TropT or Not To Be- That is the Question

Dear Bloggers

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

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

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

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

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

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

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

Family and social history were unknown.

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

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

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

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

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

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

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

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

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

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

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

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

IMPRESSION

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

Moral Of The Story

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

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

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

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

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

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

Have a great weekend !!!

Should Medicine Become Protocol Driven??

Dear Bloggers

What are medical protocols and should we be using them?

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

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

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

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

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

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

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

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

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

Please consider... :-)

An example of Good Practise

Dear Bloggers

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Keep up the good job!

Have a great day....!

An interesting brain teaser

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

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

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

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

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

She took voglibose, amlodipine and atorvastatin only.

She had no relevant family history of note.

On examination

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

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

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

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

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

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

IMPRESSION

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

There was also evidence of chronic heart failure

RESULTS AND DISCUSSION

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

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

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

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

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

Echocardiogram was normal with no vegetation.

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

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

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

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

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

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

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

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

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

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

The catheter should also be removed if possible.

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

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

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

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

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

CRP- Cannot Rule out Pathology

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

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

Broad Spectrum Antibiotics-- carBapenems Shall Avoid

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

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

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

The take home message today is:

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

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

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

Hokkaido Revisited In The Snow!!

Dear Bloggers

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

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



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

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

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

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

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

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

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

Don't Ignore Your Patient's Symptoms

Dear Bloggers

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

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

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

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

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

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

When a fuller history was taken it was revealed that

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

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

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

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

There was no history of diabetes.

She was a non-smoker.

On examination

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

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

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

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

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

Impression

The positive features from the history include the following:

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

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

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

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

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

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

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

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

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

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

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

Clinical Problems

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

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

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

4) Lower abdominal mass ? cause ? incarcerated bowel

The patient underwent further workup to investigate the above causes.

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

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

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

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

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

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

Have a good day!! :-)

Welcome to 2008-- a time for reflection

Dear Bloggers

Welcome to 2008 !!

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

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

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

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

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

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

Great Books to Read

Dear Bloggers

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

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

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

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

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

Happy reading.

Dr Aoki's Visit

Dear Bloggers

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

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


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

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


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

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.