How to make the transition from medical student to doctor?

Dear Bloggers

Today's discussion is slightly different. I would like to discuss my opinion on the transition from medical student to becoming a doctor.

I remember being a medical student and attending lectures to learn about diseases, pharmacology, anatomy, biochemistry and so on and so forth. The information in those lectures was excellent and provided the foundation of my knowledge of common diseases.

In part, I was also allowed to go to different locations for training outside the university for specialties such as surgery, paediatrics, obstetrics and gynaecology, general medicine, general (family) practice to name but a few.

In so doing, I was able to learn as a student how the information in the lectures and in the books bore relevance in the hospital system. As such, I soon learnt that the rare diagnoses such as Zollinger-Ellison Syndrome from gastrinoma are very rare, but of course, such rare diagnoses are what everyone remembers. However, the common things such as heart failure, its presentation, investigation and therapy may have only been covered in a single lecture with no emphasis on this being an important thing to know.

Hence, using the basic knowledge from medical school and seeing how it is applied in the real life scenario of the hospital system is really essential how to understand and make the transition from medical student to doctor.

One thing I always say is Common Things Are Common, and I often hear from medical students and junior doctors alike, rare diagnoses, which albeit are correct, are not the commonest presenting illness for the symptoms and signs.

How did I make the transition from medical student to doctor??

Well, I was always advised by my mentor, a famous Professor in Infectious Disease medicine, to see the patient and obtain the history and physical examination and then read about the problems in the textbooks, thereby reinforcing the medical problems with literature. This indeed was useful and I use such a method to this day. In fact, the patients are the best teachers. Going to the bedside and going through a detailed history in the correct order of how things occurred will in fact teach you a lot about the illness by itself. In so doing, the information obtained can then allow you to concentrate on areas of the physical examination that cause concern.

Then, by drawing together the positive elements of the clinical picture along with the pertinent negative symptoms e.g. no chest pain, no sputum, in a body systems review, allowed me to understand which diseases were not likely to be causing the problem.

By having a problem list from history and physical examination alone, I was then taught to consider the likeliest diagnoses from these problems e.g. central crushing chest pain, dyspnoea, diaphoresis, nausea and vomiting are more likely to be an AMI or unstable angina rather than Bornholm's disease from coxsackie virus.

It is all very good to use a medical list of causes, the one which I constructed is DIET IN HIM, an example case that I published last year maps out the different causes from the DIET IN HIM list for a particular patient problem. However, this is just the start!! One has to know the epidemiology of disease such as the age of onset, the likelihood in female or males e.g. SLE, how the disease usually presents and the salient features for diagnosis. Then one has to produce the differential diagnosis based on which is the best diagnosis to fit all the features and with less common ones below this.

Remember, this is based solely on history and physical examination alone.

In the UK, most patients admitted will been seen by the junior doctors who takes the history and physical at the bedside. There may be an ECG available and rarely have any blood tests been taken except if it is a referral from the Accident and Emergency (ER) department or another team. Then the junior doctor takes the blood tests and orders the radiological tests.

However, in the interim, whilst awaiting the results, treatment is usually commenced in anticipation of the results. Hence, treatment is not delayed waiting to see if you are right or wrong. How can this be done??

Well, it comes back to interpreting the history and physical examination. Patients with signs of heart failure get furosemide before the chest xray is performed with oxygen therapy. Patients with chest pain consistent with an ST elevation MI on ECG get the aspirin, heparin, oxygen, morphine, and thrombolysis before the CK and Troponins are available. Patients with signs of a tension pneumothorax get the needle inserted into the 2nd intercostal space in the mid-clavicular line before the CXR is taken. The patient with a good history of PE e.g. sudden onset pleuritic chest pain, cough, dyspnoea, hypoxaemia and a clear chest examination and Xray get heparin before the D-Dimer or spiral CT are performed.

The fact is, making a diagnosis based on history and physical examination is imperative. Without the proper history and poor physical examination skills, the ability to make a diagnosis can be delayed and then the reliance on machines to make the diagnosis for you increases and treatment for severe illnesses can be delayed resulting in adverse outcomes.

Problem Based Learning (PBL) using common presenting illnesses to teach how to understand differential diagnoses and which common diagnoses to consider is very important. This type of teaching is used for the famous MRCP exams in which limited data is provided and the likeliest diagnosis needs to be selected. The USMLE exams are similar in format as well. You see, patients do not present to you and say I have all of these symptoms and my diagnosis can only be X disease. There are many diseases that have overlap of symptoms and signs and the only thing that can separate them can be the timing of onset, epidemiology, sex predominance, location in the world, sexual history, so on and so on.

However, PBL is a classroom based idea and sets the mental framework about how to go about thinking of the patient problems. It is an entirely different scenario being tired and on-call at 4am and to be called to the ER to see a sick patient. This is where the use of bedside teaching comes in to play. By knowing which salient questions to ask as a discriminator to quickly get to the likely diagnosis can speed up the history taking and allows the doctor to already consider what treatments the patient is likely to require.

For example, the patient with the classical history of ischaemic chest pain is going to be questioned about the elements of the pain, its severity, its radiation, to ascertain if it is truly ischaemic or related to for example a dissecting aortic aneurysm because the treatments are different, the former being medical in most cases and the latter being emergency surgery!!

It is my opinion that training as a doctor is a vocation. When you become a doctor for the first time, you have just started on the long road to learning about diseases, their diagnosis and treatment. Medical school does not adequately prepare you for real life medicine. It neither prepares students about how to talk to patients or their families.

The best way to really make the transition is to see as many patients as possible as a student and really try and take a decent and comprehensive history including the Body Systems Review. The teaching of physical examination is really very much reliant on your teachers but you can also learn from some very good books that are available these days.

Try and practise Problem Based Learning. One UK book I would recommend is Rapid Review of Clinical Medicine (for MRCP) by Sharma and Kaushal and published by Manson Publishers. This book is available from Amazon.

Then, with this background of patients cases from real examples plus PBL examples, when you see a similar patient case in future, you should go through a similar process for the differential diagnosis and scale according to likelihood the most likely diagnosis and consider what further tests you would do and more importantly, what emergency treatments you will start.

Learn, learn, learn your medical emergencies e.g. treatment of AMI, PE, COPD, Asthma, Seizure etc.... There are many books available to do this, but I would strongly suggest you use one based on current evidence rather than on opinion.....

The ability to solve medical problems come from many years of experience and even senior doctors get it wrong on occasion because patients don't write the textbooks and doctors are human.

Good luck with your quests!

Extension for Case Result

Dear Bloggers

As you are aware, I posted a case for you to attempt to answer last week. In view that there have yet to be any replies to the case, as a consequence, I will therefore extend revealing the answers for a further week to allow you more time.

Please feel free to send in your answers anonymously.

Have a great day!

A Challenge For You All

Dear Bloggers

I have in the past presented cases and posed questions for you to answer. Today's challenge is very interesting and I would like you to post your answers on my blog for all to see and so everyone can learn.

The case has been anonymised for confidentiality as always.

A man was admitted with reduced conscious level.

He had been transferred from another hospital following a cardiac arrest on their ward. The reason for the initial admission had been vomiting and the patient was being investigated for the underlying cause. The vomiting had been occurring for several weeks following the commencement of a new Parkison's disease drug, the name of which was unknown, although that drug was eventually stopped. However the vomiting continued and the patient was developing regular vomiting of stomach contents each lunch time. The patient had never complained of much even when he had been ill in the past, so the family were unaware if he had any body pains.

The patient had a long history of constipation and had been taking medication for some time resulting in 5-6 episodes of diarrhoea daily.
The patient had not complained of any chest or abdominal pain. There was no haematemesis, malaena or haematochezia (fresh rectal bleeding). There was no complaint of any visual disturbance e.g. blurred vision, or headache (consideration of raised ICP). It is unknown whether there were any symptoms of gastroesophageal reflux (GERD).

Previous medical history included Parkinson's Disease, Constipation, Dementia, Depression and a Cerebral Infarction.

He was receiving anti-PD drugs (names unknown), Sennoside (for constipation), a tricyclic anti-depressant and Aricept.

He was a non-smoker and had previously drunk alcohol in moderation. The patient's ADLs were impaired because of the severity of the PD and he was limited to walking a few yards. However, he was nevertheless able to feed and wash himself.

The examination at the other hospital is unknown but they were investigating the suspected cause of an ileus.
The patient underwent a gastroscopy which revealed undigested food but no other abnormalities. A CT abdominal scan was also performed which revealed dilated loops of bowel but no mass lesion.

On the day of the cardiac arrest, the patient had been initially alert but soon became increasingly unconscious and then stopped breathing. A cardiac arrest ensued and he was found to be in an asystolic rhythm. He was effectively resuscitated and transferred to the current hospital. Arterial blood gas prior to the cardiac arrest revealed the following: PaO2 132mmHg, PCO2 105 mmHg, pH 7.33, HCO3 53.3, BE 23.5 (after 10L O2).

On transfer to the new hospital, his physical examination revealed the following:

JCS 300, Afebrile, pulse 50 beats per minute and regular, BP 80/60mmHg, SpO2 95% on 10L O2. Reduced skin turgor and dry mouth. No anaemia. Dark coloured, low volume urine in the catheter bag.

CVS: regular rhythm, good volume pulse, JVP not raised. Heart Sounds 1 + 2. No murmurs or added sounds.

RESP: RR 8/min, no tracheal tug or use of accessory muscles. Trachea central. Poor excursion of chest. Percussion resonant and reduced air entry throughout. No wheeze or crepitations (crackles).

ABDO: Distended, non-tender. No bowel sounds. No obvious masses. No rebound or guarding. Tympanic sound throughout on percussion. No renal angle tenderness. No abdominal hernia seen. Rectal examination-- no stool present, no mass lesion.

CNS/PNS: Pupils equal and reactive to light. Unable to perform other movements.
Moving upper and lower limbs spontaneously. Reduced muscle tone and reduced reflexes. Babinski sign negative bilaterally. Unable to test sensory or cerebellar function. Fundoscopy was not performed.

Lab Data revealed the following:

BUN 16, Creat 1.2, K 1.1, Na 134, Mg2+ 2.3, Ca 6.9, Alb 2.7, PO4 0.6, CK 850, ALT 102, AST 103, Bil 1.5, ALP 320, gamma GT 24.
WBC 38.2, Hb 9.0, MCV 82, Plt 20.0, INR 1.2

Urine revealed >100 WCC/hpf, 30-49 RBCs/hpf, 1+ protein, negative ketones, negative to glucose, 4+ bacteria.

CXR was normal apart from a raised right hemidiaphragm due to dilated bowel pushing up from below. AXR was abnormal showing loops of bowel distended with gas. No stool could be visualised on the Xray.

Questions:

1) Why did this patient develop CO2 retention?

2) Which two simple cardiac tests would you perform and why?

3) Identify as many possible reasons why this patient developed a cardiac arrest?

4) Which one urine test would you perform to investigate the cause of possible ensuing renal failure in a patient with this clinical history?

5) Taking into account the entire history, list as many causes as possible for this patient developing an ileus. Is there a Syndrome that encompasses all of these features??

6) What does the arterial blood gas show and why do you think it occurred?

Please send in your answers and in 1 week, I will publish the answers! This is not an easy case but please try and have a go-- you might just be right!

Happy sleuthing.

History is Everything-- yet again :-) !!!

Dear Bloggers

This is a case from another hospital and has been anonymised as usual for patient confidentiality.

A 45 year old lady had been playing tennis following which she had eaten lunch which included several glasses of wine. Following this, she went back to play tennis.

She developed sudden onset of lower abdominal pain which was crampy in nature. This was associated with watery diarrhoea followed by the passing of fresh per rectal bleeding only one time. The patient was so concerned that she presented to the hospital.

She had had several previous episodes of the same fresh rectal bleeding in the past and had been admitted to hospital on those occasions, and it always followed consumption of alcohol.

There was no associated nausea or vomiting.

Previous medical history included renal failure due to type 1 diabetes requiring 3x weekly haemodialysis, hypertension and paroxysmal atrial fibrillation that was refractory to recent ablative intervention.

Drugs included Valsartan, Warfarin, Flecainide, Verapamil and insulin.

She was a non-smoker and had full activities of daily living.

When she was examined on the admission day, she was afebrile, looked well, and all observations were stable.

Cardiovascular, respiratory and abdominal examinations were unrevealing except for the rectal examination. The rectal exam showed normal brown stool but occult blood was positive. There was no evidence of fresh blood !!!

Blood tests revealed normal levels of white cells, haemoglobin, MCV and platelets. INR was subtherapeutic at 1.76.
BUN and Creatinine were consistent with severe renal failure and the K was 6.5
Liver function was normal.

ECG showed sinus rhythm. No acute changes were evident.

Ultrasound scan of the abdomen was unrevealing.

Flexible sigmoidoscopy was subsequently performed which showed slight redness of the rectosigmoid mucosa but no fresh bleeding.

What was the diagnosis linking all the elements together?

Well, history here was everything.
It was clear from the drug history that the paroxysmal AF was poorly controlled as the patient, despite cardiac ablation therapy, was still using two kinds of antiarrhythmic agents. Moreover, the use of alcohol is a known precipitant of AF. The patient had suffered from this rectal bleeding problem on a total of 3 episodes and all were associated with alcohol consumption.
The INR was subtherapeutic and with PAF, the patient would be at risk of atrial thrombosis and embolism.

From the symptoms of lower abdominal pain and GI symptoms, the problem was affecting the territory of the latter transverse colon, descending colon and rectosigmoid region. The rectal exam showing normal stool with a previous bleed indicated that the bleeding must have come from an origin close to the rectosigmoid area as defecation had resulted in clearage of the blood to leave normal brown stool decending from above. Indeed, the flexible sigmoidoscopy confirmed these thoughts.

The previous flexi-sig pictures from other admissions, showed an ischaemic element to these episodes and biopsies comfirmed ischaemic colitis.

So, putting the elements of the history together with the examination, it was postulated that the patient was most likely having recurrent paroxysmal AF with resulting thromboembolism as a result of a subtherapeutic INR or ischaemia due to ensuing hypotension from fast PAF. The PAF was probably being caused by a combination of alcohol, hyperkalaemia and silent ischaemic heart disease.

However, the resident doctor thought that the patient had not had a recent episode of PAF during the tennis match. The patient was however prone to PAF during haemodialysis.

It was time to go to the bedside to take more history and then examine!

The patient was comfortable and speaking normally. On direct questioning, the patient admitted that the PAF episodes were occurring frequently and had occurred on the day that she had played tennis. In fact, this chain of questions from the senior doctor led to very interesting answers from the patient. It turned out that the patient counted her heart rate and it was irregular running at 120/min and was associated with a heavy chest feeling, radiation to the jaw and worsening paraesthesia in her fingers. The episode prior to admission also made her breathless. Following this, the patient developed the abdominal pain and bloody diarrhoea.

Examination of the heart revealed a soft systolic murmur but the patient was in sinus rhythm. Chest and abdomen were unrevealing.

In this case, it became clear that the PAF was a big problem. In fact, it was causing ischaemic symptoms to the heart and it was very possible that there was underlying coronary artery disease unmasked by the tachyarrhythmia from hypoperfusion. The PAF and subtherapeutic INR could have resulted in thromboembolism and ischaemic bowel and resulting in haemorrhage. The same would be true for an episode of hypotension resulting in bowel ischaemia from fast PAF.

On the other hand, the patient had been playing tennis. Physical activity tends to divert blood away from the gut to muscle, heart and brain etc. The patient had then eaten food requiring more blood flow to the gut after which, she went back to play tennis thereby again requiring blood flow away from the gut. With an onset of the PAF and reduction in potential blood flow, it is possible that ischaemic bowel resulted especially if there was a partial obstruction to the inferior mesenteric artery in the first place e.g. from a previous thromboembolic event or atherosclerosis.

In this case, a combination of factors were promoting frequent episodes of PAF. The potassium level was a major concern especially as she continued to be prescribed an angiotension receptor blocker to control blood pressure. Flecainide is a Class 1c agent and is can make ischaemic heart disease worse and hence, it is contraindicated in IHD!!

Using a beta-blocker to control AF and hypertension would be one option, but without knowing the cause of the bowel ischaemia could make the situation worse by exacerbating ischaemic bowel. Moreover, in diabetes, use of beta-blockers can result in loss of hypoglycaemic warning signs and hence, it would not be a first choice of most physicians.

In view of the renal failure, digoxin would not be a option as toxicity would be a real problem.

Using a calcium channel blocker (cardiac specific) at a higher dose regularly would be a option and verapamil was already being used.

In my experience, Amiodarone is the most effective anti-arrhythmic agent for AF per se. Despite its famous side-effect profile and the fear of most Japanese physicians to prescribe it, it nevertheless saves lives!
It is widely used in the UK for such difficult to treat patients and has little adverse effect on myocardial contractility. This is the drug I would have advocated in this case.

Remember that Warfarin and Amiodarone have an interaction and can cause the INR to rise.

As for investigating the ischaemic bowel, perhaps the most sensitive way would have been to do an angiogram of the mesenteric vessels. The procedure is however invasive and the patient was warfarinized and would require conversion to heparin before doing the procedure. On the other hand, a contrast abdominal CT scan might also have provided the answer.

Cardiac echo would have been essential here to rule out thrombus and if negative, a Bruce Protocol stress test to assess coronary artery disease would have been justified although failing that, a myoview scan could provide a similar answer. The gold standard of course would be a coronary angiogram.

In summary, a thorough history provided very essential clues. Simply relying on what the patient tells you is not enough. You must ask detailed and structured questions about each of the presenting complaints and previous medical history. In this case, the previous medical history of PAF was in fact, current medical history !!!!

Don't let a normal ECG fool you to exclude PAF. PAF means it is paroxysmal (intermittent) and hence, it is not always detectable !! Have a high suspicion of recurrent PAF and ask about palpitations, dyspnoea, ischaemic chest pain, and other ischaemic pains.

Always examine the drugs !! In this case, despite the history of ablation, it was clear that the PAF was uncontrolled as by definition, the patient was still taking anti-arrhythmic drugs!

Remember, STOP dangerous drugs. Examine the side effects and contra-indications. As new information becomes available you must decide which drugs should be stopped or continued or which ones to begin-- not an easy task at all.

When you think of Gastrointestinal bleeding, don't just think of localised disease such as ulcerative colitis, Crohn's or diverticular disease. Also think of system disease as well e.g. thromboembolism, systemic hypotension induced ischaemia e.g. in patients with peripheral vascular disease (ASO), endocarditis, vasculitis, congenital e.g. Aortic stenosis with bowel telangiectasia. This list of causes is wide and beyond the scope of today's discussion.

Please consider...

Congratulations Dr Aoki

Dear Bloggers

Saturday night was the celebratory party for the great Dr Aoki in respect of the publication of his revised second edition book on infectious diseases. Dr Aoki is the sole author of the book, which in itself, is a major achievement in today's medical publication era. As Prof Tierney alluded to in his speech, in modern times, the production of most major textbooks has 25-30 authors, and so a single author in a medical sub-specialty is a rarity and should be congratulated and respected. I second that.

A number of other notable business people and physicians were in attendance including Mr Matsumoto (Sakura), Professor Kurokawa and Dr Tokuda who also all made wonderful speeches.

Professor Stein sent a special telegram to celebrate the occasion and stated how Dr Aoki has contributed to the improvement of medical care in Japan especially in respect of the logical prescribing of antibiotics.

In all, about 80 people were in attendance at the party and it was wonderful to see how many friends and supporters Dr Aoki has formed over the years of hard work in promoting infectious disease medicine in Japan.

The night finished all too soon and with snow falling heavily outside, it was certainly a night to remember! :-)

I for one am hoping for the English translation of the second edition !!! :-) Now that would be fun!!

Congratulations Makoto!!!

Drugs Revisited...

Dear Bloggers

I have previously discussed drugs on this blog.

I must again reiterate the importance of not just starting drugs, but also Stopping Drugs.

There are many thousands of drugs available to use as physicians that allow us to treat a whole array of medical problems. However, on a daily basis, we perhaps use a small number to treat the most common conditions such as heart failure, angina, diabetes, infections etc...

However, although drugs have defined therapeutic effects, they may also cause adverse effects resulting in physical and psychiatric manifestations. As part of our work up of patient conditions, it is our duty to examine the list of drugs to look to see if the problem relates to a known side effect of the drug or drug combination.

Merely represcribing the drug is not enough. Knowing the drug class, knowing the common side effects and drug-drug interactions is essential. Moreover, knowing the correct dose of drugs is also necessary and to know that drug levels become altered in other diseases such as renal failure.

Carrying a drug book with you either in paper or electronic format can provide a wealth of information and help you decide whether to continue a drug or stop it either permanently or temporarily.

As real examples, a patient was admitted into hospital for work up of a skin rash. He was a known hypertensive patient for many years and had recently had the introduction of a thiazide diuretic. One month later the rash appeared which was non-painful, non-itchy, flat and purpuric-like. There were no adverse symptoms such as neck stiffness or photophobia, no diarrhoea etc.. The blood results were entirely normal with no renal failure and no rise in the inflammatory markers. The urine revealed 1+ blood only and no renal casts and no protein. The admitting resident considered this to be Henoch-Schonlein Purpura because of the distribution of the rash on the patient's arms and legs. There was also the consideration of Amyloidosis and a rectal biopsy was being planned.

The temporal sequence of commencing a thiazide diuretic and then developing a rash caused me to examine the side-effects of the drug which revealed the very top dermatological manifestation as 'purpura'!!

Hence, a trial of stopping the thiazide diuretic would have been advantageous. In the UK, a GP or hospital physician would simply stop the drug and observe and if failure occurred in resolution of the rash occurred, then further workup would be warranted.

Of course, consideration of HSP and Amyloidosis was appropriate and excluding these more serious pathologies was correct.

However, common things present commonly (drug side effects in this case) and the history was of salient importance. A common medical saying in the UK goes something like this "When you hear hooves think of horses rather than zebras."

Another case, was of an asymptomatic elderly female who was found to have a iron deficiency anaemia on her annual medical check. She had normal food intake and had not complained of malaena or urogenital tract haemorrhage.

She had a history of hypertension and amongst other drugs, she was taking aspirin. She was not taking any PPI therapy.

Her haemoglobin was 6g/dl with a low MCV of 69. Her iron levels were low with a high TIBC.

It was clear that the aspirin may have been causing asymptomatic gastritis or even peptic ulceration, which are known to occur painlessly in the elderly and which I have seen several times in the past. Moreover, she could have also had a malignancy or one of many causes of gastrointestinal bleeding. Having a negative rectal examination does not rule out chronic GI bleeding.

The resident had mistakenly overlooked stopping the aspirin when it was clearly a potential risk factor. There were more risks for continuing the aspirin than stopping it and hence, stopping the drug, either temporarily or permanently, would have been the best way forwards. That is not to say that aspirin was the actual cause of the problem, but with chronic haemorrhage, anti-platelet therapy can worsen the problem.

These two examples show that side-effects of drugs can be important even for very straight forward problems. It is important to recognise these problems and decide whether to stop drugs that can be harmful.

My advice would be to examine each and every drug on every patient you see to understand if the drug or drugs are causing the problem or at least contributing to it.

Reading about the side-effects and putting that knowledge into practise is essential.

Drug interactions are also important and carrying a software on package on a PDA e.g. epocrates (which is free www.epocrates.com) can help you decide whether there is a potential drug problem.

Please do not overlook drugs as just names on an admission sheet. Take time to look at them and the patient. It will make your workup of the patient more logical and easier to perform e.g. stopping a thiazide diuretic and observing, stopping the aspirin and arranging a gastroscopy and colonoscopy rather than performing a CT abdominal scan which might be premature or even unnecessary.

Please consider....:-)

UpDates in Diabetes Care with Potential Application To Japanese Medical Practise

The 2008 Guidelines for the Standards of Medical Care in Diabetes have been released by the American Diabetes Association.

I have endeavoured to summarize the important elements of the current ADA guidelines in addition to adding my opinion on their application to clinical practise in Japan plus any other recent evidence in support or contradicting these current guidelines to try and give an overall view of things.

Interestingly, the guidance refers to several interesting areas in particular which include:

1) HbA1c: aiming to get the HbA1c (DCCT-aligned value) as near to 7% is the goal with the aim to avoid hypoglycaemia. However, there is now the goal to get the HbA1c into the normal range if possible. The thought behind this is likely to maximise the advantage of avoiding the microscopic and macroscopic changes associated with diabetes. The HbA1c value that the ADA are advocating is to reduce it to less than 6%, if possible ,with the avoidance of hypoglycaemia.

This may of course be possible in proportionately more type 2 patients than type 1 patients as the severity of disease may be different and the former have relative insulin resistance rather than deficiency. The problem with attaining an HbA1c of <7%>

The downside to the application of such guidelines in Japan is the inability for type 2 patients taking oral hypoglycaemic agents to check their daily blood glucose levels because such monitoring therapy is not currently covered by the medical insurance system and therefore, patients are unable to know if their blood glucose levels are being well maintained on therapy or not. HbA1c measurement every 3 months is insufficient to really know if the patient is having good control. I say this because patients can have a seemingly good HbA1c result but still have frequent hypoglycaemic episodes and hyperglycaemic episodes alike.

Diabetes control can be imagined to be something like the climate and daily weather. The climate is the gradual change in temperature that beig like the HbA1c whereas the daily weather is the blood glucose level. We all know that one day there can be sun and the next there can be rain. The climate does not tell us what has happened on a day to day basis. Hence, measuring the HbA1c only tells us of an average of the glucose control over the last 2-3 months and particularly the last 1 month prior to testing. Therefore, in Japan, the clinic doctors need to ask particularly about hypoglycaemic episodes and encourage at least urine testing for glucose. However, if patients can afford to buy their own glucose monitoring kits and to manage their diabetes through empowerment and better understanding, then in my opinion, they should be encouraged to do so.

2) Carbohydrate monitoring: There is advice on carbohydrate counting and glycemic index which is of course part of the famous DAFNE thinking (Diabetes Adjustment for Normal Eating), which allows patients to adjust their insulin doses according to the amount of carbohydrate they consume. This is opposed to the traditional way of doing things where the person eats similar amounts of food every day and fixes their insulin doses. The latter can certainly work in those individuals who have a strict daily regimen, but is inflexible for young patients with hectic lives and who eat infrequently. I have seen such treatment used in the UK to good effect.

The usual regimen of insulin is the fast acting novorapid/humalog isulin for every time food is consumed and a long acting insulin at night to prevent hyperglycaemia e.g. detemir / glargine. However, such a carbohydrate monitoring regimen may not be possible in Japan because Lantus (glargine) was discontuned due to a problem of administration and as far as I am currently aware, detemir has yet to reach these shores. Hence, older regimens of longer acting insulins might be required instead e.g. insulatard, which have a shorter period of activity and can result in severe nocturnal hypoglycaemia.

Currently, some institutions are using mixed combinations of insulins e.g. novomix, three times a day with interesting results in HbA1c, in view of the lack of longer acting insulin availability, but this in my opinion, still does not provide the flexibility in insulin-food control that the DAFNE style of therapy can do. Moreover, I have yet to see any patient thus far being treated with combination of oral hypoglycaemic agent with insulin in Japan, which is standard practise in the USA and UK, with good results in HbA1c levels and reduced weight gain and lower amounts of insulin being required e.g. metformin with insulin.

3) Immunisation: The ADA guidelines suggests that all DM patients should be vaccinated for influenza on an annual basis of more than 6 months of age. Patients should also receive pneumococcal vaccination if more than 65 years of age. The pneumococcal vaccine is available in Japan and should be used in such high risk patients. I am aware though that stocks of the vaccine were previously low and hence, again, it may or may not be possible to administer such therapy depending on your local resources.

4) Lipid Management: Statin therapy should be added to lifestyle therapy (dieting and weight loss) REGARDLESS OF BASELINE LIPID LEVELS for diabetic patients:
i) with overt cardiovascular disease (CVD)
ii) without CVD who are over the age of 40 and have ONE or more CVD risk factors (e.g. hypertension, family history)

The above guidance is also in line with the International Diabetes Federation guidance (IDF) of 2005.

Statin therapy should be considered in patients with low risk if the LDL cholesterol remains > 100mg/dl or in those with multiple CVD risk factors. Aim for LDL cholesterol in those patients with low risk is less than 100mg/dl.
In patients with overt CVD, a lower LDL cholesterol level of less than 70mg/dl, using high dose statin, is an option.
In the event that LDL-cholesterol levels do not reach these targets, a reduction of LDL-cholesterol of about 40% from baseline is an alternative therapeutic goal.

5) Antiplatelet Agents:Aspirin should be used in patients with a history of CVD as secondary prevention. Aspirin should also be used as Primary prevention in type 1 or type 2 patients at increased cardiovascular risk including all patients over 40 years of age or who have additional risk factors (family history of CVD, hypertension, smoking, dyslipidemia, or albuminuria).

Aspirin is not recommended under 30 years of age due to lack of evidence of benefit in this age group and certainly not to those aged less than 21 years because of the risk of Reye's Syndrome.

Combination with other anti-platelet agents e.g. clopidogrel (Plavix) should be used in patients with severe and progressive CVD.

6) Glucose Goals: There are also guidelines for use of tight control in patients with severe illness. There have been previous trials of use of insulin in critical care patients and the overall outcome has been a benefit in survival. However, a recent German study using insulin in such patients saw a detriment in using tight insulin control.
However, when one reads the methods of the study, they measured blood glucose levels every 1-4 hours. This is a major downfall with the study leaving a potential cause for the increased mortality. In fact, when tight control is required in such patients, hourly blood sugars should be done, and a four hour delay is dangerous, in my opinion. This study was published in a famous journal and the monitoring delay, which I see as a flaw in the study design, was not addressed in the conclusions by the Authors, which is disappointing. I would not advocate a change to the current advice of tight control in critically ill patients unless there are future studies with more rigorous designs showing similar adverse outcomes.

There are many other areas of advice in the current ADA guidelines but are too much for today's blog. If you want to read more please go to Diabetes Care, Volume 31, Supplement 1, Jan 2008.

Probe Your Patients For History

Dear Bloggers

I have written about history and its importance many times on this blog and here is yet another example of why it is so important.

This case has been anonymised as usual to maintain patient confidentiality.

An elderly male was admitted into another hospital following a two-day history of chills, lower abdominal discomfort and frequency.

He had attended a local hospital in the vicinity and a UTI was diagnosed for which intravenous antibiotics were prescribed to be continued as an outpatient.

However, the chills continued and urinary incontinence occurred as a new problem prompting admission to another hospital.

At the current hospital it was elucidated that he had a long history of Benign Prostatic Hypertrophy. He had no recent sexual contacts and no change in bowel habit and no weight loss.

He otherwise had a history of ischaemic heart disease with an AMI several years before for which he had a Coronary Artery Bypass Graft (CABG), hyperlipidemia and hypertension. He had no known history of diabetes mellitus.

Medications included

• Aspirin
• Atorvastatin
• Amlodipine
• Medication for BPH (name unknown)

He was an ex-smoker and drank no alcohol. He was other wise normally fit and well.

When he was examined by the admitting resident, he was apyrexial and had normal vital sign. His cardiovascular, respiratory and abdominal examinations were within normal limits apart from evidence of a previous sternotomy scar for his CABG operation and a loud aortic systolic murmur. Rectal examination revealed a large smooth prostate which was non-tender.

Clinically the patient was admitted with a simple UTI secondary to obstruction to urinary outflow.

A catheter was inserted to drain the excess urine (residual volume unknown) and antibiotics were continued.

Up to this point, things seemed relatively straight forwards.

However, a Senior doctor reviewed the history, physical and lab data as things seemed not quite right.

There was no history about the severity of the urinary outflow symptoms. Moreover, the lab data revealed evidence of a raised CK of about 350 (normal CK-MB) and some mild renal impairment BUN 25, Creat 1.4. Previous blood tests several years ago also revealed a mildly raised HbA1c of 6.4% and a follow-up was normal.

The ECG had T wave inversion from V3-V6 inclusive and it had been initially considered to be old except when it was compared to a recent ECG within the last few weeks, and the current tracing showed NEW T wave inversion in V3 and V4 inclusive.

There was a high suspicion of an Acute MI. However, the resident clearly stated that the patient had not complained of any other problems.

The Senior doctor nevertheless went back to the bedside and asked the questions again. On this occasion, the patient had said that he had become breathless, with central heavy chest and leg pains, with him almost having lost consciousness. The pain was described in severity as 10/10 and lasted for up to 1 hour. There was no radiation to the neck, jaw, arms, back, or abdomen and no sweating or vomiting.

Asking about the urinary symptoms, the patient mentioned that he only passed very small amounts of urine, had frequency and felt he never had completely voided his urine in some time despite treatment for BPH.

Hence, from the history, it would appear that the patient was experiencing an Acute Coronary Syndrome several days prior to admission which might account for the new ischaemic ECG changes and raised CK.

Most people will now think, hey, the CK-MB was normal, so not an acute coronary syndrome! No! The serum levels of CK drop rapidly within 24-48 hours of an MI with other markers such as LDH and Troponin T remaining raised for much longer periods, the latter for up to 10 days post-infarct. Hence, it is of no surprise that the CK-MB fraction might be normal at the time of presentation to hospital.

In view of the previously raised HbA1c, it is also plausible that the patient had undiagnosed diabetes. In fact, the American Diabetes Association states that HbA1c should not be used to diagnose diabetes as a significant number of people even with normal HbA1c can still have diabetes-- it is not a fool proof test for diagnosing diabetes.

Also, having DM might also put the patient at increased risk for development of a UTI on a background of urinary outflow obstruction.

On examination the patient indeed had a loud Aortic Ejection systolic murmur with radiation to the carotid arteries in addition to left renal angle tenderness on bimanual palpation.

PROBLEM LIST

1) Outflow obstruction from BPH
2) UTI due to 1 above with complication of pyelonephritis
3) Likely Acute Coronary Syndrome ? Aortic Stenosis
4) Possible undiagnosed Type 2 DM

SUGGESTION

The senior doctor suggested the following;

• Obtain Troponin-T level
• Add Clopidogrel ( this is advocated for use in NSTEMI and was proven to be more effective when combined with aspirin than just aspirin alone in the CURE trial; a newer analogue is being trialled at present in the USA with even better anti-platelet effects when combined with aspirin)
• Increase the Statin dose (a recent meta-analysis of 14 Statin trials in Lancet 2008 has suggested that benefit from statin therapy occurs in diabetic and non-diabetic patients to the same level with the most benefit derived from patients with high LDL-cholesterol levels; however, all patients benefit with cholesterol lowering therapy independent of starting level of cholesterol. The meta-analysis suggests that for every reduction of 1mmol/L LDL-cholesterol there is a 20% reduction in cardiovascular events. Moreover, there is no lower level of cholesterol which to attain. The ADA guidelines of 2008 suggest that statin dose should be used to the maximum tolerated dose to reduce cholsterol as low a possible e.g. below 70mg/dl in patients with known cardiovascular disease.
  
• In Japan, I have often heard doctors stating that the cholesterol has reached normal levels or is normal to start with, and that they do not need to start or increase the statin dose despite the patient having had a new coronary event with them being at high risk. The international medical data and current guidelines suggests that a normal cholesterol can still be a risk, and hence, statins should be commenced or increased in 'at risk' patients. Moreover, use of statins is an acute treatment in AMI and not only helps to stabilise atherosclerotic plaques, there is also some data that it can increase the success rate of delayed PCI therapy.
• Consider switching the calcium-channel blocker (amlodipine) to a beta-blocker. The thought behind this was, firstly, the blood pressure systolic value was about 100mmHg and further anti-hypertensive therapy on top of the calcium blocker might result in hypotension and cause worsening angina. Moreover, the pulse rate was about 80 per minute. This is not ideal in patients with ischaemic heart disease. Use of beta-blockers reduced heart rate (improving blood flow time) and vasodilates the coronary arteries. They also have the effect of reducing ventricular rupture and can treat dysrrhythmias unlike a peripherally acting calcium blocker that has little chronotropic effect. A beta-blocker with both alpha and beta effects might also be useful in that it might help with the prostatic hypertrophy too.
• Obtain an echocardiogram
• Discuss with the cardiologists about a coronary angiogram
• Discuss with the urologists about a long term catheter or an operation (TURP); but to remember that an immediate operation would be contra-indicated in light of a possible ACS.
• Screen patient for diabetes with fasting blood sugar and perform an oral glucose tolerance test (the Gold Standard test for diagnosing DM).

Additional Results

The Troponin was positive at 0.72 thereby confirming an Acute Coronary Syndrome in this patient and this therefore was a contra-indication to any planned urological interventional surgery that might have been considered.

Indeed, the echocardiogram confirmed a good systolic wall motion. However, it also revealed an Aortic Valve gradient of 0.6cm2, and a maximum ejection pressure of 78mmHg with an average of 49mmHg consistent with Severe Aortic Stenosis.

It is usual for testing of DM to be performed several weeks after an AMI, unless the hyperglycaemia is obviously present and with DM then easy to diagnose, because of the phenomenon of stress hyperglycaemia. As AMI is a strong stressor, hyperglycaemia can occur but when patients recover, a significant number return to normoglycaemia in the post-infarct period.

Summary

In this case, the patient had symptoms of an obstructive uropathy with infection. The admitting medical doctors had failed to obtain a thorough history of ischaemic heart disease despite a previous history of the problem and with the patient having had a CABG. Moreover, the ECG and raised CK had not been fully appreciated.
With a thorough history retaken at the bedside with focused questions to rule in or rule out ischaemic chest pain, it was possible to elicit salient information from the patient to thereby determine that there was a likely ACS.
Indeed, with a positive Troponin T and with severe aortic stenosis being found, it is likely that the stress from the infection resulted in coronary ischaemia by means of cardiac outflow obstruction and atherosclerosis as the demand for increased blood flow could not be met.

In patients >70 years of age, the usual cause of AS is due to atherosclerotic-like changes of the tri-leaflet valve itself. Many features affecting the valve are similar to atherosclerosis but use of statin therapy does not reverse the changes, which can otherwise occur with atherosclerotic plaques in main blood vessels. Moreover, analysis of excised valves can also show bone and cartilage formation too !!
In the younger age group <70>40mmHg is consistent with severe AS (please see UpToDate 15.3).

Patients with severe aortic stenosis tend to suffer with the following problems:

1. Ischaemic chest pain e.g. angina, AMI
2. Syncope / Dizziness e.g. fall in cardiac output under stress
3. Heart Failure, as an end-stage complication

This patient had already suffered the first two symptoms in addition to echocardiographic proof of severe AS. In view that the patient was otherwise in good health, he was referred to the cardiothoracic surgeons for workup of an aortic valve replacement.

In view of the patient's advanced age and the antecedent risks of anticoagulation with mechanical valves, it was felt that a bioprosthetic valve would best suit this patient and he underwent successful valve replacement.

Moral Of The Story

The moral of this story is, don't ignore ECG changes and always compare ECGs to old ones for new changes when possible.
Never accept a raised Creatinine Kinase (CK) as trivial and always try to elicit a cardiac history in such circumstances especially when there is a previous history of such problems. Even if there is no obvious history but the suspicion of an acute coronary syndrome is high, a Troponin T should be always measured (at a minimum of 6-12 hours after the onset of any cardiac sounding chest pain).
I am afraid that using CK-MB to rule out MI is simply too unreliable and if you just use this, you WILL MISS Acute Coronary Syndromes. Troponin-T is cardiac specific but moreover, it is more sensitive a test than CK-MB and remains elevated for longer than CK.

In the presence of an aortic systolic murmur, dizziness, ischaemic chest pain, and new ECG changes consistent with an ACS, severe aortic stenosis should be considered, as it was in this case.

Hence, an apparent simple UTI turned out to be a blessing in disguise for this patient because a life-threatening cardiac condition was identified, investigated and effectively treated.

Lastly, do not expect your patients to simply tell you every aspect of their history and health. Many patients forget things and do not think unrelated events are important. It is up to you as doctors to ask the questions. The questions can be asked as part of a Body Systems Review which I have discussed at length on this blog already. For information on the Body Systems Review, please search under this topic at the top of this blog page. I would also recommend the book 'The Patient History- Evidence Based Approach' by Professor Lawrence Tierney, Lange Publishers.

Please consider....

A Benkyokai Bonanza

Dear Bloggers

Yesterday afternoon saw two acclaimed speakers attend our institution to teach the residents their wisdom.

Firstly, Professor Alan Lefor, Professor of Surgery, Jichi University presented talks on Trauma followed by Surgical Site Infections.



Professor Lefor's strident and direct approach were refreshing and it was interesting to see evidence based practise at work.

There was the presentation of several cases from the United States which showed trauma surgery at work.

There was emphasis on ATLS, including the elements of ABC, reassessment, D, E an so on.

The residents were very receptive to this different approach to teaching.

The talk on Surgical Site Infections presented the current evidence for use of antibiotics, warming the patient, not shaving patients, etc...

The two-hour set of talks were very interesting and Professor Lefor's talks are certainly well worth it!

Next was Dr Kitahara of Keio University who is also American trained with specialist interests in Infection and Haematology.

He was presented several difficult and unusual cases by the Department of General Internal Medicine and it was interesting to hear his view on the cases.



All in all, the two speakers provided an excellent opportunity for the residents of our institution to get up-to-date training on both surgery and medicine alike.

It was a really good day of teaching and it was enjoyed by the residents and myself alike.

TropT or Not To Be- That is the Question

Dear Bloggers

This case clearly demonstrates that one should always take the Troponin T level seriously even in the presence of renal failure.

The case is from an international hospital outside of Japan and it has been anonymised for patient confidentiality.

A female patient was admitted into another hospital with appetite loss.

She was a known heavy drinker and smoker with a history of poorly treated diabetes mellitus and hypertension.

She had become abruptly unwell one week before with appetite loss and apparently little other symptoms. She had refused to take food or water and four days prior to admission had stopped taking her medications.

She denied nausea, vomiting, jaundice, abdominal pain, constipation, diarrhoea, weight loss, cardiac and respiratory symptoms.

She was taking Acarbose and Perindopril and she had no drug allergies of note.

Family and social history were unknown.

Physical examination by the resident was apparently unremarkable including the vital signs.

However, chest Xray revealed evidence of an enlarged heart and signs of heart failure as evidenced by upper lobe diversion of blood.

Laboratory data revealed evidence of renal failure with a BUN 100 and creatinine of 3.2. Na & K were normal.
Liver function was abnormal consistent with an alcoholic hepaitis picture.
Blood sugar was 350.
Serum and urine ketones were negative.

CK was 1000, CK-MB was normal. Troponin T was 2.1

ABG revealed a compensated metabolic acidosis. Bicarbonate was 18 and BE -4. Lactate level had not been measured.

ECG revealed ST elevation on a background of a wide QRS complex

Senior doctors reviewed the patient and it was considered that the patient might have developed an acute coronary syndrome plus or minus diabetic ketoacidosis aside from the alcoholic hepatitis.

However, a junior resident had discussed the case with a cardiologist from another hospital by telephone, and had therefore not been able to see the patient, who considered the raised Troponin-T to be as a result of the renal impairment in the absence of an echocardiographic report.

The patient was re-examined and a pan-systolic murmur was heard near the apex of the heart with loss of splitting during respiration.

Nevertheless, it was still considered highly likely that an Acute Coronary Syndrome had occurred, as it had not been ruled out, and an echocardiogram was performed.

The echo clearly showed diffuse hypertrophy of the myocardium but with an infero-apical area of hypokinesis and rupture of the interventricular septum to a size of 5-6mm.

The renal ultrasound scan ruled out obstruction and showed the kidneys to be of normal size suggesting that the insult on the kidneys was acute rather than chronic.

IMPRESSION

1) Silent AMI due to severe, chronic diabetes mellitus
2) Rupture of myocardium due to 1 above
3) Pre-renal +/- intrinsic renal dysfunction
4) Metabolic acidosis due to AMI (lactic acidosis), renal failure, hepatic damage

Moral Of The Story

MI can present in atypical ways. In this case, the patient lost her appetite ! The diabetes contributed to the 'Silent' nature of the cardiac event. Despite renal failure being present and there being a raised Troponin-T, it does not rule out the presence of a new AMI. Certainly there have been many studies showing that renal failure increases the Troponin level correlated to the degree of renal impairment, but such patients are in fact, high risk for myocardial events in any case. Hence, a Troponin-T in renal failure has to be taken seriously and not overlooked as merely trivial.

Moreover, the idea of DKA is good because AMI can precipitate DKA in a diabetic although that is typically in Type 1 patients rather than type 2 patients, which the patient was not in this case.

The criteria for DKA are as follows:
pH < 7.3
HCO3 <15
BE > -10
Blood sugar > 200mg/dl (>11.1mmol/L)
Ketones +/++/+++ on the urine dipstick

This patient had none of the above except for the raised glucose and hence, DKA seems actually less likely in this patient.

However, renal failure with a myocardial infarction and hepatic damage seem more likely the causes of the metabolic acidosis and the fact that there was respiratory compensation goes somewhat against DKA. Most DKA patients are severely ill with Kussmaul respiration at presentation and they rarely attain a respiratory compensation. Moreover, the time scale is not compatible with DKA. This patient had a one week history of illness whereas most DKA patients (particularly type 1 patients) present within hours !

So, in summary, do not overlook the Troponin T in patients with renal failure especially when there are additional ECG changes consistent with Acute Coronary Syndrome. The raised CK and abnormal ECG were new problems, and every problem must have an assessment and a plan. You must exclude cardiac causes first. Do not let the opinions of other deter you from doing a thorough investigation of causes when the index of suspicion still remains high.

Have a great weekend !!!

Should Medicine Become Protocol Driven??

Dear Bloggers

What are medical protocols and should we be using them?

Medical protocols are a step wise guide to treating a vast array of conditions based on current evidence and moreover, on the provision of local services. We have all seen medical textbooks with 'their way' of doing things, and then pick up a different textbook to find that it is done slightly differently in that. With so many doctors using so many different opinions, it is sometimes difficult to know which one to choose. Do we base our final decision on how many grey hairs the senior doctors has or do we base it on evidence derived from trials and case-reports??

In a medical world of constantly changing medical information, it is sometimes difficult to remain up-to-date. It is important to remain appraised of new information because patients benefit directly from it. However, if we are all doing things a little bit differently, we should consider adopting a single way of 'best practise' so that there is standardisation throughout departments and throughout hospitals to ensure a basic and sustained uniformity of basic treatment.

Such methodologies do exist. Many UK hospitals have protocols for DVT, PE, Cellulitis, AMI, Stroke, Community Acquired Pneumonia etc... which are rigorously followed to be compliant with the modern evidence based practises. Hence, nevertheless who is on duty and nevertheless to the time of day or night, the basic standard of best practise can be applied.

I for one, having worked night duties, it was sometimes difficult to remain thinking clearly, quickly and precisely at 3 o'clock in the morning, and hence, following protocols for common medical conditions ensured that the work-up and treatment were followed appropriately and accurately. This can be especially useful for junior doctors who may not be accustomed to all the medical processes for safe patient care.

These types of protocols are especially good for the management of antibiotic use in the hospital inpatients and in the outpatient clinic. A protocol based on local resistance rates, severity of illness, and of course, cost to benefit, are used in many hospitals to guide the physicians on what they may be allowed to prescribe. Hence, most hospitals will not allow drugs such as the carbapenems to be utilised unless specified by a Consultant. More traditional antibiotics are used in combinations to provide effective broad spectrum cover and this cuts down on the abuse of antibiotics plus gives definite rules to the doctors on prescribing. In a World of ever expensive treatments, being cost effective is now very important. Protocols can help with this process.

Some may say that they do not want their autonomy taken away from them and they should have the ability to make changes and do things the way that they see fit. Indeed, for a seasoned senior doctor, the use of a protocol may not be necessary because they may have the knowledge to know what treatments should be administered and why. This is not the case for junior doctors who are simply trying to survive the long nights of sleeplessness and barrage of the daytime problems. The use of a protocol to guide them exactly how it should be done is both helpful and safe.

If a problem was to occur, then the junior doctor would also have the legal protection that they had followed the pre-specified hospital protocol.

Of course, not all things in medicine can be fastened down to a rigid protocol as there needs to be leeway and flexibility. However, for common medical problems as I have laid out above, the use of hospital adopted protocols that are available on every ward or outpatient in paper or electronic format can ensure that any doctor can appropriately investigate and administer the correct treatments at any time of day or night.

I for one have trained in a system that began to adopt the protocols for medicine several years ago and I found it extremely helpful.

Please consider... :-)

An example of Good Practise

Dear Bloggers

Having travelled to Hokkaido recently, I was able to see an example of good practise at the hospital to which I went.

The medical team who is headed by Dr Kaneko, run a Ward Round based system whereby all medical patients are reviewed daily by the senior physicians along with other staff doctors, junior residents, nursing staff and ancillary staff such as the speech & language therapist. This multi-disciplinary approach is excellent, as it is possible for all members of the team to understand the current clinical problems and of course, the social problems of patients to thereby be able to comprehend the full picture of the patient's current state.

This is an excellent example for learning at the bedside and making decisions based on history, physical and review of laboratory and radiological tests.

The fact that the patients are seen daily by senior doctors is a safe-guard for the patients in case errors are made by less experienced physicians or difficult-to-make decisions are required.

This is a very similar system to that of most UK hospitals whereby all medical patients are seen daily and where the Consultant will see the patients several times per week.

However, some hospitals in Japan do not have such a Ward Round based system whereby junior residents have to muddle through due to a lack of senior support. Moreover, medical meetings are held away from the bedside so that only history and physical, derived from perhaps an inexperienced junior resident, is heard, and decisions are then based on that plus the usual laboratory and radiological tests. There is of course no way to know if the resident has interpreted the history or physical findings correctly which thereby allows potential inaccuracies to become propagated through the inpatient stay unless the errors are identified early by a senior physician.

Such a no-hands-on approach can lead to errors which an experienced eye may pick up and soon avert.

In view that history taking and physical examination are not emphasized heavily in most Japanese medical schools, how can one expect junior residents to realistically pick up all the problems effectively?

Unless the emphasis of medical student training can be changed to reflect the changing needs of medicine, then the emphasis needs to be focused heavily on junior resident training.

Hence, a hands-on review by the senior doctors is essential to prevent mistakes being carried through into an admission and to teach the junior doctors appropriately to prevent the same problems occurring again in the future. A ward based approach is extremely important for the patient and for the resident training, rather than looking at numbers and pictures in a closed room. Some things cannot always be explained and it therefore requires a visit to the bedside to understand the problems.

Such senior doctor-led ward rounds of all the medical patients, a so-called 'business round' in the UK, is great for passing on 'gems' of information to the junior doctors with respect to history, physical, natural history of the disease and treatment plus how to understand the management of multiple clinical problems. Unfortunately, most books of clinical medicine deal only with distinct diseases rather than diseases in combination which a great number of patients have. That is the downfall of clinical books. However, the best teacher for this type of medicine comes from the Ward Round based teaching and discussion of evidence and experience of previous patient examples.

I, as a junior doctor, found it very helpful to also see the approach of the Consultants and how they dealt with difficult situations, such as telling bad news. To see how the different approaches worked allowed me to learn a great deal and to emulate the good examples. To see how the patients were treated with dignity and respect was also a good learning experience.

We do not start our lives as doctors and we are all human beings at the end of the day. Just because we become a doctor with a license does not mean we have all the necessary knowledge to manage patients at the start; far from it. We all need good role models to learn those things which are in no book, cannot be written down and can only be gained by approaching with a senior doctor to the bedside of the patient and seeing together. This is the basis of a medical vocation.

I think the experience in Hokkaido reminded me that there are many different ways to practise Medicine in Japan in addition to other good ways to learn medicine too.

Keep up the good job!

Have a great day....!

An interesting brain teaser

A patient was admitted to another institution with fever. She was a poor historian due to a background of dementia. Hence, obtaining a thorough history was not possible and moreover, the patient did not complain of any problems.

The fever had been going on for several weeks and was not associated with chills or rigors.

There was no respiratory,abdominal or urinary symptoms. There were no complaints of joint problems or skin problems. There was no facial or ear pain. There was no history of dental work or recent gastrointestinal endoscopic examinations.

There was no history of other people developing such fever in her nursing institution.

Her previous history included dementia, type 2 diabetes, hypertension and hyperlipidaemia.

She took voglibose, amlodipine and atorvastatin only.

She had no relevant family history of note.

On examination

Fever was 39 degrees and the patient looked well. She had digital clubbing.No splinter haemorrhages or Janeway lesions.

CVS: pulse 100 per minute, regular, BP 110/70mmHg, JVP elevated to her ears, heart sounds normal.Peripheral oedema ++

RESP: Respiratory rate 16/minute, Sats 95% on room air, tracheal central, no lymph nodes, bilaterally decreased air entry at both bases posteriorly.

ABDO: Soft, non-tender, no organomegaly, normal bowel sounds,no renal angle tenderness or suprapubic tenderness, rectal examination normal.

MUSC: No joint pain or swelling, no evidence of DVT.

Examination of the urine in the draining Foley catheter revealed murky fluid.
The catheter had been in situ for several weeks.

IMPRESSION

The impression was of a urinary tract infection causing the fever and grossly abnormal urine.

There was also evidence of chronic heart failure

RESULTS AND DISCUSSION

The urine examination revealed 3+ bacteria and 3+ fungi.

It was initially considered that the fungi were present due to long term catheter placement. However, the bacterial component of the urine was treated initially with meropenem, then ceftriaxone and finally with vancomycin without a specific culture result being present.

Despite these antibiotics being used, although the urine was cleared of bacteria, the fever continued unabated!!

Hence, it was considered by the attending physicians that the fever was due to some other reason.

A series of computed tomography scans was engaged but they just confirmed the presence of congestive heart failure. The effusions were small and hence, it was difficult to attempt aspiration of those.

Echocardiogram was normal with no vegetation.

A senior physician was asked to help elucidate the cause of the fever and suggest treatment.

The attending physicians were unable to fathom why the CRP was negative despite the fever.

The senior doctor reviewed the history, physical and reviewed the laboratory data and scans.

It became clear that there were two urine analyses that showed a heavy presence of fungi. Moreover, the patient was diabetic with a catheter in situ.

It is not uncommon in the elderly to have fungal and bacterial contamination of the urine in chronically catheterised patients. However, when there are symptoms such as a fever and tachycardia, such contamination may actually be causing infection.

In this case, several broad spectrum antibiotics were used without resolution of the fever despite resolution of the bacterial infection.

It was suspected that the cause of the fever was a fungal urinary tract infection. Risk factors for this included being an elderly female, catherterised and being diabetic.

This type of problem is called antibiotic non-responsive infection and with fungi being present in the urine, and evidence of infection e.g. fever and tachycardia, such organisms should not merely be considered as contaminants.

The usual cause is candidal species and blood cultures are frequently unhelpful.

Treatment should include Fluconazole 200mg per day for 14 days or if non-responsive, due to resistance, Amphotericin B or 0.5mg per Kg for 7-14 days or Caspofungin.

The catheter should also be removed if possible.

In view that Fungal infection of the urinary tract can cause Bezoar formation and therefore cause obstruction, a search for such entities should be considered by ultrasound or CT of the urinary system and consideration of cystoscopy of the bladder.

In view of the digital clubbing, which can be caused by infective endocarditis, and because of the persistence of fever a repeat echocardiogram was advised.

The workup of a Fever of Unknown Origin can be difficult. Usually a good history and physical examination can provide several clues. However, in this case, no helpful history was obtainable and physical examination was not particularly revealing.

However, as with all FUOs, infection should always be ruled out first.
The longer a fever continues without an obvious source of infection being found, the less likely it is that it is an infectious cause, and therefore, no infectious causes should be considered.

Always remember that infections are not just bacterial. The can occur from viruses, fungi and protozoa as well. Laboratory results should always be compared to the patient's clinical presentation and whether such results are consistent with infection or not. Usually, the presence of fungi in the urine is of no consequence, but heavy colonisation, peristent fever and tachycardia despite antibiotics should raise the question of fungal UTI.

CRP- Cannot Rule out Pathology

The CRP was negative in this patient which proved to be an unhelpful test. CRP can certainly help guide investigation and treatment, but it is non-specific and can be negative in the elderly despite overwhelming sepsis. CRP is in my opinion, over used and overly relied upon by many physicians. It is more important to look at the patient than the CRP as the patient is the best model and when you treat a patient, you are not treating the CRP you must treat the patient.

CRP is predominantly a marker for inflammation/infection. It can be raised by many processes such as infection, malignancy, coronary artery disease and collagen vascular diseases. It shows that there is a problem but it is a non-specific marker. Reliance on non-specific tests can lead the physician into a false sense of security and lead to misdiagnosis. Absence of CRP does not mean that there is no problem and immune suppressed patients may not mount an appropriate response to an infective organism.

Broad Spectrum Antibiotics-- carBapenems Shall Avoid

The use of such broad spectrum antibiotics in this cause is also inappropriate. There are many other antibiotics that can be used for infection of the urinary tract that are very effective. The patient could have been given a penicillin drug such as amoxicillin-clavulanate or a second generation cephalosporin plus gentamicin initially rather than using a carbapenem. The problem with using carbapenems is inducing resistance. This should be avoided. Once there is resistance to the carbapenems, no penicillin/cephalosporin will work-- not a nice thought.

Use of fluoroquinolones is also another good option such as ciprofloxacin or levofloxacin. The use of Trimethoprim orally can also clear a bacterial infection and in fact, it is the antibiotic of choice for UTI by general practitioners and hospital physicians alike in uncomplicated urinary tract infections in the UK.

The fact that Vancomycin was used for potential MRSA urinary infection is a surprise. Vancomycin can indeed be used for urinary infections and sepsis syndromes, but MRSA UTI is not common and moreover, it had not been grown from the urine culture or blood cultures. It would seem suprising to find this and once again, going back to the patient, she looked well. Most patients with MRSA bacteraemia are very sick and in this case, MRSA would be less likely.

The take home message today is:

• In patients with antibiotic non-responsive urinary infections, consider ruling out fungal infection. Remove urinary catheters if possible in fungal infection and consider a fuller examination of the whole urinary tract.

• Try not to rely on CRP as it is a non-specific test; use your patient as a guide instead.

• Use of antibiotics should be with combination of more traditional antibiotics first giving broad spectrum cover and then narrowing the spectrum once culture results are known. Try not to use the carbapenems as first line to reduce emergence of resistance. Use of Vancomycin should be considered in the context of the clinical situation e.g. is the patient sick? is the focus possible in the organ system you have identified? has MRSA been identified etc...

Hokkaido Revisited In The Snow!!

Dear Bloggers

Yesterday saw my return to Hokkaido to teach the resident doctors on history and physical examination.

On arriving I was delighted to see it snowing. It has been many years since I have seen real snow and to see the beautiful white blanket covering much of the terrain was very pleasing.



The afternoon started with rounds seeing all the medical inpatients with a short medical history and discussion of the current problems. It was good to see medicine being practiced to a good standard. I was able to provide my alternative opinion on several patients which I hope my have helped with their future workup.

Moreover, the second session was composed of a case history and physical examination. I cannot reveal the case on this blog due to anonymity but suffice it to say, it was a rare problem and something that you as physicians may only see once in your working life times! Through history and physical in addition to review of the laboratory results and radiological scans, I was able to offer an informed opinion on this complex problem.

Lastly, I provided a lecture on the serious problem of acquired severe cardiac valve disease. This was supplemented with a case vignette from a real scenario. The purpose was to show the residents what is expected when asking about non-specific symptoms. Because the specificity of such symptoms is low, one has to ask many varied questions to ascertain some idea of which system is contributing to the problem. In doing so, one may then focus of potential positive areas of the physical examination.

After this 5 hour total session, we went out to enjoy a nice evening with great food, great beverages and of course, great people.

We ended the evening with a trip to an open air onsen with the outside temperature of minus 7 with snow all around us on the ground and also falling from the sky....The perfect way to end a perfect day.

Today involved contributing to the elucidation of a fever of unknown origin in a bed ridden patient who was otherwise asymptomatic. After many investigations and scans, a cause had not been identified. No history of relevance was obtained from the patient but physical revealed digital finger clubbing, leg edema, and probably urinary tract infection. Hence, the possibilities of infective endocarditis came to mind despite the absence of an audible murmur.
Moreover, malignancy was a possibility as well. The patient also had bilateral effusions although too small to sample. However, one should always entertain the possibility of chronic pulmonary embolism which can cause a fever and mimic infection.

Finally, I returned to the warmer climates.....a whirlwind trip with great delights.

Don't Ignore Your Patient's Symptoms

Dear Bloggers

I hope that you find this next case interesting. It has been anonymised as usual.

A patient was admitted to a hospital following worsening of nausea, vomiting, and fatigue.

She had been seen at several other hospitals over several months for control of her rheumatoid arthritis for which she took predisolone and tacrolimus.

It was noted that her renal function had gotten slightly worse and it was considered to be a result of the tacrolimus, which is nephrotoxic, and it was therefore stopped.

However, the renal dysfunction did not resolve and she was seen at another hospital where no further investigations had been instigated.

Her symptoms of fatigue, nausea and vomiting were worsening and the patient was advised to attend the hospital's ER department if symptoms worsened. Indeed, those symptoms did in fact worsen and she was then admitted to a different hospital.

When a fuller history was taken it was revealed that

• She was increasingly breathless on exertion over several months. She was unable to walk for more than 10 minutes on the flat and when at home, it took her 10 minutes to walk up 13 stairs whereas previously she could do the stairs without problem. Her legs and face had also become swollen.
  
• She had noticed a change in her bowel habit with alternating constipation and diarrhoea for one month. She had noticed no blood but the stool colour was yellow.
• She had lost her appetite over several months and her weight had decreased by 5 kilograms
• Several months ago, her urine production suddenly decreased compared to usual and she had become worried by this. She attended a different hospital and this was blamed on tacrolimus therapy, which was stopped.

Previous medical history included operated right sided breast cancer with localised radiotherapy, RA, Sjogren Syndrome, hypertension, mild chronic renal failure and hyperlipidemia.

She had been taking tacrolimus, but was still taking prednisolone, H2 blocker, aspirin, an Angiotension Receptor Blocker (ARB), and a calcium channel blocker (CCB) and atorvastatin.

On further questioning, she had only ever been on prednisolone before taking the tacrolimus therapy for the RA.

There was no history of diabetes.

She was a non-smoker.

On examination

She was afebrile, looked unwell and had an obvious 'moon face' and thin skin with subcutaneous haemorrhage consistent with long term steroid administration. She had finger clubbing.

CVS: Pulse 100/min, regular, JVP not raised. BP 160/80mmHg. Heart sounds loud 1 and 2. No murmurs evident. There was pitting edema to both knees.

RESP: Obvious operation scan on right chest. Resp Rate 20/min. SpO2 96% on room air. Percussion was dull posteriorly at both bases with reduced tactile vocal fremitus.bilaterally . Auscaultation revealed crepitations throughout both lung fields.

ABDO: Distended. Hard non-tender mass in the right iliac fossa with no cough reflex. Supra-umbilical region revealed an obvious tender mass. Percussion of the mass produced a dull note. There was no rebound or guarding over the area of the mass. There was no loin tenderness.
Percussion of both flanks revealed a dull note with evidence of shifting dullness.
Bowel sounds were present.
There was an obvious arterial bruit in the right lower quadrant.

Musculoskeletal examination revealed classical RA features of Z deformity and Swan-neck deformity. Otherwise, other joints showed normal range of movement. There was no evidence of any flare of the RA.

Impression

The positive features from the history include the following:

• Nausea
• Vomiting
• Appetite Loss
• Weight loss
  
• Facial Swelling and Leg swelling
• Change in bowel habit
• Yellow stool and a tender mass in the supra-umbilical area
• Bilateral effusions
• Probably ascites
  
• Abdominal bruit
• Right lower quadrant mass
• Previous breast cancer
• RA and Sjogren's syndrome
  
• Use of steroids, tacrolimus
• Use of ARB and aspirin
• Use of a statin
  

The change in bowel habit, the yellow stool, an abdominal mass, nausea and vomiting, ascites suggest malignancy perhaps of the pancreas or biliary system e.g. cholangiocarcinoma. Yellow stool could represent steatorrhoea from a malabsorption process e.g. pancreatic insufficiency or small bowel problem e.g. coeliac sprue. In view of the autoimmune disease association with coeliac disease and its association with lymphoma, it is a possibility at best although it is unlikely in view of its higher predominance in Caucasians from Europe e.g. Ireland.

The history of a sudden reduction in urine could have been due to the tacrolimus, from renal failure although at the time when it was stopped, the creatinine was 2.0. However, if the patient had had a fuller history and examination taken, it would have become clear that with a mass present, an obstruction to urinary outflow was perhaps more likely to be the problem.

Moreover, with the presence of an abdominal bruit and with the patient being on aspirin and an ARB, the latter drug can cause renal failure through the reduction of renal perfusion. Aspirin is known to be nephrotoxic by its action on the reduction of the vasodilatory prostaglandins in the kidney. Both drugs should have also been stopped once it was established that the renal failure was progressing without a known diagnosis.

The history of breast cancer is important because the history would suggest from operation and radiotherapy that the original tumour was invasive and hence, the possibility exists of metastatic disease.

The history of RA and Sjogrens is important here because RA causes immunosuppression (along with the drugs that also treat this condition). Moreover, RA is associated with Sjogrens syndrome. Patients with Sjogrens >7 years can increase the likelihood of developing Lymphoma. This patient admitted that she first developed absence of tears 20 years before suggesting that the problem had been in existence for more than 7 years. Moreover, the use of immunosuppressive drugs can interfere with cancer surveillance by the immune system thereby increasing the likelihood of developing a malignancy.

One should also consider the possibility of a pancreatitis as a cause for the mass. Pancreatitis can cause an inflammatory mass. The use of steroids and a statin can both induce pancreatitis.

In fact, this patient had a mildly elevated amylase and ALP level. The BUN and creatinine were 80 and 6 respectively with a K of 5.6 and Na of 124. A mild anaemia was also present. Bilirubin was normal.

Abdominal ultrasound revealed a dilated right kidney from a hydronephrosis and a small left kidney.

Abdominal CT scan revealed the same information plus the presence of ascites and a mass in the location of the pancreas.

Chest Xray revealed bilateral pleural effusions as found by physical examination.

Clinical Problems

1) Severe Renal Failure through combination of likely ureteric obstruction, and drug induced actions on a background of possible renal artery stenosis

2) An abdominal mass - likely pancreatic, although lymphoma, metastatic breast cancer and cholangiocarcinoma were also possible candidates

3) Fluid overload from renal failure causing non-cardiogenic pulmonary oedema.

4) Lower abdominal mass ? cause ? incarcerated bowel

The patient underwent further workup to investigate the above causes.

What is important here is to ask the right questions and not to make assumptions.

If the above detailed questions had been asked, e.g. weight loss, bowel habit changes etc.., then the severity of the problems could have been better appreciated. Moreover, the physical examination findings of the abdomen were inescapable with the presence of a mass.

Taking time with eliciting a more thorough history, and examining the abdomen adequately can be difficult in a busy outpatient clinic when you may have only 5 minutes per patient. However, asking questions which may flag up serious problems such as change in bowel habit, constipation and diarrhoea, yellow stool, weight loss (despite edema being present), sudden and reduced urine output with a background history of malignancy, autoimmune disease and use of immunosuppressive therapy requires more investigation than just following a patient in the outpatient clinic.

As a bare minimum, in a situation such as this, tacrolimus levels should have been taken in addition to stopping the drug. Moreover, aspirin and the ARB should have also been stopped. An ultrasound scan of the kidneys, ureters and bladder would be the next step, which is quick and easy to perform. Investigation of the abdominal mass would have also been with an ultrasound scan followed by CT.

For further information on stopping nephrotoxic drugs such as ACE-inhibitors and ARBs, especially in the presence of hyperkalaemia, there is a good review article in the New England Journal of Medicine in 2004 (Ref:Volume 351: 585-592. August 5th 2004).

The moral of this story is-- listen to your patients. Take a thorough history and examine the patient thoroughly.

Have a good day!! :-)

Welcome to 2008-- a time for reflection

Dear Bloggers

Welcome to 2008 !!

After the bonenkai season has drawn to a close and the New Year holidays have finally ended, life is now getting back to normal.

On a more serious note, I sincerely hope that 2008 sees the world become a more peaceful and safer place. There are many struggles going on throughout the world which often lead to violence; only a peaceful way forward can ever lead to long lasting peace and cooperation.

I pray that all people be treated with equality and fairness on Earth.

I wish for the suffering of people to end and for there to be joy in their lives and an end to famine and war.

Let us all for one moment hope that such tragedies and inequalities can be righted in our lifetime.

All the best...... :-)

Great Books to Read

Dear Bloggers

There are several books I wish to recommend to you that may be able to help you with history taking and physical examination.

One book is Cope's book on Early Diagnosis of the Acute Abdomen (21st edition), revised by William Silen and published by the Oxford University Press. This book deals with the basics of history taking for the acute abdomen and the features of abdominal pain. It is a mini-bible of the abdomen and concentrates on the traditional elements of history taking, physical examination and anatomical structures that can cause pain in the abdomen. It is not a large book, being less than 300 pages, but the English usage of words might prove somewhat difficult for the non-fluent Enlgish speaker. However, all is not lost because there is a Japanese version too!! I would strongly recommend all doctors, fresh out of medical school or seasoned ones too to have a look at this most excellent book even if it is to refresh the knowledge once known but long forgotten.

Another great book is called Physical Signs in General Medicine by Zatouroff and published by Mosby. This is packed full of pictures, over 800 in fact, with explanation of the various clinical diseases plus when they were first described and by whom ! Hence, this book not only teaches about physical signs but it also teaches you about the history of medicine! In fact, this book starts off teaching you what is normal for you to be able to understand what is abnormal. Some photos are very subtle and the problem is not immediately evident until the author refers you to the problem and it becomes clear. Some problems are rare and related to third world countries whereas there are variations of presentation of common problems too. Hence, this book deals with problems amongst various races e.g. caucasian, middle eastern and afro-carribean populations to avoid missing diagnoses. I would highly recommend this book. There are no CT or MRI pictures :-) but this book will be very helpful for teaching dermatology, neurology and especially general internal medicine.

Finally, when it comes to taking a History, the best book around is the book by Professor Tierney called The Patient History- Evidence Based Approach, published by McGraw Hill. This book covers in depth all the major symptoms of disease and the differential diagnoses to accompany them plus the list of Red Flag diagnoses to alert the doctor to excluding such serious pathologies. Again, I would highly recommend this book and at almost 600 pages, it is well worth the money.

All the above books can be obtained in large book stores or more conveniently through Amazon on-line.

Happy reading.

Dr Aoki's Visit

Dear Bloggers

Yesterday saw the great Dr Aoki visit our institution again to impart his wisdom to us all.

He was presented with a most unusual case of a patient with multisystem problems including confusion, pneumonia, and skin rashes.


The patient had a varied and extensive history and the sexual and social histories provided for many areas of thought for considering different diseases.

The session went very well and a lot was learnt by all who attended.


At the end of the session, Dr Aoki was presented with a number of the second edition of his own book on infectious diseases to sign for the residents!