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!

Dehydration-- How To Recognise It and Avoid Disaster.

Dear Bloggers

Today I would like to discuss about inpatients and one of the biggest problems that can cause morbidity and mortality -- Dehydration !!

Yes, dehydration. Patients who are admitted with severe illness usually have a deterioration over several days before being admitted to the hospital. In that time, they may have stopped eating and drinking and have already started to dehydrate. Moreover, with the onset of confusion, they may have abolition of thirst and be unaware of the fluid loss. Addition of fever and a warmly heated hospital ward all year round means that fluid loss from sweating can become a real problem.

We as doctors have to acknowledge that dehydration can occur in patients and that it can even occur in hospital.

How to recognise dehydration and how to deal with the problem requires knowing what to look for and communicating with the nursing staff. For example, asking the nurses whether the patient is drinking by themselves and the total quantity is a basic question but useful as it indicates that the patient is alert and whether they have an intact thirst mechanism.

Asking how much urine the patient has been passed is equally as important because low urine output is a red flag danger sign that no doctor should miss.

Examining the patient is very important. The fingers should be felt for reduced temperature which can indicate vasoconstriction. Next the pulse for assessment of tachycardia followed by checking the skin turgor. The finding of 'tenting', where the skin pulled up into a fold, usually on the forearm, taking several seconds to flatten can also indicate dehydration. In the elderly, with loss of connective tissue, the sign is not entirely accurate, but it should be interpreted in the context of the clinical situation. Checking the mouth mucous membranes and tongue to assess how wet it is (dehydration cause salivary glands to cease production of saliva) is again a reasonable sign although it can be misleading if the patient is mouth-breathing. Obviously, knowing the blood pressure and assessing if there is a drop in blood pressure (>20/10mmHg) when sitting or standing is an indicator of hypovolaemia or sympathetic dysfunction. In children, looking for sunken eyes and reduced pulsation of the anterior fontanelle is a good indicator of volume depletion.

Examining the peripheral lower limbs can also reveal skin mottling which is a purple discolouration of the lower limbs in a non-specific lace-like pattern that ascends from the feet to the thighs with reduced skin temperature indicates reduced circulatory volume, although by this time, the patient can be severely unwell.

Finally, checking the urine volume and colour in a catheter bag can be helpful. Dark coloured urine is usually indicative of the concentrating ability of the kidneys and if working normally, a small volume, highly concentrated volume is produced. It can be dark for other reasons such as jaundice, anti-TB drugs, glomerulonephritis, fistula from bladder to bowel, myo- or haemoglobuniuria, alkaptonuria (only on standing in air for oxidization) etc..

Hence, there are many indicators of dehydration and hypovolaemia. These cannot be identified by CT or MRI scan and require the physician to examine in some detail at the bedside.

Of course, blood and urine analysis can give extra information such as the severity, but actually going to the bedside for making an assessment is essential.

I have heard of many cases in Japan and the UK, where the renal function begins to deteriorate and things such as infection, drugs and collagen-vascular disease are thought to blame, and in some circumstances, that may be so. However, in several cases, when going to the bedside to examine the patient, an element of dehydration and hypovolaemia is invariably present.

There is a constant concern that too much IV fluid can cause heart failure from 'fluid overload'. Yes, too much fluid can cause heart failure, but too little fluid will cause hypovolaemia, multi-organ dysfunction and especially, pre-renal failure. Which is the worst of both evils, heart failure or renal failure??

Well, if too much fluid is given to a patient, there are several therapies to treat heart failure such as loop-diuretics, nitroglycerine, CPAP, and even haemodialysis if necessary. However, for pre-renal failure from dehydration, there can only be one therapy and that is WATER. Haemodialysis will not resolve pre-renal failure. All haemodialysis does is remove toxins but it does not change the causative problem. That can only be sorted with fluid administration.

Hence, the worst problem in my view is renal failure rather than heart failure. Therefore, the concern of giving too much fluid and causing heart failure is unfounded. In fact, these sorts of patients with dehydration and hypovolvaemia may have several litres of fluid deficit and require significant replacement.

In a recent case reported to me from another institution, a patient had developed a pneumonia in hospital and it had been noticed that the BUN and creatinine were rising. There was concern that the drugs were causing the renal failure or the sepsis. However, when going to the bedside, it was clear that the problem was severe dehydration from the signs described above. The patient was having 1.5 litres of fluid in per day but only 500ml out in urine. The doctor was concerned about giving more fluid without obvious reason as the patient had no signs of heart failure.

The in-out volumes were unbalanced because of the concentrating ability of the kidney in response to hypovolvaemia through increased Vasopressin release and upregulation of the renin-angiotension-aldosterone axis and hence, it was no surprise that this was the clinical picture.

It was suggested to double the daily input (at the very least), and after several days, the patient's kidney function had normalised from the replenishment of water.

Water makes up 70-80% of the human body and depletion of it can kill.

Common things are common -- dehydration in the elderly is very common and should never be forgotten or ignored. Giving adequate fluid replacement can make the difference between your patient improving quickly or developing worsening renal failure. This can be completely avoided.

Please do not be scared giving IV fluid.

There are several equations available for assessing the estimated weight of a patient and working out the fluid loss by calculating measured Na against target Na, which may all be very helpful. However, we are not machines. We are biological organisms and one equation does not fix all. Sometimes, giving fluid and reviewing the urine output, blood pressure, chest sounds for new crackles [assessing for heart failure] and pulse rate can determine whether your iv fluid replacement strategy is on target, under- or overshooting.

At the beginning and the end of the day, it comes back to being around the bedside and examining the patient using your clinical skills of assessment to see if your treatment is working and adjusting it accordingly.

Please consider.... :-)

US Navy Meeting 3- Sexual History Wins The Day

Dear Bloggers

Yesterday was the 3rd combined US Navy medical meeting with our institution.

The session started off with one of our excellent English speaking first year resident's, Dr Tsunoda., who presented a case of a young patient with a history of what appeared to be consistent with meningitis. The case took a twist as the patient had an additional problem of an abnormality in the left frontal lobe on CT scanning which was considered by some to be a contusion and by other to be an abscess or even a lymphoma.
This was a so-called 'Grey Case' as there was no definite answer, but it provided an excellent opportunity to raise discussion on the possibilities that existed for generation of a differential diagnosis and work-up of the patient.



Following on in the second half, a US Navy resident, Dr Suzuki, presented a case of a patient with diffuse arthralgia & tenosynovitis and skin lesions on the hands and feet. The case took on a whole new slant when a sexual history was enquired about and the diagnosis unravelled nicely just based on this set of questions. The patient had had risky sexual encounters. The senior members of our institution got the diagnosis just based on the history, but particularly the new element of a strong sexual history, and a few photos of the skin lesions. I was very proud to hear them say-- disseminated neisseria gonorrhoea and the diagnosis was later confirmed as this.

By grouping together the significant parts of the history such as sexual exposure, arthralgia & tenosynovitis and skin lesions made the diagnosis relatively straight forwards.

It was interesting to hear that the rate of gonorrhoea infection in Japan may in fact be higher in prevalence than in the USA ! Moreover, cultures to try and identify the organism are usually negative! Hence, a high suspicion of this infection needs to be borne in mind.

The evening went very well and the cases presented made us all think and they provided a great forum for discussion.

As I emphasize on many occasions, take a sexual history. Being married is not the beginning and the end of a sexual history. Probing deeper about sexual partners, foreign travel for sex, types of sexual encounter e.g. bisexual, types of sex e.g. oral, anal, are very important and should be pursued in your questioning especially if you think that the problem is a sexually transmitted infection. In knowing the answers to the above allows one to consider which places to examine and where to obtain cultures.

Moreover, contact tracing for partners is essential as part of a well organised public health programme because stopping the spread of sexual infections such as HIV, gonorrhoea, syphilis and chlamydia and education on safer sexual practices will hopefully reduce some of these most devastating infections known to mankind.

A Great Case of Twists and Turns

Dear Bloggers

This case is a great example of how to work up a Medical Patient and it shows how being too specialised in ones approach can cause the physician to lose sight of the bigger picture. This case wins by the fact that a senior doctor did not lose focus of all the medical problems and considered a unifying diagnosis under the principles of William of Okham, so-called Okham's Razor.

Case

An elderly gentleman was admitted into a hospital with a 6 month history of Gynaecomastia.

He had noticed breast enlargement and tenderness six months previously at which time it was noted that it was probably due to the spironolactone used for his heart failure and the drug was subsequently stopped. He had no galactorrhoea.

However, the gynaecomastia did not improve, so his local hospital measured the serum prolactin level which was found to be mildly raised (approximately 1.5 x normal) and he was sent to another hospital for more intensive investigation.

However, one week before admission to the next hospital, whilst walking, he developed sudden onset of lower back pain. The pain remained even at night and stopped him from sleeping. He was then having difficulty walking because of it.

On further questioning, Body Systems Review revealed a problem with urination as it took him some 5 minutes to void his urine. Moreover, he had no had an penile erection in 10 years. He had not lost any body hair although he had never had a lot in the past.

Body Systems Review also revealed no loss or change in vision and no headaches, nausea or vomiting.

Previous Medical History included ischaemic heart disease, heart failure, and COPD.

Drugs included furosemide, candesartan, beta-blocker and aspirin plus an H2-blocker.

He was an ex-smoker and drank 2 glasses of wine per day.

On examination, the patient was in severe pain and was lying still in bed but when moving, he screamed in pain.

General inspection showed mild gynaecomastia and loss of skin turgor plus dry skin. Temp 36.5, BP 124/78 (lying)

Cardiovascular examination revealed a pulse of 80 per minute and regular. JVP was raised to the angle of the jaw and showed a systolic 'v' wave consistent with Tricuspid Regurgitation. No murmur could be identified. No leg oedema was seen.

Respiratory examination showed a resp rate of 20/min, SpO2 of 95% on room air, central trachea, slightly hyper-inflated chest and normal vesicular breath sounds throughout the chest fields.

Abdominal examination revealed a slightly distended abdomen that was soft and non-tender with no abdominal masses. Bowel sounds were present. There were no hernial orifices and no AAA. Rectal examination had not been done !!! :-(

Neurological examination of the Lower Limbs was abnormal. Straight leg raising caused pain on the right leg at 70 degrees but immense pain of the left side at only 30 degrees-- a positive test.

The patient was unable to raise legs spontaneously due to pain. Reflexes showed hyper-reflexia throughout in upper and lower limbs but were absent at the ankles. Babinski sign was normal bilaterally. L5 dermatome on the left lower limb revealed loss of sensation (skin sensation below the knee).

CNS examination revealed normal cranial nerves throughout and there was no evidence of bitemporal hemianopia.

Examination of the lower spine was not painful to touch.

Lab data revealed a normal CBC, Normal Na & K but BUN was 50 and Creat 1.6.
Liver function was normal.
Calcium was 10.6 (mildly elevated)
Prolactin level was 1.5 times normal.
Thyroid function was normal
FSH/LH were 20-30 times normal and testosterone was low normal
Cortisol, GH and ACTH were normal.

CXR revealed a small area of scarring at the lateral right upper zone consistent with old TB but no evidence of malignancy.

Clinical Impression From History & Examination and Lab Data

Okay, this patient had in fact been admitted into hospital for a TRH stimulation test because of the raised prolactin. The back problem had not been known about until the patient had been admitted and had complained of the problem.

This patient therefore had several problems

• Gynaecomastia and Hyperprolactinaemia
• Renal Failure
• Hypercalcaemia (mild)
• Back pain of sudden onset with Lower Motor Neurone Signs.
• Probable Tricuspid Regurgitation
• High LH/FSH and low-normal testosterone (testicular failure)
  

In this case, I think the patient has developed gynaecomastia from hyperprolactinaemia and spironolactone. But, the drug was stopped. Prolactin can be raised for several reasons but most people immediately think Pituitary Tumour and do a reflex MRI head scan. Well, in view that the LH / FSH levels are high as well, one might naturally think it to be a pituitary source. However, pituitary adenomas in males present LATE and are usually macroadenomas (>10mm in size) and tend to cause Visual Disturbance. This patient had no obvious visual impairment.
The Raised LH and FSH should have caused a raised testosterone level, but they did not in this case because of the low-normal level (which is inappropriately low) thereby suggesting Testicular Failure.

In Testicular Failure, in response to low testosterone levels, the feedback loop of the pituitary axis is for LH and FSH to rise. Hence, the rise in these levels is unlikely to be due to a tumour. Moreover, LH-FSH secreting pituitary adenomas are rare. Also, prolactin when raised to very high levels e.g. 20x normal with prolactin secreting adenomas, there is inhibition of LHRH and reduction in LH & FSH; hence, in this case, with LH and FSH being high, it was unlikely to be caused by an adenoma. The fact that the other anterior pituitary hormones were left intact goes against panhypopituitarism.

History was important here because on Body System Review, it was elucidated that the patient had had no sexual activity in 10 years due to erectile failure, which again would fit with Testicular Failure. This patient did not offer the information of erectile failure spontaneously, but it was the clever junior doctor that asked the question and the patient then was able to answer to the affirmative.

The raised prolactin from a Prolactinoma, I would expect to be higher and as I say, I would expect some visual disturbance because of the nature of the presentation of pituitary adenomas in men.

However, one obvious cause of hyper-prolactinaemia is Hypothyroidism because of raised TRH in response to low T3/T4 also drives Prolactin release. In this case, all thyroid function was normal. Hence, it was not entirely clear why a TRH stimulation test was being performed at all. Some authorities advocate a TRH stimulation test, but it does not really tell you what or where the problem is. A TRH stimulation test is perhaps more useful when combined with a LHRH and insulin stress test for patients with suspected hypopituitarism, usually performed post-operatively for pituitary adenomas.

Perhaps, the most obvious cause of the Prolactin being elevated was renal failure induced by the Candesartan (ARB) plus furosemide [dry skin, reduced skin turgor].

There are numerous causes of hyperprolactinaemia which are detailed in any good textbook and are beyond the scope of today's talk.

Now, why did this patient get back pain?? Well, hypotestosteronaemia in men can result in osteoporosis. Referring back to the history, this patient was walking when he suddenly developed severe back pain. This suggests either a vertebral fracture or intervertebral disc herniation. One always has to considered serious causes of neurology such as cauda equina syndrome whereby the lower spinal nerves roots become compressed in a lower motor neurone distribution. Even worse is the conus medullaris syndrome with compression of the spinal cord that can lead to permanent paralysis of one or both lower limbs. In such conditions, patients can develop urinary problems such as retention and then overflow and hence, incontinence and the same can occur with the bowel giving constipation and then overflow diarrhoea.

That is why a rectal examination is so important !!! Rectal examination should always be done in patients with back pain and abnormal neurology affecting the lower limbs.

In this situation, it is useful to check TONE by asking the patient to squeeze with their anus on the examiners finger. Loss of tone is an ominous clinical sign. Moreover, checking sensation around the anus for numbness is also suggestive of a compression problem.

Rectal examination is also important in this case to identify possible prostate cancer as it might also account for the prolonged micturition symptoms and if metastatic, could result in a vertebral fracture.

Hence, a senior doctor who saw this patient suggested the possible diagnoses

1. Iatrogenic Renal failure with secondary Hyper-Prolactinaemia
2. Testicular Failure with Hypotestosteronaemia, raised LH and FSH
3. Osteoporotic fracture due to hypotestosteronaemia
4. Lower motor neurone signs of the left lower limb due to nerve impingement syndrome from likely intervertebral disc herniation
   

However, a pituitary adenoma would have needed to be ruled out by MRI head scan but in view of the previous insertion of coronary artery stents, the patient could not have such imaging. A CT head scan was not performed.

Results

Lumbar Xray did confirm a new vertebral disc fracture at the T12 position when compared to Xrays taken several months before and this 'biopsy' of the radiological archives indicated that he had been experiencing back pain for some time, although it had worsened on this admission due to the new fracture.
The ARB and furosemide were stopped with some improvement of the renal failure.
Moreover, PSA and a Myeloma Screen [renal failure, raised calcium and back pain] should also have been checked in view of being elderly and male.
The patient's back pain improved during the admission and there was no weakness of the lower limbs and he was subsequently discharged home for follow-up as an outpatient.

In summary,

1. Not all hyperprolactinaemia is due to an adenoma. Think of more common things e.g. drug induced renal failure, anti-dopaminergic drugs, lung cancer
   
2. In men, consider also osteoporotic fractures not just osteoarthritis.
3. Think of hypotestosteronaemnia, multiple myeloma, prostate cancer and hyperthyroidism as possible causes of vertebral fractures in men.
4. If you find back pain you must examine the neurology of the lower limbs, check sensation and do a rectal examination. Such patients require urgent imaging by Xray and MRI and may require urgent neurosurgery.
5. Remember, drugs can cause renal failure and the drugs should always be examined in detail and if there is a concern that they are the cause, they should be STOPPED. As in this case, the patient also had COPD and was also taking two bronchospasm-promoting drugs !!! e.g. aspirin and a beta-blocker. Other drugs such as ticlopidine / clopidogrel can be used in place of aspirin and beta-blockers used for hypertension can be switched to other classes such as a calcium channel blocker. If used for anti-arrhythmic purposes there are many agents out there that can be used in place of a beta-blocker.
6. Remember to Ask Questions from Body Systems Review- you will find symptoms that the patient never thought were a problem and that they never thought you would ask and it will save your patient and you too.
7. Men with osteoporosis due to hypotestosteronaemia may benefit from testosterone replacement and reduction of fractures with the use of bisphosphonate drugs or the newer recombinant human parathyroid hormone ( teraparatide ), which should be strongly considered in this case. Note: when starting testosterone therapy, prostate cancer should be initially ruled out because hormone therapy can accelerate this type of cancer.
   
8. Most compression neuropathies from intervertebral disc herniation improve with time, but if severe e.g. severe pain, loss of function, then disc surgery should be considered.
   
9. Remember, Rectal Examination, Rectal Examination and finally, Rectal Examination. Never Forget to Do It !!!!!!!!
10. In view that this patient had biochemical evidence of testicular failure, the genitalia should have also been examined. Never forget to examine this area.
    

One excellent reference for principles of history taking (and hence, Body Systems Review) is:
The Patient History: Evidence-Based Approach (Paperback)
by Lawrence M. Tierney & Mark Henderson

Please consider....

Juggling The Balls of Uncertainty

Dear Bloggers

A 70 year old female was admitted into another hospital in Japan, following 3 episodes of gastrointestinal haemorrhage.

She had first noticed dark, black stool the day before admission and she had slight lower abdominal discomfort.
However, by the next day, this was followed by fresh red blood on defecation. There was no information about how much bloody stool was produced.

The patient had no other symptoms including no nausea, haematemesis, vomiting, epigastric pain, dizziness, dyspnoea, palpitations etc...

The patient had known severe coronary artery disease and had had a previous myocardial infarction resulting in 100% stenosis of the RCA, LCX arteries and a patent LAD which housed a stent to maintain its patency. Not only that, an apical thrombus had been diagnosed due to dyskinesis of the left ventricle, several months before for which anticoagulation was used.

The patient was also receiving aspirin and ticlopidine but no proton pump inhibitor (PPI).

The patient was not using alcohol. There was no history of any previous GI complaint.

Previous medical history apart from the above also included Diabetes Mellitus (Type 2) for which a sulphonylurea was used for control.

She was a non-smoker.

On examination the patient looked unwell and pale. The blood pressure was 80/40 despite having received 3 litres of crystalloid fluid. Pulse was 120/min and regular. Temp 37.0
Resp Rate 14/min and O2 sats 97% on room air.

CVS: Pulse quality was reduced at the radial artery; it was difficult to find. Left hand middle and ring fingers were cold to touch. JVP was not elevated. No heaves or thrills. Heart sounds were normal. No peripheral oedema was found.

RESP: Trachea was central. Hyper-expanded chest. Slight crackles evident at the right base only.

ABDOMEN: Soft, non-distended, no organomegaly, palpable colon from faeces only. No rebound or guarding. Bowel sounds increased. Rectal examination: Fresh Blood and no masses.

Bloods revealed a raised BUN/Creatinine ratio, Hb 6.0, INR 3.0. Normal CK and normal Liver Function Tests (three hours before, the Hb was 11g.dl)

One area with highest risk from bleeding was the Upper GI tract such as the stomach or duodenum in view of the history of anti-platelet agents and malaena, although lower GI haemorrhage could not be totally excluded because of the lower abdominal discomfort that was non-specific. Sometimes, a caecal focus of bleeding can produce stool that looks similar to malena. A raised BUN to Creatinine ratio can signify upper GI haemorrhage but in this case it might also be as a result of renal hypoperfusion from shock-- there is simply no way to accurately tell unless a gastroscopy is performed !

However, this patient was not straight forwards because despite the bleeding, by reversing the coagulation might result in either stent thrombus or embolisation of the apical thrombus. This is a so-called Catch 22 situation i.e. you cannot win either way. You are damned if you do and damned if you don't..... :-(

It was clear that by not reversing the coagulation disturbance the patient would exsanguinate.

A senior doctor who reviewed the patient was suspicious that the combination of warfarin plus two anti-platelet agents was the cause for the bleeding. It was suggested that the following things should be instituted:

1. Blood replacement to aim for an Hb>10g/dl especially as coronary heart disease
   
2. Reduce the INR with Vitamin K (low dose e.g. 0.5-1.0mg only), plus Fresh Frozen Plasma (FFP) to aim for an INR of 1.5 or thereabouts
   
3. Intravenous Proton Pump Inhibitor
4. Stop anti-platelet agents (temporarily)
   
5. Urgent gastroscopy and colonoscopy. The former was suggested because of the raised BUN to Creatinine ratio.
6. Insert a Foley catheter to measure hourly urine output
7. Aim for systolic BP >100mmHg
8. Repeat echocardiogram
   

However, in the end, only Vitamin K was used and only a colonoscopy was performed which is shown below:

The colonoscopy showed generalised mucosal bleeding suggesting platelet dysfunction and coagulation disturbance. There was also evidence of Diverticular disease with bleeding, and although it is common for these to bleed, it by itself does not account for the generalised bleeding. Thus, the bleeding had resulted from an iatrogenic source-- DRUGS!

A gastroscopy was not performed and hence, an upper GI bleed was never excluded here.

Repeat transthoracic echocardiogram revealed that the thrombus located at the apex had become smaller in size as one would expect on treatment.

In this case, what one has to decide is which problem is going to be immediately life threatening, in this case, GI haemorrhage. Hence, once the bleeding had been stopped e.g. by clipping bleeding vessels and stopping harmful drugs temporarily e.g. aspirin, ticlopidine and warfarin and reversing coagulation disturbance, then treatment to prevent stent thrombosis / thromboembolisation would be the next step.

In view that the thrombus had reduced in size (and was more likely to be organising) and that with time, stent thrombosis is relatively less compared to the time when they are initially inserted, the relative risk of thrombosis/embolisation versus uncontrolled haemorrhage tipped the scales in favour of concentrating on stopping bleeding first. Remember the emergency ABC- without a Circulation the heart will have no blood supply for itself or for the rest of the body! Hence, stopping bleeding and maintaining the circulation is essential.

There were certain areas with this cases where management could have been optimised, for example:

• Performing Gastroscopy to exclude an upper GI source of haemorrhage (remember, there was malaena too and raised BUN/creatinine ratio!)
• Use of FFP-- essential. Reversing the INR (in this case, probably an incomplete reversal of INR would suffice) until all bleeding had ceased then followed by intravenous heparin for cardiac protection. Use of heparin is preferred in such circumstances because if bleeding recurs, the heparin can be immediately stopped and if need be, protamine sulphate can be used to reverse it. The only concerns here would be recurrent bleeding and the potential Heparin-Induced Thrombocytopaenia. HIT does not happen immediately and the risk increases the longer the heparin is used, usually over several days to weeks.
  

Vitamin K was used which would have returned the INR to near normal although it takes several hours for new clotting factors to come into play and this might be too late for someone bleeding rapidly. Always consider using FFP. FFP contains pre-formed clotting factors and hence, it will temporarily normalise the INR whilst Vitamin K allows new intrinsic clotting factors to be produced.

Hence, the idea that hoping to maintain a high INR for coronary protection and at the same time clipping bleeding areas in the face of generalised mucosal bleeding that could result in multiple torrential sites of bleeding at any time and anywhere needs a re-evaluation. It is like trying to plug holes in a kitchen sieve- a self-defeating objective. Not performing a gastroscopy again needs reconsidering because this patient had generalised mucosal bleeding and was probably bleeding from every part of the GI tract.

Remember, it is not just GI tracts that bleed on warfarin with dysfunctional platelets, anywhere can bleed, but especially the brain. The GI tract is a good guide (and the skin too) to know what is going on with coagulation in the rest of the body and with mucosal bleeding then be warned because your patient could have a intracerebral bleed. The important thing here was to control the clotting first and thereby control the bleeding to make the patient haemodynamically stable and then image the GI tract and then consider starting the heparin to protect the heart.

In this case, the patient's INR was reduced to 1.4 on Vitamin K alone and the repeat colonoscopy reconfirmed multiple areas of previous haemorrhage.

These kinds of case are not described in your average medical text book as no case is the same as the next. Doctors should always expect the unexpected and hope for the best, but plan for the worse. An element of uncertainty is always going to occur in a case such as this, and sometimes, keeping your nerve and following long-upheld evidence based rules but at the same time taking a leap of faith into the unknown is required in order to help your patient.

Please consider...

Medical Residency System In The UK

Dear Bloggers

It may well be known how the USA medical residency system works by Japanese residents because of the wide-spread American influence in Japan. However, I am certain that little is know about the UK medical residency system which I will endeavour to unveil in this article.

It may be best to explain the infrastructure of the system to see how it related to the residency system.

Basically, in a usual district hospital there are 10 medical teams which are usually Cardiology, Respiratory, Gastroenterology, Diabetes and Elderly Care medicine who although have their own speciality, they also practise General Internal Medicine and therefore see all medical problems.

Each respective team will usually have a first year doctor, and more senior doctor who may be anywhere from a second year to a fourth year doctor. There will also be a Registrar doctor who will be sometimes assigned to two teams within the same speciality thereby covering four doctors below him/her. These days, the number of Registrar level doctors has increased and therefore, it is likely that a Registrar will cover only one team. Each team has its own consultant who will also have a respective speciality and who also practises general medicine.

Each team will look after around 20-30 patients and the work will be split between the first year doctor and more senior doctor or they will see all the patients together. This thereby allows all the patients to be seen usually in a morning and all the jobs are carried out by the afternoon. If a patient gets sick then one doctor is available, usually the senior, to sort it out whilst the junior continues to see the other ward patients.

The Registrar is a more Senior doctor who is in training to become a Specialist consultant. The Registrars are usually engaged in a combination of Outpatient clinics and Ward work and hence, if patients are sick they are usually called upon to resolve matters especially if the less senior or junior doctors cannot solve the problem.

If all else fails, the Registrar may defer to the team consultant who has responsibility to try and resolve the problems.

Hence, there is an upward chain of command whereby the ultimate responsibility for all the patients lies with the consultant of the team. It is therefore in the consultant's best interest to know what is going on with the inpatients and this is done by twice weekly ward rounds in most cases.

The UK ward rounds involve the whole team seeing all the inpatients whereby the consultant can be updated on recent tests and blood results, but more importantly new history and physical changes. This is a great opportunity to learn as all the junior members of the team (everyone else lower than consultant level) have a chance to learn if they have been doing things correctly and get feedback from the consultant. This is also a safety mechanism for the patient as they will be seen by an experienced physician who will take more history and examine them and review drugs, interactions and start or stop such drugs. They will also make further plans and decide on discharge. Such an interaction between junior doctors, the consultant and the patient is a great opportunity for learning about history taking and physical examination but it also provides skills on how to manage inpatient problems, multi-organ system problems and how to decide on when to call the more senior doctor and when to discharge the patient.

Doctors do not stay in the hospital after 5:00pm if their work is finished. They are able to go home and rest--- or study !

If they are on-call, as a team, they will also admit ALL new medical patients referred from community GPs, other hospitals (transfers) and the outpatient clinic plus Emergency Room (Accident and Emergency [A&E]). Thus, all patients are admitted under the care of a single consultant on-call and that may be anywhere from 10 to 30 or 40 patients in a 24 hour period.

The on-call team work from 9am to 9pm and then go home. A night team who work for a week of nights take over from 9pm to 9am.

On the morning of the next day, the team do a Post-Take ward round to see all the new patients. Again, history and physical are reviewed by the consultant providing a great learning opportunity for the Residents. This is a legal requirement for all patients to be seen within 24 hours by a consultant when admitted to the hospital. This provides great training in emergency medicine.

On-call varies and may be once in a week or may involve a week of nights or a whole weekend, but no on-call session lasts more than 12 hours.

Why is this important? Well a fatigued doctor makes mistakes. A recent lecture given by Dr Landrigan in August 2007 at the National Institute of Health gives an indepth explanation of fatigue in doctors and increased chances of making medical errors and driving accidents after doing long on-calls and with sleep deprivation [ http://videocast.nih.gov/ram/ccgr082907.ram ]

Hence, the UK system having implemented the famous Working Time Directive has stopped most doctors working more than 56 hours per week.

I for one who worked under this system felt fatigued working 12 hours straight when on-call and was relieved to be able to get a good night [or day] sleep after on-call. I also worked under the old system which meant a full 24 hours on call or 72 hour weekend (Friday, Saturday and Sunday) without much sleep and hence, I know the acute differences that the Working Time Directive implemented and I am sure that it caused a reduction in the frequency of mistakes within the hospitals throughout the UK.

In the USA, some hospitals are trying hard to reduce doctors hours but they are by no means in line with the standards currently employed in the UK system.

In summary, the UK system has many doctors per team with a chain of command upwards when a less experienced doctor does not know what to do, which incorporates multiple checks and balances for the patient to try and avoid accidents and misdiagnoses. The consultant has a responsibility to see all new patients and all the inpatients, the latter, several times during a working week. Residents never work more than 12 hours at a time unless under exceptional circumstances and hence, it is hoped that this will reduce mistakes by doctors.

Resident educational is somewhat informal as it takes place during ward rounds and post-take ward rounds, but there are also educational sessions carried out by all the consultants on an ongoing rota once a week to teach specific topics. Moreover, the Registrars also do training sessions for the junior doctors and medical students.

Grand rounds take place weekly as do journal clubs. Other training for higher exams the doctors usually do Self-Directed Learning and they may also go on training courses. Registrars also go on specific training courses. For advanced exams (MRCP) the consultants and Registrars will usually rotate on a training scheme whereby they will take the senior doctors to a patient and ask them to examine a body system. They will then provide their advice and constructive criticism on how the doctor can improve their examination skills in order to pass this high-level exam.

The MRCP exam concentrates on history and physical examination with little emphasis on scans such as CT or MRI.

All training sessions take place at lunchtime in most hospitals with food provided.

Moreover, I have never seen a UK doctor fall asleep in any meeting.

In summary, I think that the UK system is comfortable for working in but also for having free time as well; the so-called Work-Life Separation. Doctors do not need to remain in the hospital out of hours as any problem is handled by the on-call team for that time, and that includes speaking with relatives.

There is an upward chain of responsibility by every member of the team and a very good but informal way of training the junior doctors on frequent wards rounds at the bedside plus formal teaching sessions.
Training focuses on the patient and not on interpreting radiological scans.

This is a different system to that found in Japan and such a system may be somewhat of a surprise to you.

Have a nice holiday :-)

Professor Tierney, Dr Aoki and Some Great Cases

Dear Bloggers

Today Professor Tierney visited our institution for just two hours, but it was two hours of brilliance.



The first cases consisted of a patient with pharyngitis, fever and shoulder pain. This was presented by our fourth year resident Dr Fukuda. Professor Tierney lectured on the quality of information about platelets and how you can predict either marrow failure or consumption just by observing the change in absolute numbers. The result of the case was meningococcal septicaemia with infiltration into the CSF without laboratory data indicating meningitis.


Professor Tierney and Dr Aoki were lecturing on how they had seen previous cases of meningitis without cells in the CSF; rare but still possible ! Never say Never.

However, during Dr Fukuda's presentation, he was being called to say his wife had just given birth to their second child--a daughter. Looks like Professor Tierney is a Lucky Charm too.




The second case presented by Dr Ban, was a very interesting case of a young female with a previous diagnosis of Diffuse PanBronchiolisis (DPB) and Immune Thrombocytopenic Purpura (ITP). The patient had been admitted with recurrent respiratory problems and there was a concern that the original diagnosis was in doubt.


The patient also had hypogammaglobulinemia.

Professor Tierney went through this case methodically and came up with differentials such a Histiocytosis X, Immotile Cilia Syndrome, Kartagener's Syndrome and potentially, Cystic Fibrosis.


However, pulling all the elements together, he considered that the initial diagnosis of DPB, made some 10 years before, was wrong and in fact, he considered it to be a congenital condition called Common Variable Hypogammaglobulinemia otherwise known as Common Variable ImmunoDeficiency (CVID).



I had also been consulted on this very same case a week before and my opinion was also CVID and it is good that two minds can think alike.

The disorder is rare and Prof Tierney admitted only ever seeing 2 previous cases in his whole career and this made his third.

UpToDate 15.3 covers CVID in some detail although I am sure any good medical textbook will detail this condition.

The two hours flew by and it was a shame that it had to end. Anyhow, there is always next year ! :)

Lastly, Congratulations to Dr Fukuda and his Wife on the Birth of their Second Child.

Hypoglycaemia masquerading as Hyperglycaemia !

A recent case at another hospital is a caveat for a common problem-- hypoglycaemia.

A female patient with a history of type 2 diabetes was admitted following several episodes of unconsciousness lasting up to 12 hours each time. The patient eventually presented to the hospital because of concern as to the cause.

On the first episode, the patient had collapsed to her right side with no associated seizures or incontinence. She awoke some 12 hours later.

The second episode, she collapsed whilst eating and again, this lasted some 12 hours. At that time, she was noted to be disorientated and could not remember how to cook or wash up dishes. She was also found to have some cerebellar dysfunction. These symptoms spontaneously resolved.

When she presented in the outpatient clinic, her blood sugar was high, approx 200mg/dl.

It was initially considered by the admitting doctors that it was an unusual neurological problem although the subsequent MRI was normal.

However, another doctor suggested examining the daily drugs that the patient took to see if these phenomena were drug-induced. Sure enough, the patient was taking metformin and glimepiride 1mg-- diabetes drugs !

One junior doctor suggested that this could not be hypoglycaemia because the admission blood sugar was normal-high and that the patient had no warning signs of hypoglycaemia. This reasoning was not correct for the following reasons:

1) Most cases of hypoglycaemia are drug induced e.g. sulphonylureas / alcohol / insulin and as a consequence, they can cause a decline in blood glucose levels. The reflex reponse of hypoglycaemia is the output of Growth Hormone, Adrenaline, Glucagon in additon to Cortisol, whereby there is glycogenolysis and gluconeogenesis. Of course, this mechanism then over shoots and causes hyperglycaemia. This is the Sygomni Effect and is often seen in the early morning e.g. 3am when the patient wakens with sweats or wakes up on the floor with a headache having had a nocturnal seizure ! Some patients don't get symptoms of hypoglycaemia. Either this is because of beta-blocker use and hence, the adrenergic response to hypoglycaemia is blunted or the patient has been having recurrent hypoglycaemia which is associated with reduced warning signs.

2) Hypoglycaemia can therefore self-correct through the correcting mechanisms described above and when the patient is admitted to hospital may have a low, normal or high glucose level. The latter two scenarios DO NOT EXCLUDE an episode of hypoglycaemia.

However, some patients blood sugar can go extremely low and they may experience neuroglycopaenia and subsequent brain damage and hence, hypoglycaemia must always be treated.

With such a history of prolonged unconsciousness with periods of normality punctuating such episodes in a patient with diabetes on hypoglycaemic agents, one must allows consider this to be drug induced until proven otherwise.

The glimerpiride drug is a once daily dosing 3rd generation sulphonylurea. Because of its long period of activity, it can induce hypoglycaemia. Metformin rarely causes hypoglycaemia by itself.

Hypoglycaemia should always be considered in diabetic patients who have an HbA1c <7% (DCCT-aligned) who take insulin or an SU drug. This was demonstrated in the DCCT study when the more intensive the diabetes was treated, and hence the lower the HbA1c towards to the population normal range, the higher the recorded refequency of hypoglycaemic events. In this case, the patient had an HbA1c of 6.8% (non-DCCT aligned) and hence, it is difficult to say exactly what the DCCT aligned HbA1c was without the appropriate adjustment to DCCT.

Patients with suspected drug induced hypoglycaemia should receive iv glucose infusion (50ml 50% glucose) and the diabetes medications should be halved in dose or in some cases stopped and changed to a shorter acting agent e.g. glibenclamide changed to gliclazide.

In this case, the glimepiride was stopped. It is better to allow the DM control to run slightly high for several weeks so as to allow the mechanisms for hypoglycaemia to auto-correct before trying to attain tight control again. Hence, earlier warning for hypoglycaemia can hopefully be restored.

Finally, patients with hypoglycaemia have to got through several steps to correct their hypoglycaemia 1) They have to have warning signs 2) They have to recognise those warning signs 3) They have to consider how to correct the problem e.g. decide to eat some food 4) They have to put the thought into motion e.g. eat some food.

Anywhere along the way, such patients can have a failure to correctly manage a step, resulting in hypoglycaemia being uncorrected. For example, a patient may have warning signs and recognise them but fail congitively to consider how to correct the problem or fail to eat food despite wanting to.

Remember: Patients with hypoglycaemia can present as unconscious, confusion, aggression, appear drunk, appear with hemiparesis or seizure etc.... CT / MRI are nice tests for making nice pictures, but never forget to check a blood sugar and check the drugs as something simple as 50% 50ml Glucose can correct the problem in seconds and save a life, and save embarrassment for you too.....

Please consider ! :)

Prof Tierney Back in Town

Dear Bloggers

Professor Tierney is back in Town. Today he began his 3-day whirl wind lecture tour at C.

There were three morning sessions organised, two of which Professor Tierney presented his own cases acquired from other hospitals in Japan. The middle session involved a case presented by the C residents to put Professor Tierney to the test.



In view that Prof Tierney may be presenting his other cases at his future hospitals in Japan, I will not reveal their contents. It is a surprise !

However, the C case involved a female who presented with an intermittent nocturnal non-productive cough, fever and hypoxaemia. The diagnosis was made from history and physical examination and later inferred by chest roentogen / CT, which was extrinsic allergic alveolitis. This was a simple diagnosis for this Professor of Medicine :)


One odd thing was the request of a resident to have Professor Tierney to sign his wallet!!! Perhaps the strangest request he has ever had !

Absence of Fever

The elderly are a unique subset of the patient population. When the elderly get sick, it is time to throw the book out of the window for adult medicine because there are not firm & fast rules.

When I say this I mean for example about sepsis. In sepsis, elderly patients do not always have a fever, they do not always mount a white count or even a rise in C-reactive protein.

Patients do not always get headache, Kernigs or Brudzinski sign in meningitis and alot of elderly patients have a stiff neck just from age related osteoarthritis rather than from meningism.

Hence, relying on the patient not having a fever, a normal WCC and CRP does not exclude sepsis.

Patients can present with confusion and low blood pressure and a tachycardia. The observations of the patient and looking at the patient from the bedside can sometimes be more revealing than the blood results.

Therefore, don't be mislead by seemingly normal blood results. Remember to always take cultures of blood, sputum and urine, and if warranted, CSF to check for meningitis / encephalitis or even stool culture / toxins.

A good example was of a recent case from another hospital of a male patient with a 3 week history of worsening cough. The patient had otherwise been remarkably well despite having severe aortic stenosis. However, the patient lost his appetite and the cough worsened precipitating a hospital admission. All the observations were normal. No fever, normal blood pressure and pulse and SpO2 was 96% on room air.

Even the white cell count was normal. CRP was only slightly raised at just above 1.

Examination was most revealing as the patient appeared weak and tired and slightly confused. Chest examination revealed dullness to percussion and crackles with the addition of increased tactile vocal fremitus. JVP was not raised but peripheral edema was evident.

The concern was of rather than just a straight forward pneumonia, it was considered that there could be heart failure plus pneumonia.

The patient's sputum examination revealed gram positive diplococci consistent with streptococcus pneumoniae.

Echocardiogram and BNP exams were also ordered.

In this case, the patient had a pneumonia plus suspected heart failure from severe AS. Despite these problems he only manifested loss of appetite, weakness and mild confusion. No obvious problem with his vital signs and no fever.

Please remember that patients do not write the textbooks---doctors do. A typical case is a typical case, but patients sometimes do not fit the mould and do not obey by the rules of illness as defined by doctors.

Hence, when it comes to the elderly don't just label them as demented when they turn up to your hospitals with confusion, it could be due to overwhelming sepsis!

Please consider.... :)

Back In The Saddle

Dear Bloggers

It has been almost 2 weeks since my last blog for which I apologise. Unfortunately, I was unwell and I underwent various and extensive medical tests. I am now getting better and I hope to be back to writing my regular blog articles from now on.

I have been extremely impressed with the speed of the medical services here at my hospital. The process of undergoing tests is streamlined and well practised. I have only ever been used to the British hospital national service which is also very good. However, when you become a patient in another country it can sometimes be daunting about what tests will be done and how quickly and particularly the communication. However, I can understand many Japanese medical terms these days plus usual communication, so I did not find that too taxing.

I have had no complaints at all. In fact, I was very, very impressed. I also noticed that people showed concern and were caring. Hence, the Caring Profession.

Although I have no wishes at all to be a patient, I did feel I was in good hands.

I am now Back in the Saddle..... :) It is sure good to be back!!!

Changes to this Blog

I have decided to make some changes to the design of the blog page and I hope that it is now easier to read than before.

This new format should now fit the entire page of your computer and the text should be easier to read than before.

I have also removed the restrictions on this site for posting comments. You no longer require a Gmail account and you can simply post a comment although all comments will be reviewed by me, the site moderator! :)

Be warned, I will only publish comments that are relevant to this site and not comments for people wanting me to advertise their books in America !

Please pass any feedback to me on how I might be able to improve this site in future.

Navy Meeting II: Journal Club

Last night we were invited to the US Navy base in Yokosuka to partake in their alternate month Journal Club.

We started the session with delicious American pizza with some refreshing beverages followed by the presentation of two recent journal papers.

The first paper was presented by one of this years interns and it featured the topic of male circumcision for the prevention of HIV transmission. This idea was put forwards over 20 years ago when HIV was first discovered but for some reason it has taken until now to have been taken seriously. The results of the paper and several others show a 50-60% reduction in HIV transmission rates simply by circumcising men. This, apart from condom use and total abstinence, is probably one of the major factors identified for reducing HIV transmission in sexually active men.

The second paper featured the topic of obstructive sleep apnoea-hypopnoea in children. The paper discussed about adenotonsillectomy aiding children who have the OSAH problem and where diagnosis with polysomnography can be helpful to determine those patients who require surgery and those who do not.

Both papers were quite long and somewhat complicated even for natural English speakers, but both Navy interns did remarkably well and spoke very eloquently with congent perspectives on the papers.

The US and British style of Journal club activity is more combative in style with questions and opinions being thrown at each other to see what other peoples opinions are in return. In a UK or USA type journal club setting, the opinion of the person presenting the paper should also be heard.

For example, the presenter may agree with the paper's findings or on the other hand, they may find other errors with the paper and disagree with the findings. Just by conveying the Author's opinions is not enough. As doctors, we can all read a paper and appraise it ourselves without a presenter.

The purpose of the presenter is to compare, contrast and constructively criticise the quality of the paper. There are many papers produced each year, some with dubious results, each trying to persuade us to change our practise in some way or other. If we were to believe everything we read then we would be pushed and pulled in sorts of directions and not necessarily the right ones.

A journal club is there to try and concentrate the presenter to give his or her opinion why they agree or disagree with the findings and then to justify that opinion. It is not always the best way to just agree with the Authors of a paper as the Authors may be wrong and have come to the wrong conclusions. It is sometimes good to be critical because as doctors we are presented with information from drug companies each and everyday who are trying to get you to use their drug and convincing you that their drug is the best for a particular condition.

When they provide you with the 'evidence based papers' you need to be critical of such studies and try and find other studies that agree or disagree with such findings. It is a real problem because drug company studies are generally funded by the drug companies themselves and they sometimes are in control of the data collection and analysis-- this is a gross conflict of interest that the medical professional has little power to do anything about. Hence, it is sometimes dubious as to whether we can believe the findings of such papers. Therefore, the purpose of a Journal club is to teach you how to critique a paper and how to pose questions to those who produce a paper or to drug representatives.

Asking drug reps how and why we should use their drugs and what evidence they have is not something to shy away from. When we use new a treatment we need to know that it works, it is better than the previous treatment, that it does not harm the patients and if it is more expensive than before, that it is going to prove cost effective and actually make a clinically significant difference in the long run.

Hence, a Journal club is not just a nice meeting for a friendly discussion, it is a serious thing that can teach us all a great deal and it is great to hear other peoples opinions even if they are different from our own.

These meetings are proving to be very helpful and provide an insight on how matters are discussed differently among different cultures.

Dr Makoto Aoki-- What a Great Guy !!

Dr Makoto Aoki visited out institution to answer to a case on meningitis. He went through the various types of meningitis and stressed the importance of taking a sexual history.

He reminded us about 'aseptic meningitis' such as vasculitis (SLE, Behcet), malignancy (metastases), drugs (NSAIDs), Infective ( viral: HIV, mumps, enterovirus, herpes simplex virus; bacteria: partially treated meningitis, TB, syphilis; fungal: cryptococcus, candida ). Moreover, bystander meningitis e.g.caused by a paravertebral abscess is another important cause.

He also reminded the doctors that being married does not exclude patients from engaging in sex with the same or opposite sex and hence, sexually transmitted infections are an important cause of meningitis. Hence, a sexual history is an extremely important part of the work up of infectious diseases.

The turn out of doctors at the tutorial session was great ! The doctors were able to answer Dr Aoki’s difficult questions intelligently and more importantly, correctly !!

Dr Aoki’s sessions are always great fun and he tells some good jokes as well. These sessions provide a valuable time for the residents to learn new things and to relax from the busy daily schedule.

I for one am looking forwards to his next visit here in December.