Sicko and State run Healthcare Systems

Dear Bloggers

I recently saw the new film Sicko which is a real-life compilation of different peoples stories about how the American health system has failed them because of the insurance run practices that exist in the United States.

Some of the stories are shocking and reveal how some insurance companies refuse to pay out on the medical bills because of their own corporate decisions, rather than the advice of the treating physicians, that the treatment is not necessary or considered experimental.

Despite the first world American leading in medical advancements, or at least that is what we are led to believe, still some 50 million Americans have no healthcare insurance and as such, if they get sick, then they have a problem ! Sick-O-No!

Then there is a comparison to state run health care systems that are described as 'Socialist' run systems, which are in fact, State runs and which exist in Canada, France, UK and Cuba !

These State run health care systems are funded by Taxation from the working population that is then FREE at source for ALL members of the society. These systems work very effectively by cutting down on unnecessary costs, inpatient stays, increased outpatients procedures, scrutinisation and implementation of evidence based practices and cost to benefit for particular treatments and use of generic drugs to keep down the costs of overall expenditure. This is at least the way it carried out in the UK system.

The Author of the film was amazed when speaking to the various doctors in the four different countries with State run systems that the Health care systems actually do WORK. He was also amazed that there was no payment desk in ANY UK hospital as patients DO NOT pay anything for their hospital stay as it is paid totally through the high taxation.

I am sure the Film was certainly an 'eye opener' for most Americans who have seen it, but for me, who has come from the UK where health care is free at source, I feel saddened that people without insurance will not benefit from the best medical intervention.

Does this have implications for Japan?

Well, the Japanese system sits somewhere between the British and American systems. There is an insurance system plus state cover for expenses. Despite the large part of the expenses being covered by the Government, there is still some 30% or so that will need to be paid by the patient or the patient's family unless, this is covered by the particular insurance programme.

Of course, if the patient has no family to foot the bill and no personal insurance, then it leaves a financial problem for the patient, who should not be worried about health costs when they are sick and moreover, a financial problem for the hospital.

How can this problem be solved??

Could a Government run medical system funded by taxation alone work here in Japan? This would mean a higher taxation on the working population to support an ever growing elderly population.

However, in doing so, the Government would have the ability introduce legislation to cut costs on medical expenditure such as having effective antibiotic and drug protocols to provide effective medical therapy but at a cost to benefit sliding scale. No one would ever be worried about accessing medical treatment and all medical expenses would be free in the time of need....sounds good !

However, from my experience of the UK medical system, there are delays in treatment directly as a result of this State run service.

In the UK, hospitals are provided with their annual money and they then need to manage their finances effectively by juggling services to try and stay within their financial provision. However, some treatments which are expensive, e.g. new cancer drugs with limited evidence, may be refused to patient (see UK National Institute of Clinical Excellence [NICE] Guidelines ). Moreover, some planned surgical lists may be postponed because the funds are not available to pay for the surgery. Waiting lists for outpatient surgery can be several months although emergency surgery and cancer surgery tend to be very fast.

Patient awaiting a new hip, of which there are many in the UK, sometimes have to wait for a year before they are operated on. It has been known, that some patients have travelled to France or Germany for their operation and the National Health Service (NHS) reimburses those foreign hospitals. The system clearly has some problems.

To get an outpatient appointment at a hospital to see a specialist in the UK is not like in Japan. You cannot just walk into a hospital and see who you want. You must first see your General Practitioner (GP) in the local community who then has to refer you by letter to the hospital in the locality. The GP practice usually will use only one hospital as it is that hospital from which it purchases the services for their patients. Hence, there is no choice of where you can be referred. The wait to actually be seen can be several months for non-urgent conditions and from my experience, the same day or the same week for more urgent conditions e.g. deterioration in diabetes control.

So, there is no ability to choose the hospital of choice....the UK are trying to now change this, which seems logical. The Canadian system is also paid by taxes, but you have the ability to choose whichever hospital you want to receive a consultation or treatment. Again, it is free! :)

As with any system, there are good and bad perspectives. There is a trade off for having a free system such as reduction in expenditure, generic drug usage, evidence based practice which drives down expenditure, more use of clinical skills such as history and examination with less reliance on radiological services unless deemed necessary BUT longer waits to see doctors in outpatients and longer waits for non-urgent surgery.

However, the Emergency treatment is rapid e.g. stroke, AMI. Even ER waiting times are not too long. Non urgent conditions can be seen within a few hours and more urgent conditions more rapidly. In the UK system, new legislation means that no patients wait more than 4 hours in the ER department before being moved to a ward. Hence, this means that the patient are seen within 4 hours, treatment is commenced and they are moved to a ward where therapy can be continued.

From my experience, the Japanese medical system works well but in my opinion, it could be enhanced in many ways.

I would hope that in the future, Japan can learn many things from these State run medical systems in order to help Japan reduce expenditure its health care system, provide cover for all which is free to utilise at source and so to therefore avoid what has happened to the American medical system so that 'Sicko' does not occur here.

DISCLAIMER: These comments are my own personal perspective on the health care systems within which I have worked and are not in any way endorsed by my hospital or anyone else.

American Navy Hospital Meeting

I am happy to finally announce that after negotiations with the doctors from the Yokosuka American Navy Hospital, we have set up a monthly Conference for exchange of interesting cases with all cases and discussion to be done in English starting this month.

This will provide an excellent opportunity for the Residents of this hospital and the Navy Hospital to create presentations, learn more about how to present in English and then to discuss about the disease(s) and of course, having to answer to direct questions!

There will be an alternating exchange of interesting cases e.g. we will present to the navy hospital one month and the following month they will present to us and vice versa.

I think it will provide excitement to the Residents and it will be a unique situation where Japanese, American and British physicians can come together and have a discussion about history, physical, workup and therapeutics.

This will be a sort of mini-international conference between hospitals and it may well be unique in Japan especially as the whole time everyone will be discussing matters in English.

As a hospital, we are eagerly expanding our horizons and with such a combined conference being created, the junior and senior residents will have yet more exposure to international medical practices which will be a most valuable experience.

Although the training at this hospital can be busy, the flux of inpatients is so high that a junior doctor can easily see many common and rare conditions as the rare problems have usually been rejected by other local institutions.

The patients are the best teachers as one can mentally recall all manner of different patient situations rather than chapters in a book. Through high patient turnover the junior doctors soon become knowledgeable and experienced compared to other doctors of the same level in some other institutions.

It is hoped that in the future, this hospital will be one of the front leaders in Internal Medicine training which will continue to provide an International style system concentrating on reducing time and cost and maximising on efficiency on reaching the diagnosis and treating it promptly and of course, getting the patient home as soon as possible.

The ways of achieving such a level are for training history and physical, how to work up the patient and at the same time, having an open atmosphere for discussion and use of evidence rather than just accepted doctrine.

I think this is a definite achievable step and as a hospital many steps have already been taken towards that goal..... maybe you would like to help us achieve that goal as well.....!

Please consider.....

Depression

We have all seen patients with depression. We may or may not have realised it though.

The elderly have a high rate of depression but may not exhibit the usual signs. They may stop eating, become withdrawn, have irregular sleep patterns or exhibit signs that resemble dementia.

The usual patient admitted to the hospital is the 'overdose' who is looking for help from us, the medical profession. In my experience, doctors are somewhat dismissive of the depressed patient and don't want to ask too many details about the underlying cause for their depression.

I have seen with my own eyes how depression can have fatal consequences.

A friend of mine was also affected by depression and to see her consider suicide and watch her mental state and body weight decline was a wake up call that depression should never be considered trivial or just a mere problem that we send to the psychiatrists.

Depression can be mild and that is something we have all experienced at some time or other. However, severe depression can be cause severe morbidity or can even be fatal if the patient takes their own life.

As doctors we must take depression seriously and when taking a history ask the patient if they feel depressed. A simple question ! However, asking about other symptoms such as appetite loss, weight loss, impaired sleep, impaired concentration, suicidal ideation etc should be other such questions to move on to if you suspect depression.

Remember, that some symptoms have no identifiable physical cause and they can be due to somatisation which can be associated with depression.

Depression should not be left untreated especially in the elderly. Treatments such as the SSRIs, SNRIs are very effective albeit that they take several weeks to show an effect.

If sleep is a problem then the older drugs such as the Tricyclic antidepressants can be of benefit but remember that there are frequent side effects especially anti-cholinergic and they can cause daytime drowsiness in the elderly and precipitate falls.

SSRIs and Tricyclics should not be prescribed together and there should be at least a two week 'wash out' period before starting a new anti-depressant.

In the UK, severe depression unresponsive to drug therapy is sometimes treated with ECT (Electroconvulsive therapy) which is said to have good effect.

Remember that in your elderly patient with the label of 'dementia' it may be depression and there is little harm in providing a trial of SSRI / SNRI therapy once organic causes of dementia have been ruled out and that depression remains the most likely diagnosis.

Please consider...........

Peak Flow In Asthma

I have recently been teaching doctors about the use of Peak Flow Meters for use in Asthma.

It appears that most physicians here rely on listening for resolution of wheeze when deciding on whether asthma is improving.

Although this is a relatively good measure, it does not provide the physician with any means of equating what is normal or the extent of improvement or worsening of the patient's respiratory condition.

Some Japanese physicians use peak flow meters, but there is no consistent use from what I have observed thus far.

Peak Flow Meters (PFM) are commonly used in the UK and USA to grade the severity of asthma as they are a guide to the extent of air trapping in the lungs. Hence, the more severe the asthma, the worse the peak flow reading.

The are normal predicted values for both males and females in Japan and these peak flow values are slightly less than for caucasian patients.

By taking a Peak Flow reading in an asthma attack, and comparing to the predicted normal value for a patient of particular age, sex and height, a percentage from normal can be calculated.

This percentage value can then guide the physician on how severe the asthma attack is and with treatment, it can show if there is any improvement in the Peak Flow percentage and also whether the improvement is sustained as a result of the treatment.

Peak Flow measurements should be done before asthma treatment is commenced and after the treatment to see the extent of the improvement.

The British Thoracic Society in the UK has excellent guidelines from 2003 which can easily be accessed for free on the internet and they give the emergency / internal medicine physicians firm guidance on how to assess, treat and whether to admit the patient or send them home.

As an example, the use of a PFM helped with the care of a patient in the UK with an infective exacerbation of asthma. The patient was seen in the outpatient clinic and given beta-stimulant therapy but with recurrence of wheezing soon after the initial therapy. However, the patient wanted to go home and a decision needed to be taken as to whether it is was safe. Hence, PFM was used and showed that the peak flow was 66% of predicted which was sustained several hours after repeated therapy in the clinic. The patient appeared to be improving and in accordance with the UK guidelines it was considered acceptable to allow the patient home despite PEFF being less than 75% of predicted as there was a sustained improvement. However, on returning to a booked appointment in the outpatient clinic 48 hours later, the asthma was still a problem and the peak flow was measured again, and it showed to be less than 50% which precipitated a hospital admission for more intense therapy.

Without such use of the PFM, the doctor would have had no other way to convince the patient that admission for more intense therapy was absolutely necessary. With inpatient hospital nebulisation therapy, iv steroids and ipratropium (no aminophylline !!!) the patient made a good improvement and the asthma stabilised as evidenced by improvements in the PEFF measurements.

Hence, if you have not used a PFM then you should be. The guidelines on use of PFMs have been available for many years and are well established and are incorporated into the UK asthma guidelines. Please see my blogs on asthma from april and march 2007.

Please consider..........

ANTIBIOTICS AND LOGICAL PRESCRIBING

Today, I would like to discuss about antibiotic choice.

I come from a country where antibiotics are restricted for certain conditions and hence, it is not possible to use certain antibiotics unless there is an agreement from the pharmacy department but especially from the hospital Microbiologist.

The Microbiologist in the UK is a Doctor who trains in medical microbiology and it is they who decide on specialist use of antibiotics not the junior doctors.

For example, if a seriously ill patient is admitted and a resistant organism has been identified, then the doctors will either consult to the Microbiologist directly or they will be contacted by the Microbiologist.

The Microbiologist will then decide on what antibiotics are most appropriate for the condition taking into account local resistance, cost and benefit plus side effect profile etc...

For example, if a junior doctor was to commence a carbapenem antibiotic for a condition that could be treated by an antibiotic of a different class, then it would be stopped by the Microbiologist thereby overriding the junior doctor.

The purpose of this practise of restricting antibiotic use is to prevent resistance. Resistance is an ever increasing problem and those antibiotics which have the least resistance should be used last not first !! If you use these antibiotics then resistance will soon occur to these, leading to a situation of having nothing to fight the bacterial enemy, a situation similar to the pre-antibiotic era.

As doctors, we have a responsibility to look after the FUTURE and not to just think about the now.

A resident I met at another hospital said 'I have to think about the patient in front of me now'. I make no criticism of that comment at all but to me it shows a flaw in the intrinsic understanding of antibiotic knowledge. I always hear, that we should start with a broad spectrum antibiotic and then narrow to a specific one. This is indeed a reasonable way to look at things, but one has to consider the cause of the infection in the first place, to consider the likely organisms involved and from there choose antibiotics that will provide appropriate cover. This is my understanding of using broad spectrum cover. To just inject the 'naypalm' type antibiotics of the carbapenem group with no idea of the cause is irresponsible with the excuse that it is 'broad spectrum'.

As an example, I heard of a patient with a stroke at another hospital who developed a fever and upper respiratory infection. The doctors had no idea of the cause of the infection and hence, they started a carbepenem antibiotic. This was clearly a wrong decision. When one considers the likely cause of the infection, one has to think of aspiration pneumonia e.g. anaerobes, oral streptococci in addition to the usual causes of infection such as penumococcus, haemophilus influenza etc... Of course, nosocomial infections should be considered but this depends on the timing of when the patient develops the infection in hospital. Hence, pseudomonas and MRSA should also be of consideration.

I would have commenced such a patient on a regimen of pencillin with a penicillinase antagonist or a cephalosporin plus anaerobic coverage with a licosamide e.g. ABPC/Sulbactam. In the UK I would have probably used amoxicillin/clavulanate or a 2nd generation cephalosporin plus metronidazole which would provide cover for most of the infections considered above.

Yes, it is always possible to consider the rarest of bacteria with the potential resistance and that every patient has MRSA etc, but common things are common. Pneumococcus causes most pneumonias, stroke patients suffer with aspiration....MRSA pneumonia is in fact, quite uncommon. MRSA tends to cause line infections in hospital and of course, soft tissue infections e.g. cellulitis / infetced ulcers where of course a different antibiotic would be considered in that case.

Hence, the use of the 'broad spectrum' carbapenem shows that the actual cause of the infection was not appreciated, because if it was, then antibiotics within a selective area would have been considered instead.

I also hear that the worse the condition of the patient, the stronger the use of the antibiotic. This again is not a logical statement. When one thinks of infection, one has to consider the bacteria but also the Immune reaction of the Patient. It is a two way process. The same bacteria in one patient may cause just a minor infection whereas in another it may produce septic shock. The bacteria is the same and will respond the same to the identical antibiotic. So, why should a stronger antibiotic be used????

One has to remember that bacteria produce Exo- and Endo-toxins that activate the immune system in various ways and result in cytokine release and it is the cytokines that produce manifestations such as septic shock. It is our own immune system reactivity that results in the severity albeit driven by the presence of the bacterium.

Hence, one needs to consider the sensitivity of the bacteria to killing by an antibiotic, the volume of distribution of the drug, its solubility, renal/hepatic clearance from the circulation etc, and not just how severe the patient is. Remember, the severity is due to the immune system and cytokine release!

For example, I would be more than confident to use benzylpenicillin in a patient with a severe pneumococcal pneumonia with a septic syndrome rather than using a third generation cephalosporin. Even if there is resistance (PRSP) Benzylpenicllin can still be used effectively, albeit at high dose. In the UK, we commonly start Benzylpenicillin with a daily total dose of over 14 mega units per day.

Only if treatment fails to work by a failure of clinical improvement and / or if culture results reveal resistance that categorically show that the current antibiotic regimen will not work, does one then switch to a stronger regimen of antibiotic cover.

The severity of a patient needs to be always be looked at separately as such patients may require a CV Line for fluid management, large quantities of fluid and potentially, catecholamine support until the septic syndrome abates.

Hence, I hope that you can in some way appreciate that my training has come from within a system of where there are limited use of 'strong' antibiotics and patients are generally treated with penicillin e.g. amoxicillin, anti-staph penicillin (flucloxacillin), first and second generation cephalosporins, macrolides, aminoglycosides and fluoroquinolones, and patients still get better from their infections !!! :)

The UK Microbiologists routinely reserve the use of Vancomycin, Piperacillin, Third Generation cephalosporins and especially the Carbapenems. They must be consulted first . If such a system of microbiologist / ID specialist consult existed in all major hospitals, and that there was consistent guidance to all Japanese doctors in hospitals and in the community, I feel sure that resistance to current antibiotics would slow down although it will never be possible to extinguish such resistance.

Please do not abuse the use of antibiotics and consider carefully the cause of the underlying problem and choose your antibiotics according to this. There is no harm in using more than one antibiotic to cover different organisms in different groups so that a broad spectrum cover is then possible.

Do not use the last antibiotics that are left without considering the vast armory of other antibiotics that will still do the same job.

Please look at the following Adobe PDF files below that are NHS Guidance from a Scottish Hospital in Fife produced in 2006 showing that for common infections that require hospitalisation, simple antibiotics are still very much used. Please also check out the use of antibiotics in the community setting. Note that no where will you see carbapenems being used as first line treatment except in ICU patient who have failed on other treatments.

For a more detailed analysis and perspective on antibiotics please read the books by Dr Makoto Aoki.

Meningococcus

Dear Bloggers

Sorry for the lack of new articles but I have been busy with teaching plus nursing my recent head cold which has left me feeling unwell....

A recent case was passed to me about a patient from another hospital who was admitted with an alteration in consciousness. The patient could not speak very well following a sub-arachnoid haemorrhage some years ago that left the patient with paresis and required a VP shunt to be placed in vivo.

The patient had developed a drop in consciousness and vomiting. There was no fever or other symptoms from the patient.

The salient clinical signs included a high blood pressure (systolic >200) and a disseminated haemorrhagic rash on both forearms (patient was not taking warfarin).

CSF examination revealed a high WCC, High protein and low Glucose but no visible bacteria.

These findings were consistent with a Meningococcial Meningitis and Septicaemia.

However, the high blood pressure concerned me that there may have been a blockage in the VP shunt due to infection causing a Hydrocephalus.

CT film showed an old infarction area, the VP shunt but evidence of a dilated anterior horn on the contralateral side to the shunt. There was no midline shift.

The patient was started on Vancomycin, Ampicillin and Ceftriaxone which is the standard therapy for meningitis when the organism is unknown.

Patients with meningococcus infection can develop complications including:

1) Disseminated Intravascular Coagulation (DIC)
2) Adrenal Failure (Friederichson-Waterhouse Syndrome) from DIC
3) Haemorrhagic rash (from DIC)
4) Renal Failure
5) Death

The rash may intially present a small areas of non-blanching haemorrhage around or within the white of the eye (sclera) or it may progress to diffuse ecchymosis.

Blood cultures should always be done!! Don't ever delay using the antibiotics for fear of a negative CSF gram stain / culture because the longer you wait the greater chance of death.

In fact, in the UK, GPs routinely will give Benzylpenicillin intravenously / intramuscularly if they suspect meningitis in order to start treating the disease before they reach the hospital. They will not delay treatment.

Apparently, CSF can still yield a positive culture up to 4 hours after antibiotic use (CMDT 2007, Tierney, L. Lange press). If such CSF exams reveal no bacteria and suspicion of meningococcus is high, then consider checking the CSF for meningococcal PCR. Also consider nasal and throat swabs for the organism as it is in these two places where meningococcus can be found and where it is considered to invade in the later location.

REMEMBER all close contacts e.g. family members / nursing home residents / kissing contacts / and RARELY medical staff need TREATING WITH RIFAMPICIN as prophylaxis (600mg twice daily for two days) to prevent them from developing meningitis or spreading the organism they may harbour derived from the sick patient.

This treatment can be done as an outpatient, but it should not be forgotten or delayed.

Patients with meningococcal sepsis / meningitis should ideally be treated on an ICU / HCU ward until stable.

Please consider....

Medical Student Visits and Ways of Thinking

This week and last week has seen the usual influx of medical students from throughout Japan coming to see how this hospital works.

I have as a result been very busy with my daily rounds teaching history and physical examination to the students so that they can also understand the patient problems.

When I am asked by Residents what the problem is, I naturally produce a differential diagnosis but I then throw the question back to the Medical students. I usually get but only a few answers.

I am aware that in Japan, because of the hierachical structure of the senior doctor to the junior that in some cases what the senior doctor says is final and with little or no questions from the juniors / medical students as it might be seen as embarrassing or insulting.

Well, I do not mind questions. I think questioning seniors is good. In fact, fresh medical students / junior doctors fresh from medical school can sometimes have the right answer as they know the most uptodate information.

Sharing of ideas and challenging why a diagnosis has been made allows all the members on the round to understand the thought process behind diagnosis. By questioning the senior doctor allows everyone to understand and to find out the evidence / experience of the senior doctor and hence, all can learn from this type of interaction.

I had a discussion just yesterday with several medical students and I advised them that they should always read about the patients that they see. In doing so, they truly learn about the conditions and the associated problems, workup and treatments.

As a medical student / doctor you need to read to fill in the gaps in knowledge that everyone has. No doctor is perfect-- except perhaps Prof Tierney ! :)

By reading, one can learn about the evidence base of current diagnostics and therapeutic measures and why old treatments lose or regain favour etc...

Never just rely on the notes taken at university as they soon become out dated and moreover, they are sometimes opinion of the lecturer rather than based on evidence and fact.

The take home message today is always question in your own mind what is being said to you and never just accept that it is correct. Go away and read about it and decide for yourself if that is correct or not. In so doing, you will grow as a physician and become better diagnostitians.

Let's Get Physical-- Let's Get Training

During my time in Japan I have been able to assess the medical students way of examining patients and to some extent the skills that have been taught are sometimes inadequate for finding common clinical signs.

This is a concern for me because some of the students are soon to become junior doctors.

For example, I have recently seen several medical students miss a basal pneumonia that was identifiable from loud wet crackles. The reason was the students only examined half the lungs ! Each made the same mistake.

They only placed their stethoscopes half way down the chest at the back and said they could hear no problem. Only when demonstrating the surface anatomy of where the lungs commence (at the apex) and where they finish (12th ribs posteriorly) were they able to then understand that the lungs fill the entire space and hence, they should listen at the lung bases as well.

Even after doing this, only one student was able to identify the sounds suggesting that the practical, 'hands on' ability to detect through physical examination was previously not taught to them optimally.

Moreover, one medical student started examining with his stethoscope through the patient's clothes, which must not be done as it is not possible to always differentiate the rubbing of the clothes from the sounds in the patient's chest.

So, why are some Japanese medical students unable to identify pathology / diseases through physical examination? The problem may be when they start learning physical and how they learn it.

In the UK, modern medical school teaching starts with physical examination right from the first year. This is not the case in Japan where physical only starts from 3rd/4th year onwards. Moreover, some medical students have also said to me that the opportunities to examine patients at medical school in Japan are too few.

Hence, by the time some medical students start to visit other hospitals to decide where to do their two-year residency, it becomes clear to me that some institutions training in physical examination is not optimal. Of course, this is a generalisation and on a case-by-case basis, but a final year medical student in the UK would be expected to be able to examine the three main systems (e.g. cardiovascular / respiratory / abdominal) and to pick up straight forward diagnoses such as pneumonia, pleural effusions etc...

The utility of percussion of the chest for signs of consolidation or effusion is not universally taught in Japan as some medical students have never seen this done before until they visit me at my hospital. They have been reliant on the chest xray / CT to make the diagnosis for them. Even if some students have seen percussion done, they have not fully appreciated its significance or the great utility that it has to offer until they come to this institution.

Examining simple things such as the hands and the quality of the pulse are, in my experience, not considered by medical students as important, and hence, if one were to start from the eyes, as is done in Japan, the patient's physical examination misses a vital area. Essentially, the patient has no arms as no parts of the upper limb are examined !

Things such as clubbing, splinter haemorrhages, Beau's lines, Janeway lesions, Osler's nodes, Dupytren's contracture, nerve palsies, metabolic flap, collapsing / slow rising pulses are MISSED because they are not examined for. Serious diagnoses can therefore be missed.

I also did a local seminar last weekend where I presented a case of a dissection of the aorta. I was asked whether Review of Systems questioning was necessary and worthwhile because it took so much time. I am glad that such a question was asked and of course, it is indeed very important because it is a safety net for the patient and the doctor to pick up additional information that might help with the diagnosis / diagnoses that may have been overlooked by the patient and the doctor.

Taking a little bit of extra time at the beginning might save the doctor time in the future by cutting down on unnecessary tests / scans.

Communication with the patient and thorough history taking is Essential. I am somewhat concerned that medical students do not find that this might be useful because of time constraints. This may also be because of the reliance on laboratory data, xrays and other advanced radiological studies rather than the basics of a good story of the problem and then having the appropriate skills to find the problem(s) by physical examination.

Whilst medical students come to visit here for three days only on their tour of different institutions, it is never possible to show just how the basics of being a doctor can provide quick and straight forward answers that might otherwise not be obtainable by any scan ! However, they are able to see how classical physical examination should be and how it is possible to dissect and rebuild a junior doctor's patient history so that the problem(s) can be elucidated and hence, following that, how appropriate investigations and treatment should be considered.

For those interested in improving 'level up' on history and physical, they should consider coming here for more than 3 days as it is otherwise insufficient time to obtain the true nature of what is on to offer to the medical students.

Essentially, with an ever growing elderly population and few doctors and with a large medical expenditure in Japan, I believe it will become evermore important for doctors to take more time on history and physical so that instead of doing 'blanket' blood testing and scanning otherwise referred to as the 'pan-man' scanning, the doctor will order tests related only to their considered differential diagnosis rather than doing lots of tests without really knowing what to look for and hoping to find something, as this is not efficient or cost effective.

If you are interested in an externship or a longer period than three days then please let me know on skghjpn@gmail.com

Trip to Hokkaido

For tyhe past few days I have been in Hokkaido for purposes of teaching junior residents.

There are several medical residents working under General Internal Medicine and they get to see some interesting cases in addition to the everyday 'bread and butter' cases.

I was presented several cases of unusual general medical conditions. One case required for examination of the Central Nervous System wherein I was able to determine both old and acute neurological dysfunction because of history and examination only.

The scans presented to me after the physical exam confirmed my suspicions.

I was also there to teach opthalmoscopic examination with the handheld opthalmoscope. The doctors were able to identify the optic disc of the patient which is perhaps one of the most important tests as it is necessary to check the optic disc in patients with suspected raised intracranial pressure e.g. meningitis and hence, I hope the doctors were able to gain some valuable experience from this practise.

Following this, I went on a 3 hour sightseeing trip and the pictures of that experience are below:

Type 2 Respiratory Failure and Therapy

In my years as a doctor I have seen many patients come to hospital with worsening respiratory failure due to all sorts of underlying diseases.

The classic example is with the patient with underlying heart failure who gradually gets breathless with worsening oedema who then is so breathless at rest eventually calls for an ambulance.

Of course, in some instances, the paramedics are unaware of the underlying problem and give high flow oxygen.

When the patient reaches the hospital, they can sometimes have a low conscious level which in some instances makes the doctor think of an intracerebral cause and the patient gets sent for a CT head scan which comes back as normal.

In this case, the patient has CO2 Narcosis and hypoxaemia causing the reduced conscious level.

A history from relatives or even the patient plus a detailed examination can provide a wealth of data that can quickly narrow down the cause and differential diagnosis to provide swift treatment.

When examining the patient-- START WITH THE HANDS. Assess for warmth and sweatiness that one can get with CO2 retention. In addition, red palms can also be due to this problem. However, the Gold Standard test is to look for a CO2 retention flap of the hands.

This can quickly tell you if there is a major problem and the likely cause. It is referred to as a Metabolic Flap as it can be caused by CO2 retention, Liver and Renal Failure in the main.

Pulse is an excellent measure. Not checking just the rate, but the QUALITY too. CO2 retention gives a Bounding Pulse that is easy to find. The blood pressure may also be high.

Check the JVP to see if it is raised. There are several causes of raised JVP such as heart failure, cor pulmonale of Type 2 respiratory failure, dysrhythmia, valvular dysfunction, tamponade, superior vena cava obstruction, pulmonary embolism, severe respiratory failure etc...

However, this is where a good history will be of help to try and make some discrimination as to the cause such as being a heavy smoker, previous evidence of myocardial infarction, thromboembolic events in the past, being on oral contraceptives.

Listening to the heart sounds may provide an answer such as obvious heart murmur or reduction in heart sounds as in tamponade. Feeling the apex to assess if has shifted laterally can reveal the chronicity of the problem as in chronic heart failure.

Listening to the chest may reveal the dullness and reduced air entry associated with a pleural effusion plus the classical sounds of bronchial breathing. Moreover, in heart failure, the appearance of widespread wet crackles aids the doctor to make the diagnosis at the bedside. Wheeze is not so easy, as it may signify asthma, COPD or even heart failure. That is why a history helps to refine the mental diagnosis along the way.

Feeling the abdomen for ascites and organomegally can provide further clues about heart failure and lastly, checking the legs, buttocks and abdominal wall for oedema and of course, around the face can also provide salient clues about the extent of heart failure.

Hence, a basic clinical diagnosis can be made at the bedside without a chest xray or blood results. However, these tests DO need to be done, but that should not stop you as doctors from providing emergency treatment whilst awaiting such results.

Basic life saving treatments include:

• Appropriate oxygen therapy. For example, in the patient with hypoxaemia and a high respiratory rate, high flow high percentage oxygen is likely to be appropriate. However, in the patient with heart failure / COPD and a low respiratory rate, hypoxaemia and reduced conscious level, low percentage oxygen may be more appropriate. The percentage oxygen provided should be guided by arterial blood gas analysis, not just by saturation probe monitoring.

• Percentage oxygen should be given throw a Venturi Mask and not nasal cannulae. I have seen in the past doctors trying to put 4 litres through nasal cannulae. The idea is flawed because the maximum effective amount of oxygen that can be put through nasal cannulae is only 2 litres. Moreover, if the patient is mouth breathing, there is no way that even 2 litres will give the desired effect. The only way to really ensure an adequate percentage of oxygen is via the Venturi system of facial mask.

• Normally oxygen starts at 24% and increases upwards to maintain an oxygen saturation of about 92%. In patients with Type 2 respiratory failure, such patients rely on hypoxic drive for respiration. If the drive is abolished by high flow oxygen, the CO2 rises and the patients respiratory status worsens. Patients need to have careful oxygen replacement in order to maintain this hypoxic drive. Of course, when the patient is established on the right percentage of oxygen, a repeat blood gas needs to be obtained to ensure that the oxygen saturation is adequate and that the CO2 is beginning to fall. Additionally, acidosis, should it be present, should be seen to improve.

• If the Venturi oxygen mask fail to ameliorate the problem of Type 2 Respiratory failure such as persistent hypoxaemia, rising CO2 and acidosis e.g. pH < style="font-weight: bold;">BIPAP. Such therapy is very effective to reduce CO2 and improve acidosis and at the same time raise the oxygen saturation. This can be used in COPD and heart failure, and in the latter condition, the positive pressure helps to push fluid out of the lung tissue and into the vasculature. In such events, reducing the fluid inside the lung alveoli improves compliance of the tissue and reduces the alveolar-capillary barrier thickness and thereby improves oxygenation.

• Again, once established on BIPAP, blood gases need to be taken to ensure the patient is improving.

• However, intubation and ventilation is sometimes the eventual progression of these disorders, but instituting such therapy should be the last option as in doing so you put the patient at risk of not being able to be weaned off the machine. Only after a few days of ventilation by a ventilator, the intercostal muscles start to waste and hence, this makes the patient ventilation capability worse if they were to come off the ventilator.

Other measures to improve respiratory outcome:

• If heart failure is the main problem then using nitroglycerine and furosemide are standard therapies. Nitroglycerine reduces venous return and hence, preload of the heart is decreased. Furosemide has a similar effect and also cause diuresis and reduces afterload. These therapies are relatively safe as long as the patient has a sustainable blood pressure. If the clinical opinion is heart failure, giving such therapies is unlikely to do harm.

• If wheeze is the predominant problem, giving steroids and beta-stimulant nebulisers may help. Even if the cause of the wheeze is not clear, such as a suspicion of heart failure, but a smoker and previous history of COPD, such therapies should not be withheld. Sometimes, it is not clear which condition predominates and so as a result, treatment for heart failure and COPD/Asthma are given until more information is available to refine the diagnosis. Withholding such life saving therapies to ascertain the true nature of the problem which could take several hours is not good practise because the patient suffers. It is better to sometimes treat several suspected problems at the same time on admission to the hospital as an inpatient and with further test / scans the treatments can be stopped or continued depending on the outcome. Hence, the patient has the life saving therapies from the start and comes to no harm from the disorder as treatment was not withheld. This way of practising medicine is common place in the UK and USA.

1. Sit your patients up!!! Yes, it is a simple thing to do but very rarely done in Japanese hospitals. I have been to several hospitals in Japan, and in almost every one, patients with COPD and heart failure are nursed flat. This is not standard treatment. Patients who have cardiorespiratory diseases often find it easier to breath when sat up. For example, in COPD, such patients rely on diaphragmatic contraction for breathing as their hyperinflated 'barrel' chests poorly expand. If the patient is sat upright, the use of gravity is enhanced and patients can also sit forwards to fix their chest to enable deeper breathing. By lying COPD patients flat abolishes this advantage and worsening respiratory function can ensue. Heart failure patient rely on gravity so that the pressure in the upper lungs is less than the higher pressure in the lower lobes. This can help with respiratory function. Lying such patients flat equalises the pressure and breathless gets worse. This is why one sees the phenomena of orthopnoea in COPD and CHF and Paroxysmal Nocturnal Dyspnoea in CHF when lying flat. Just by sitting you patients up may improve their oxygen saturations !!!! However, please let your nursing staff know that the patient must be nursed in that position because failure of you as doctors to communicate such orders will find the patient put flat and situation repeats itself.
   

• Dysrhythmias should be treated if pathological. For example, fast atrial fibrillation should be treated. It should not be left as a mere matter to observe. AF can lead to worsening heart failure and cardiorespiratory function can worsen as a result. Such patients need to have a echocardiogram to exclude thrombus formation, thyroid function tests and cardiac enzyme level measurement to ensure cardiac damage has not occurred.
  

• Patients with renal failure and fluid overload can develop respiratory failure. Such patients may have a metabolic acidosis and poor urine output. Consideration for dialysis / haemoflitration to reduce circulatory volume should be considered on an urgent basis.

The above is by no means an exhaustive guide, but basic patient management with oxygen, positioning and standard basic drugs can make a world of difference to your patients care and hopefully prevent them from progressing to a worsening state.

Remember, the patient comes first. Please consider......

Electrolyte Disturbance, Spasm and ECG Disturbance

A case presented to a hospital and has been anonymised for patient confidentiality.

An elderly male was brought to the hospital with a reduced conscious level and evidence of respiratory distress.

No history was obtained from the patient, but there was the possibility that the patient had developed aspiration from poor swallowing.

The patient had known dementia and had previously undergone a thyroidectomy some years before.

Drug history was unknown as was the family history.

The patient apparently lived alone prior to admission to the hospital.

Physical examination on admission confirmed a right basal pneumonia and the patient underwent intubation, ventilation and antibiotic therapy was initiated.

The laboratory data revealed a low K of 2.7 and a low Ca of 4.7 in addition to evidence of infection with raised white cells and inflammatory markers.

A senior doctor suggested that the patient might have tetany to account for the breathing difficulty, and also for a potential swallowing disturbance. Moreover, the tentany may have resulted from the thyroidectomy in the past and hence, the patient probably had hypoparathyroidism and hypothyroidism.

On examining the patient, there was a loss of the outer 1/3 of the eye brows and a swollen face with pale skin consistent with hypothyroidism. There was a necklace scar confirming a thyroidectomy had occurred in the past. The reflexes were generally absent.
Applying a blood pressure cuff to the left arm provoked CarpoPedal Spasm (Trousseau's Sign) and Chvosteck's Sign was negative.

These physical features indeed suggested tetany and hypothyroidism.

ECG revealed atrial fibrillation and T wave inversion in the lateral leads.

It was suggested that a magnesium levelshould also be obtained in addition to thyroid hormone tests and a troponin T level.

The resident gave intravenous calcium gluconate and started K replacement whilst awaiting the results of the other tests.

However, the K level dropped further despite replacement. This was because the Mg proved to be half the normal level. The K cannot be corrected if the Mg level is Low.

Hence, the resident then gave an infusion of magnesium and within a few days, the K level had normalised and the Ca level was also increasing towards normal.

The ECG improved with normalisation of the T wave to the upright position and the patient was in sinus rhythm.

The thryoid tests came back with a TSH of 14 and low T3 and T4 confirming hypothyroidism. The Troponin T test was negative.

Thyroid hormone was commenced at low dose of 25 micrograms/day in view that the patient was elderly and might have underlying ischaemic heart disease.

Diagnosis in this case include:

• Tetany due to combined Hypocalcaemia dn Hypomagnesaemia
• Hypokalaemia due to Hypomagnesaemia
• Iatrogenic Hypothyroidism
  
• Iatrogenic Hypoparathyroidism
• Aspiration pneumonia
  

It was considered that the dementia-like state might improve with thyroid replacement as such problems can occur in profound hypothyroid states.

Moreover, this was a great example of how tetany can present. Tetany can be due to low Calcium or Magnesium, and in this patient, both were present.

The low Magnesium would have precipitated low potassium and the combined electrolyte and thyroid hormone dysequlibrium would have caused muscle weakness which could have lead to problems with swallowing and hence, aspiration pneumonia.

The lessons to be learnt hear are:

1. Always go back to the patient to test a hypothesis. In this case, the low calcium prompted the search for physical signs of Tetany. The positive physical sign and low K, lead to the thought of low magnesium that might otherwise have been missed.
2. If the patient has dangerously low electrolytes, they must be corrected on an urgent basis
3. Thyroid hormone replacement should be started at low dose in the elderly and gradually titrated up until the TSH and T4/T3 are normalised.
4. Electrolyte disturbance can cause ECG abnormalities that can resemble an ischaemic ECG. Moreover, low Ca and K can each precipitate a Long QT syndrome and hence, such patients are at risk of Torsade de Pointes. Thus, reversing such electrolyte abnormalities is required urgently.
   
5. Thyroid deficiency can cause reduced conscious level and even a dementia type picture. When starting replacement, always start at low dose in the elderly.

For a more detailed description, please see an appropriate textbook.

Please Consider......

Lonny Ashworth Welcome Back

Today has seen the return of Lonny Ashworth to our hospital, on this occasion, teaching the new first year residents about the use of ventilators.


Lonny has 33 years of ventilator experience and currently works at the Boise State University, USA.

Over the next few days, he will also be teaching nursing staff from around Japan about ventilator usage and they will be able to get hands on experience of modern ventilators and how
to manipulate the machine settings to provide optimal respiratory care for sick patients.



Lonny's knowledge of these machines and the physics / mechanics is just amazing and it is very worthwhile experiencing his annual visits to Japan.

Chest Pain, Collapse and Vomiting

A patient to another institutions ER department who presented with:

• Chest Pain
• Collapse

The patient had gone to a care centre earlier in the day, and on arriving there, the patient fell to the floor which was witnessed by her carer.

The patient had not lost consciousness but complained of severe chest pain followed by three episodes of vomiting.

The patient was then brought by ambulance to the ER department.

The patient suffered from dementia and was only able to say that there was chest pain. Sometime later, the patient said that there was also upper back pain.

There was no description from the admitting doctor of the quality of the pain or radiation.

The vomitus was of food only and contained no blood.

The previous medical history included dementia and untreated hypertension.

No other history was known.

On initial examination by the ER staff, the patient was afebrile, pulse 90 beats per minute, blood pressure 190/110, respiratory rate 18 per minute with oxygen sats of 90%.

Blood pressure in both arms was said to be the same.

Chest examination revealed bilateral crackles only with normal heart sounds.

Abdominal examination was said to be normal except for some epigastralgia but the chest pain at that time had resolved.

From history and examination differential diagnoses were formulated and included:

• Dissecting aortic aneurysm
• Acute myocardial infarction
• Unstable angina
• Acute perforation of an abdominal viscus
• Biliary colic
• Pancreatitis
• Oesophageal spasm

The ECG showed an old inferior myocardial infarction but nothing acute. The chest Xray was abnormal with evidence of possible tracheal shift to the right and a right paratracheal mass. The right basal lung appeared to be collapsed and there was an effusion at the left base.

This was an unexpected finding from the history as there was no apparent serious illness with this patient in the past.

The patient appeared confused but in obvious pain from the wincing of the face but pain was denied on several occasions.

Hands were cold and the radial pulse was felt to mildly collapse. There was still a wide pulse pressure in the blood pressure despite intravenous anti-hypertensive therapy in the ER. Quinke Sign, Corrigan Sign and DeMusset Sign of aortic regurgitation were negative.

JVP was not raised. Frank sign of the earlobe was positive suggesting some coronary artery disease.

Trachea was depressed (tracheal tug) and mildly deviated to the right. There were no cervical lymph nodes present.

Heart examination revealed a very subtle murmur of aortic regurgitation with the occasional Austin Flint murmur that was no present on every cardiac cycle.

Lung examination revealed dullness at both bases with right basal crackles. On pressing the sternum, this reproduced some central chest pain but it was uncertain whether this was the same as the presenting chest pain as the patient could not describe the problem.

Abdominal examination revealed no AAA but on auscaultation there was a left renal bruit.

Pulses were equal in the upper limbs and femoral areas. The left dorsalis pedis was weaker than the right.

In summary, this patient had a sudden collapse without loss of consciousness, onset of central chest pain and upper back pain followed by vomiting. The patient had later complained of epigastralgia .

The examination had revealed a collapsing pulse and the murmur of aortic regurgitation, right basal crackles and an left renal bruit with a slight inequality of the dorsalis pedis arteries.

Pulling all the main features together to make one unifying diagnosis, it was considered to be a Proximal to Distal Dissenting Aortic Aneurysm.

CT scan showed some minor right basal lung collapse, no obvious apical problem, but the aorta was slightly abnormal.

The advice was to

• Obtain expert radiological advice on the CT scan
• Obtain an urgent cardiac echo to observe the aortic valve and to check for a potential tamponade
• To obtain a doppler study of the kidneys to assess blood flow to ascertain if there was an obstruction to the arterial orifice from a dissection.

The radiologist had confirmed that the CT findings were consistent with an aortic dissection and the patient was admitted under the appropriate specialty.

DIAGNOSIS: Aortic Dissection

This case markedly shows how a history and detailed examination with the basics of an ECG and chest Xray can lead one to the diagnosis of dissection.

Never rely purely on upper limb pulses being equal; they can be equal and there can still be a dissection.

A chest Xray can aid with the diagnosis if there is a widening of the mediastinum and in some cases there can be a left sided pleural effusion which can be a haemothorax due to the dissection. In this case, there was a left sided pleural effusion, but the effusion was not tested , so it remained unknown as to its origin.

Echocardiography is very important as it can show valvular insufficiency and tamponade.

The abdominal bruit was a gift sign in this case as it signified narrowing of an arterial foramen which suggested abdominal extension of the dissection.

The CT scan here was helpful to give more weight to the diagnosis although it was used to confirm the diagnosis rather than to make a surprise diagnosis.

Rectal, Rectal, Rectal !!!!!

Dear Bloggers

This case has been anonymised for patient confidentiality.

An elderly female patient with a two month history of watery diarrhoea was admitted to another hospital. The diarrhoea had started gradually and built up to a peak which had plateaued at 15x per day!! The diarrhoea was described as painful and in the lower abdomen. There was no blood and no mucus in the stool.

The patient described loss of appetite, weight loss of 7 kg and night sweats for the preceding 1 month prior to admission.

On further questioning, the stool was described as looking like 'paper' as it was thin when she produced it, just like paper.

However, the patient had been seen at another hospital where she was told that the problem was irritable bowel syndrome.

Having asked the patient if any doctor had in the last 2 months performed a rectal examination, the answer was NO.

The patient presented to hospital because of the development of urinary frequency, stool-coloured urine and production of gas per urethra at the end of micturition (pneumaturia). The patient also had a feeling of always needing to go to do stool which is known as Tenesmus which is usually an ominous symptom of cancer.

There was no previous medical history and the patient was taking no medications.

There was no relevant family history whatsoever.

Review of systems: No joint pain, no eye discomfort, no myalgias, no bone pain, no chest complaints.

Physical examination revealed a fever of 37.9 degrees C, normal vitals otherwise.

Cardiovascular and Respiratory examinations were unremarkable.

Abdominal examination revealed tenderness in the suprapubic and both iliac fossae. There was no costovertebral angle tenderness. There was no rebound tenderness and no guarding. An indiscrete mass could be palpated.

Bloods revealed a neutrophil leucocytosis, raised CRP and LDH. All other bloods were normal.

CXR was normal.

Differential Diagnosis

From the history of weight loss, appetite loss, night sweats, increasing diarrhoea without blood/mucus and new onset symptoms of UTI are consistent with an advanced colonic tumour NOT irritable bowel syndrome.

Other differential diagnoses should include inflammatory bowel disease but this is somewhat unusual in the absence of bloody diarrhoea. Also, patients will sometimes develop extraintestinal manifestations affecting the eyes (iritis), joints (arthritis), skin (erythema nodosum) etc, which this patient did not have.

Diverticulitis should also be considered, as post-inflammatory masses can occur which cause stricture and can invade the bladder.

CT scan of this patient revealed a colonic mass attaching to the bladder and with air seen inside the bladder which was unsurprising.

Two mistakes were made in the management of this patient.

Firstly, no Rectal Examination was ever done. 45% of all colonic malignancies present in the rectum and are therefore detectable with the tip of the finger! If performed two months ago, this could have perhaps been picked up at a stage when it could have been more amenable to surgical therapy.

Secondly, this patient had a fever and urinary signs of infection including faeces in the urine, white cells >100/hpf , 2+ bacteria and blood. However, the fatal mistake was to rely on urine culture which was negative. Hence, no antibiotic therapy was given on admission. This was clearly wrong as the patient has symptoms and signs of a UTI. Moreover, only 50% of urine cultures prove positive despite a UTI being present. Therefore, giving antibiotics such as a fluoroquinolone antibiotic would be advisable e.g. levofloxacin, as the patient was not being sick, the fluoroquinolones are rapidly absorbed and are effective against gram negative bacteria.

However, the diagnosis could have soon been established by performing a rigid sigmoidoscopy o admission to hospital as again another 25% of colonic cancers can be picked up where they occur in the sigmoid area. [please note 5% occur in the descending colon, 10% in the transverse colon and 15% in the ascending colon].

Thus, 70% of colonic tumour can be potentially picked up with the aid of a finger tip and a rigid signmoidoscope. Simple but rapid and effective in establishing a cause.

The Lessons to be Learnt here include:

• In patient with any lower GI symptoms ALWAYS DO A RECTAL EXAMINATION. It is negligent to avoid doing one, and relying on CT to make a diagnosis in this circumstance is incorrect. CT is a guide only.

• The patient had symptoms of OVERFLOW DIARRHOEA. This occurs when there is a blockage in the colon either by a internal occlusion [for example constipation, tumour] or external compression [e.g. invading non-colonic tumour]. Hard stool is unable to pass through the small hole produced by the compression. The liquid stool within the right colon migrates over the obstructed harder stool and through the stenosis of the colon to produce tape-like stool or diarrhoea, just as in the case of this patient. Thus, taking a decent history about the consistency of the stool should have set of warning alarms to do a rectal examination and rigid sigmoidoscopy at the bedside.

• The patient clearly had developed a fistula from bowel to bladder with subsequent infection. Relying on culture alone is not correct. Look at the history, physical, vital signs [such as fever] and other laboratory data and they ALL point to a UTI. Hence, patient should have been treated on suspicion of infection which might otherwise progress to a complicated UTI.

Please consider..............

Devil's Grip

A young adult male was admitted to another institution with severe upper chest pain that awoke him from sleep.

He had been previously well and had no serious underlying problems.

The pain was located in his upper chest and was severe (9/10) and made worse by lying flat. The pain was squeezing in nature, radiated to his back and was non-pleuritic. There was no associated breathlessness, cough, sputum or haemoptysis. The pain did not radiate to his neck, jaw or arms. He felt nauseated and sweaty but had not vomited.

He also complained of right upper quadrant abdominal pain. He had no other abdominal symptoms including the absence of diarrhoea, constipation, jaundice or malena.

On direct questioning, he denied doing any recent heavy lifting. He complained of no neck pain although he did mentioned that he had new onset 'katakori'. He did not have a stressful occupation.

Previous history included hyperlipidaemia, appendicetomy.

He was taking no regular medications.

He was a previous smoker having given up last year.

When he was initially examined there was a positive finding of fever which was low grade. The chest examination was unrevealing. Abdominal examination showed some right upper quadrant tenderness but no organomegally.

All bloods were normal except for a raised neutrophil count, low lymphocytes and rising CRP.

Initial differential diagnoses included;

• Acute MI
• Unstable angina
• Variant angina
• PE
• Aortic dissection
• Spontaneous pneumothoraces
• Spontaneous rupture of oesophagus with surgical emphysema
• Oesophageal spasm
• Gastritis
• Pericarditis

The serial ECGs revealed no pathological changes.

Chest radiograph showed no evidence of surgical emphysema, pneumothorax or enlargement of the superior mediastinum.

CT chest was performed and dissection was ruled out.

Echocardiogram of the heart revealed some mild left ventricle asynergy and abdominal scanning was normal.

In view of the abnormal echocardiogram result, the patient underwent coronary angiography which was normal.

Hence, despite the serious pains, no major abnormality could be found.

On further review on attending the same institution for review, the pain had mostly resolved, but he was left with some persistent abdominal discomfort and blood tests were still abnormal.

Examination was completely unremarkable.

The only major abnormality was the evidence of an inflammatory /　infective episode. The mild LV asynergy made me consider a coxsackie infection. However, the CK and ECG were normal.

The diagnosis to be somewhat unusual and referred to as Bornholm Disease, but also known as Pleurodynia or Devil's Grip.

This is a viral infection caused by Coxsackie B virus (1-5 isotypes) affecting the diaphragmatic and intercostal muscles. It causes painful spasm and fever, and it can simulate the painful and potentially serious pathologies consider above. The condition occurs in summer months (hence, at this time) and adults are affected to a greater degree than children.

Having reviewed several texts, the general description is poorly reported with there being no definite bedside diagnostic criteria although a rising titre of anti-coxsackie antibody should be normally be checked . However, this is a diagnosis of inclusion when all other serious diagnoses have been ruled out.

Pleurodynia generally resolves with 6 days and treatment is with analgesics.

Don't Ignore Your Patient's Symptoms

This patient was admitted to a hospital and details have been anonymised.

The patient is an elderly male with a long history of rheumatoid arthritis who been admitted with non-specific symptoms of

• fever
• malaise
• back pain

The patient was vague and confused so was not able to answer questions clearly, but it appeared that there were no localising symptoms to the chest, CNS, abdomen, genitourinary tract, joints or skin.

There was no other significant history.

The patient had been taking long term steroid (prednisolone 5mg / day) and NSAIDs. The patient had not been on any DMARDs.

Physical examination performed by another doctor was described as generally unrevealing except for the signs of cold shock, and features of chronic steroid administration which included a Moon Face, a Buffalo hump, Centripetal obesity and the obvious signs of advanced RA of the hands.

Blood results suggested renal failure, sepsis and DIC, and he underwent renal ultrasound scanning which revealed an infected hydronephrotic right kidney.

As the coagulation was deranged, the patient who would have normally had nephrostomy tube insertion instead had a double J stent inserted from renal pelvis to bladder in order to allow drainage of the infected kidney.

Microbiological results revealed the infecting organism to be Proteus mirabilis.

He was also treated with broad spectrum antibiotics and received iv steroid replacement in view of the real potential for an Addisonian crisis in view of his prolonged period having received oral steroids for the rheumatoid arthritis over the years.

The patient's inflammatory markers began to settle and the renal failure improved. However, the patient developed an ensuing haemolytic anaemia with raised bilirubin, raised reticulocytes, but normal Coombe's test. Other testing for GI evidence of bleeding was negative.

It was clear that there was some process still driving the haemolysis despite the improving infection from the Genitourinary tract.

The back pain had essentially been overlooked because the patient had had a long history of back pains and of course, an infected kidney can also cause back pain. However, other pathology such as infection which could be causing this back pain had not be investigated and excluded and moreover, the infection was supposed to be improving and therfore one would have expected the back pain to also get better!

When the patient was questioned, he said that the pain in his back had changed and had become worse than usual. It was so painful, that the usual pain medications were not proving to be effective.

It was therefore decided to perform a CT scan of the lower abdomen and back which astoundingly revealed a psoas abscess!!!!!

What this case shows is not to ignore or overlook the most trivial of symptoms as they may lead to a diagnosis that had clearly not been considered on admission to hospital. Back pain is a very common symptom especially in patients with arthritis. However, never forget that RA patient by dint of their autoimmune state are relatively immunodeficient and in addition, the patient had been taking steroids further impacting on immune suppression. That puts them at greater risk for infections.

The change in the nature of the back pain and the fact that it was enough for the patient to complain about it was enough for it to be investigated. Just because a patient has a chronic condition does not mean to say that it should not be investigated during an admission to hospital as the condition may have deteriorated or become complicated, as in this case by infection.

Let's suppose the patient had COPD. Just because the patient has a chronic pulmonary condition does not mean to say if breathlessness gets worse then it should not be investigated, does it?! Without such investigation, a pneumothorax, infection, PE, tumour etc would be missed. Hence, the same is for other areas of the body including the back or any other chronically affected area / organ system.

Basically, this boils down to Listening to Your Patient and taking them seriously. Sometimes in these chronically ill patients, it is better to over investigate and come up with normal results than to under investigate and miss the diagnosis.

Remember, that patients who are elderly or immunosuppressed for whatever reason will not always show a raised white count, fever, tachycardia etc in response to infection. In such patients, have a low threshold for treating.

It proves that in this case, despite an abscess being present, the inflammatory markers were improving!! The main feature for making certain that the patient was scanned, was the fact that there had to be a severe pathological process driving the haemolytic anaemia.

The haemloysis was probably due to localised-subacute DIC and the anaemia resolved once the abscess was drained.

This patient underwent retroperitoneal drainage of the abscess and full microbiological results revealed Proteus mirabilis as in the urine.

Things to Remember:

• Listen to your patient
• Examine all the areas complained about by the patient
• Investigate affected areas
• Treat !