar case when he went for the PACES examination and had been stumped by this question. The answer was easy for us and we were able to confirm that she had an earlier operation for repair of coarctation of the aorta.
I did include this in ACES for PACES page 201 so that candidates preparing for the MRCP PACES would be aware of such a possibility. The late complications of coarctation of the aorta include aortic valve disease because of associated bicuspid aortic valve.
One of the signs the trainee missed was the opening click. I know that this is one of the features that examiners at the PACES often question the candidates on and hence it is important not to miss it.
We went thorough the method of auscultation of the heart and reinforced the importance of heaving a robust method and sticking to it. Placing one’s stethoscope over the praecordium and listening to what one may hear is not enough. One must go through each phase of the cardiac cycle and analyse each component. (See ACES for PACES pages 165-169 summarised on page 170)
Another important point illustrated by the presentation of this case is the importance of a complete diagnosis. Replaced aortic valve, no leak, sinus rhythm, no heart failure, aetiology bicuspid aortic valve associated with coarctation of the aorta.
In other words the four components of diagnosis (ACES for PACES chapter 3)
Saturday, August 04, 2007
We went through some of the sections and I pointed out what the colleges were expecting from the candidates. He was completely unaware of what was expected and had approached preparation in the wrong way.
The booklet clearly states what knowledge and skills are expected of the candidates at each station and then gives the mark sheets so that one may get an idea of how marks are awarded.
It is surprising that many candidates are unaware of the existence of such a publication and hence their preparation is misdirected and incorrect.
I would recommend that those who are taking the exam should go through this booklet and use this to guide their preparation.
Sunday, July 29, 2007
I spoke to a candidate who had failed the MRCP PACES at his last attempt. We discussed presentation of findings to the examiners and in particular how to present one’s diagnosis.
I asked him how he had presented the diagnosis of the cases he had seen at the examination and the information he gave me was inadequate. He gave basic information but left out very important facts concerning function of the system concerned and aetiology.
This led us to discuss diagnosis in detail.
I realised that this candidate had not analysed what is meant by diagnosis and had not studied this in depth.
When coming to a diagnosis it is important to make this as complete as possible and find out about the organ or system concerned, the pathology affecting the organ or system, the aetiology of the illness and the function of the organ or system
In other words it is important to elucidate the four components of a diagnosis:
Anatomical diagnosis (where is the lesion)
Pathological diagnosis (what is the pathological process)
Aetiological diagnosis (what is the cause of the lesion)
Physiological diagnosis (what is the function of the organ or system concerned)
If one presents one’s diagnosis in this manner it will demonstrate to the examiner that one is thinking clearly and this is likely to influence the marks obtained.
For an analysis of diagnosis, the four components of diagnosis and checklists for use in situations where it is difficult to come to a diagnosis; see chapter 3 of ACES for PACES
Sunday, July 22, 2007
He had a case of fibrosing alveolitis (interstitial lung disease). He said he easily made the diagnosis and knew everything about fibrosing alveolitis and was waiting for the examiners to ask him about fibrosing alveolitis so he could display his knowledge.
Unfortunately for him this was the MRCP PACES and what was being assessed was demonstration of practical examination and evaluation skills not, encyclopaedic knowledge of theory.
He was asked how he would demonstrate clubbing (see ACES for PACES pages 107,126) and he was then asked about the causes of clubbing (see ACES for PACES pages 126,254)
He was also asked about cyanosis and the types of cyanosis (see ACES for PACES page 116)
He made crucial mistakes in these basics and did not satisfy the examiners.
This is quite a common error. Many candidates prepare for PACES by studying all the details of likely cases rather than going through the basics. The examiners are looking to see if the candidate demonstrates ability to examine a patient correctly and then interpret the signs obtained.
Theory knowledge has already been assessed in parts 1 and 2 and will not be assessed here.
Sunday, July 15, 2007
They all said the first thing they look at is how well the candidate examines the patient. If the candidate does not demonstrate correct technique or if they do not examine with ease then they would fail the candidate.
If the candidate passes this first hurdle the next step is whether they detect the physical signs present. With regard to physical signs they would not mind if a difficult sign was missed but they all said they would definitely fail the candidate if they “ made up physical signs”. That is if the candidate tells the examiner that the patient has a physical sign that is not there then, the examiners will definitely fail them. I asked several candidates how they prepare for the exam and they said they memorise the physical signs of the likely cases in the exam.
This technique of exam preparation is incorrect.
This is the reason why a lot of candidates fail the exam despite examining correctly and making the correct diagnosis. Memorising the physical signs and repeating this at the exam instead of telling the examiners the findings that are present in the case in question is why most candidates fail.
So in summary the main reasons for failing the MRCP PACES physical examination stations are:
1) Incorrect technique
2) Making up physical signs
Saturday, June 23, 2007
They stressed that what was most important was correct method. They observed the candidates going through history taking, clinical examination and communication and noted whether they appeared competent in the skill they were demonstrating. If they demonstrated competence they were most likely to pass.
If the candidate failed to demonstrate competence at history taking, clinical examination and communication then they would fail even if they got the findings right.
One of the examiners gave me two examples of candidates who examined the abdomen and the respiratory system. Both had what he described as appalling technique but both were able to give all the findings when asked. However, both failed, as the exam is a judge of the ability of the candidate to demonstrate or show competence in clinical method rather than an ability to memorise the findings in a given condition.
The secret of passing the PACES examination is practising clinical methods (history taking, physical examination and communication) over and over again until you can do it without even thinking about what comes next. Then you will pass with ease
Saturday, June 02, 2007
We discussed this further using examples of scenarios.
The first thing to remember is that most of the stations involve simulated patients or relatives. They have been told what to say regarding a certain condition or situation. If one asks a question they will answer according to the instructions given. If they are not sure, they will give you the answer rather than risk hiding an important fact and prejudicing the candidate’s chances.
What are the questions one should ask?
The questions to be asked in history taking are standard and these should not present a problem. (Presenting complaint, past illnesses, drug history etc)
The questions that one should ask to make the history more relevant and display maturity on the part of the clinician are the extra questions that are not yet considered standard.
These questions are regarding the beliefs, expectations, anxieties or concerns of the patient. If they are not asked very important information is missed out and this is usually the cause of failure especially in the communications and ethics station.
If one does not take into account the thoughts and views of the patient or the concerned party, then the explanation will lack focus on the situation in and will simply be a general explanation which may not suffice in that particular situation.
To make sure that you take into account these additional parts of the history, use the mnemonic:
I PASSED By Employing ACES (see ACES for PACES chapter 4, chapter 18)
The second part of these stations is delivering an explanation to the patient or concerned party regarding the situation. This explanation is best given by telling them in simple language what one’s own beliefs, expectations and concerns are regarding the situation (ACES for PACES chapter 18)
By having such a framework for assessing and explaining, the whole process becomes methodical and thus simplified.
We went through several scenarios using this method.
A scenario concerning a pregnant woman who has a deep vein thrombosis; the concern of the patient is that the treatment will cause harm to the foetus. If this concern is not elicited and addressed the explanation would be deemed unsatisfactory.
Similarly, a patient with a stroke and the scenario is regarding feeding, the relation may be concerned that not feeding and starving the patient may cause distress or on the other hand the concern may be that feeding would prolong the patient’s suffering. Hence it is important to elicit these thought and views and address these anxieties.
Sunday, May 27, 2007
The presentation was as follows:
The patient is an elderly gentleman who is of average height and weight. There are no signs of bacterial endocarditis. Pulse 80 beats per minute regular, no collapse.
JVP not elevated
Apex 5th left intercostal space, medial to the mid-clavicular line
First heart sound was soft. There was a pan systolic murmur best heard at the apex with radiation to the axilla. The murmur increased in intensity during expiration.
He was then asked the diagnosis and replied that the patient had mitral regurgitation.
We then thought we would go through the patient again. This time we went more slowly, following the method (ACES for PACES pages 157-171), we meticulously went though each step and analysed one step at a time
We started with a general examination.
The patient was an elderly gentleman of average height and weight. He was lying propped up in bed and appeared tachypnoeic. We paused to think what this would indicate and decided that on this information and the fact that we were examining the cardiovascular system, the patient must have heart failure.
We looked at his head, quickly went though the general examination and then looked at his nose. His alae nasi were flaring; in keeping with the suspicion that the patient had heart failure.
On examination of his mouth we noticed that the patient had a high arched palate.
On examination of his hands, there was no abnormality of his nails but on examination of the skin we noted multiple bruises. In the context of the cardiovascular system this could indicate that the patient was being treated with an anticoagulant.
His pulse rate was 80 beats per minute, regular in rhythm and volume no collapse, normal character, no radio-radial, radio-femoral or brachio-radial delay.
We asked the patient to stretch his palms out, there was no tremor. We asked him to spread his finger wide apart and cock his wrists back and noted that the patient had a flapping tremor. We thought about the causes of a flapping tremor and decided that of the many causes pf a flapping tremor; this patent’s tremor was most likely to be due to heart failure (see ACES for PACES page 446 causes of flapping tremor)
On examination of his neck there were no abnormalities on general examination, no goitre, muscles normal. His JVP was elevated to his ear lobe. The trainee remarked that he had noted the pulsation in the patient's neck but thought that this was carotid pulsation. We then went through how to differentiate pulsations in the neck (see ACES for PACES page 162)
The predominant wave in the JVP was a systolic wave, which was expansile, a V wave, and this suggested that the patient had tricuspid regurgitation.
The carotids were normal; the trachea was in the midline.
There was no structural abnormality of his praecordium, skin was normal and there were no visible pulsations.
The apex beat was in the 5th left intercostal space just medial to the mid-clavicular line and it was diffuse in nature. There was no left parasternal heave.
The heart sounds were regular in rhythm 80 beats per minute. The 1st heart sound was soft. This made us think that the patient had mitral regurgitation.
The 2nd heart sound was normal in intensity and not split.
There was a pan systolic murmur at the apex and this murmur radiated to the axilla. The murmur increased in expiration. This was in keeping with the earlier suspicion that the patient had mitral regurgitation.
There was a pan systolic murmur at the left sternal edge. It was difficult to say whether this murmur increased in inspiration. The murmurs were in keeping with mitral and tricuspid regurgitation, which we suspected from our earlier findings.
On examination of the back we looked at the neck and spine and traced our fingers down the spine as recommended in the method and this enabled us to readily observe that the patient had sacral oedema, in keeping with our suspicion that the patient had heart failure.
On auscultation of the lung bases we noted that the patient had fine bilateral basal crepitations. Further evidence in favour of our suspicion that the patient had heart failure.
Mitral and tricuspid regurgitation
Congestive cardiac failure
We discussed the differences in the amount of information obtained and came to the conclusion that following the method and concentrating on one step at a time enabled us to obtain much more information.
The recommendation to the trainee was to read the method over and over again and practice over and over again until the method became second nature to him. Read, practice, read again ad infinutm.
What is the cause of the mitral regurgitation? (See causes of mitral regurgitation ACES for PACES page)
Advanced level question:
Is it primary valvular disease or regurgitation secondary to cardiac dilatation?
The absence of a loud 2nd heart sound makes it unlikely that the patient has developed pulmonary hypertension and further the absence of left parasternal heave makes it unlikely that that patient had developed right heart failure secondary to chronic left heart failure and pulmonary hypertension.
Hence, the valvular regurgitation was more likely to be due to heart failure and cardiac dilatation.
Notes on mitral regurgitation :
Saturday, April 21, 2007
She was of average height and weight.
On examination of her head, the only abnormality seen was flaring of the alae nasi in keeping with the impression that the patient was in heart failure.
On examination of her hands there was no abnormality.
Her pulse rate was 90 beats per minute regular in rhythm and volume. The pulse was large in volume and collapsing in nature. This was a definite collapse and a good example. We went through the technique of demonstrating a collapsing pulse (ACES for PACES page 159) We discussed the causes of a collapsing pulse (ACES for PACES page 194) and the trainee concluded that in the context of the PACES examination, a collapsing pulse would most likely indicate aortic regurgitation.
There was no bisferiens pulse. This made mixed aortic valve disease less likely.
On examination of her neck it was noted that the jugular venous pressure was elevated about 5 cms above the manubriosternal angle. This was further evidence in favour of the impression that the patient had heart failure. In this patient a pulsation in the neck could also be exaggerated carotid pulsation , Corrigan’s sign ( ACES for PACES page 200 abnormalities of the carotid pulse)
Hence, it was important to differentiate between this and the jugular venous pulse. We went through how to analyse pulsations in the neck (ACES for PACES page 162)
The trachea was in the midline.
On examination of the chest it was noted that there were no deformities or pulsations of the praecordium. The apex beat was in the 6th left intercostal space in the anterior axillary line and it was thrusting in nature.
A displaced apex in the context of a trachea in the midline would suggest the heart was dilated (not mediastinal shift).
See ACES for PACES page 201-203 abnormalities of the apex beat
This was in keeping with the impression that the patient had aortic regurgitation.
The thrusting apex was also in favour of this diagnosis.
There was no parasternal heave and there were no thrills.
There was an ejection systolic murmur in the aortic area, which did not radiate and there was a decrescendo early diastolic murmur at the left sternal edge, which increased in intensity when the patient leaned forward and held her breath in expiration.
On auscultation of her lung bases bilateral basal crepitations were heard.
On auscultation over her femoral arteries a systolic bruit was heard.
Aortic regurgitation, sinus rhythm, heart failure
We went through the questions that could be asked in relation to this case.
First, what are the causes of aortic regurgitation and after that how does one assess severity (ACES for PACES page 216)
Next, how does one investigate the patient? (See planning investigation ACES for PACES pages 571-574)
How does one manage this patient? (See planning management ACES for PACES pages 574-577)
Notes on aortic regurgitation :
On examination of his head the trainee noted that the patient had xanthelasma on his lower eyelids. She concluded that they were probably of no significance in relation to the patient’s respiratory problem.
On examination of his hands the trainee noted that the patient had clubbing (increased nail bed fluctuation, loss of the nail be angle, increased curvature of the long axis of the nail; stage 3 clubbing see ACES for PACES page 127). At this point we emphasised the importance of recalling the causes of clubbing with special reference to the causes in relation the respiratory system (see ACES for PACES pages 127,254).
There were no other abnormalities detectable on examination of the hands.
There were no abnormalities detected on examination of the neck. The trachea was in the midline.
On examination of the chest the trainee noted that the chest was normal in size and shape with normal respiration with equal movements of the two sides of the chest. The respiratory rate was 16 per minute; the apex beat was in the 5th left intercostal space just medial to the midclavicular line. Vocal fremitus was normal and equal on the two sides; respiratory movements by palpation were equal on the two sides. Percussion note was resonant and equal on the two sides. Breath sounds were vesicular. There were fine late inspiratory crepitations at both lung bases. This made the trainee consider the causes of fine crepitations at the lungs bases (see ACES for PACES page 264 –265). She thought of fibrosing alveolitis. In association with clubbing this was the most likely diagnosis. Vocal resonance was normal and equal on the two sides.
Fibrosing alveolitis, not in respiratory failure clinically
Next, we considered the questions that could be asked
First, we went through the causes of fibrosing alveolitis (ACES for PACES pages 239-240)
Next, we considered the investigations that one may arrange on this patient (see planning investigation ACES for PACES pages 571-574)
Finally, we considered management of the patient (see planning management ACES for PACES pages 574-577)
Saturday, April 14, 2007
On examination of the upper limbs there was no major change in size or shape of the limbs; the skin was normal.
On examination of the muscles the trainee noticed that there was some wasting of the small muscles of the hand involving the thenar eminence bilaterally and the interossei. However, the wasting was not uniform. She also noted fasiculations in the triceps muscles.
At this point we interrupted and asked what her thoughts were. The reply was that with a combination of wasting and fasciculation the most likely diagnosis was motor neurone disease.
On examination of power, the trainee noted that there was weakness mostly distally (small muscles of the hand) the distribution of the weakness was not uniform. This added more weight to the initial suspicion that the patient had motor neurone disease.
Reflexes were exaggerated bilaterally and Hoffman’s sign was positive. Exaggerated reflexes were evidence that the upper motor neurones were involved and this suggested that the patient had amyotophic lateral sclerosis.
There were no overt cerebellar signs and there was no sensory deficit. This was further evidence in favour of motor neurone disease.
Amyotrophic lateral sclerosis
Revise the degenerative disorders of the motor neurones ACES for PACES pages 439-440
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
Saturday, January 13, 2007
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.
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
Friday, January 05, 2007
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
As there was marked weakness of the lower limbs it was not possible to test
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