Why Are Troponins Ignored?

Dear Bloggers

Dyspnea has a wide differential diagnosis that can potentially involve the cardiac, respiratory, abdominal, haematologic, neuromuscular, metabolic systems etc. Because of the vast number of causes of dyspnea, it is essential to take a detailed history, as much as possible, and examine carefully for various serious causes.

Performing of a chest radiograph, electrocardiogram (ECG), cardiac biomarkers, a complete blood count and an echocardiogram, etc, are essential components for the work up of the cause of the dyspnea and on occasion, there may be several overlapping causes.

Silent myocardial infarction resulting in new onset or worsening heart failure should always be considered. New ECG changes suggestive of ischemia e.g. dynamic T wave changes, should alert the physician that there is a cardiac cause.

Checking of the Troponin-I is currently regarded as the Gold Standard test to confirm a myocardial cause. Previously, it was considered that Troponin-T (TnT) was specific for cardiac muscle but studies have shown that skeletal muscle can also release TnT e.g. rhabdomyolysis. Only Troponin-I (TnI) is considered to be most specific to cardiac muscle. It is more sensitive and more specific as a cardiac biomarker than the CK-MB fraction.

Evidence Based Medicine (EBM) texts and international guidance now make mention that TnI (or TnT) should be measured and that measurement of CK-MB is no longer necessary for the diagnosis of an acute coronary syndrome. Moreover, the TnI levels stay elevated for up to 10 days, whereas CK-MB levels drop much more quickly, making it possible to still diagnose a recent myocardial infarction even if other less sensitive or specific biomarkers are negative.

TnI can be used to examine for re-infarction too. A rise of >20% from the last measurement can assist in the diagnosis of re-infarction. CK-MB is again no longer required for making this diagnosis.

It is an unfortunate situation that many Japanese medical students and junior physicians are still being taught that they should check CK-MB and that many still are uncertain about the utility of TnI. Some physicians are not inclined to check TnI or take an elevated TnI level seriously e.g. in renal failure citing that it is purely the renal failure causing the rise.

Recent evidence has actually suggested that patients with a raised troponin level without proven acute coronary aetiology actually have a worse prognosis than in patients with an obvious acute coronary syndrome. One reason for an increased mortality rate may have been the physicians did not take such a rise seriously enough, considering it unrelated to coronary heart disease and therefore, further follow-up was not performed timely enough for such patients. The American Journal of Medicine (2011) 124, 630-635

Other common causes of elevated troponins include

•myopericarditis
•aortic dissection
•cardioversion
•cardiopulmonary resuscitation
•subarachnoid hemorrhage
•severe sepsis
•trauma / contusion
•fast atrial fibrillation
•heart failure

Stress-induced cardiomyopathy (Takotsubo) can cause heart failure, ECG changes and TnI rises. It is said that in some cases the physicians will observe the myocardial echocardiographic changes only and then (somehow) will diagnose this disorder. However, "Takotsubo Heart" cannot be diagnosed unless the patient's coronary arteries are deemed normal by angiography; thereby ruling out an acute coronary syndrome.

Essentially, we cannot ignore a potential acute coronary syndrome as evidenced by worsening dyspnea, ECG changes consistent with ischemia and a TnI rise. Although echocardiography can be useful to look for wall motion abnormalities typical of myocardial infarction, it cannot completely rule out the diagnosis especially as ultrasonographic observations have operator error and there may be poor views depending on the anatomy. In such situations emergent angiography or coronary artery computed tomography may provide the answer.

An elevated pulmonary artery pressure can be helpful to assist in the diagnosis of heart failure given a consistent history, in addition to an elevated B-Natriuretic Peptide (BNP). It is worth noting that in a recent study BNP levels were found not to be superior to physical examination of the right and left sided heart pressures by cardiology experts. The American Journal of Medicine (2011) 124, 1051-1057

Hence, it comes back to history and physical examination and understanding what common things present commonly and what important differential diagnoses should not be missed. Acute coronary syndrome is very common and Takotsubo Heart is not common at all. New onset dyspnea or worsening symptomatic heart failure should make the physician consider silent myocardial infarction in the differential diagnosis. Consistent ECG changes and elevated troponins assist in the diagnosis of this disorder.

Finally, one should not forget about pulmonary embolism (PE). This can also result in worsening heart failure and acute, sub-acute or chronic dyspnea. ECG changes can occur although they are usually right sided in origin on the ECG e.g. Tall R wave in V1 (>7mm), biphasic T waves / ST depression in V1-V3. However, a normal ECG is common and the "classic" S1Q3T3 is very unusual to see yet it seems that this is the only ECG change that students and residents seem to remember. However, BNP and TnI can both be elevated in PE, and when elevated together, they are associated with a worse prognosis.

In essence, elevated troponins should not be overlooked. Instead, further examinations should be undertaken. If silent myocardial infarction cannot be ruled out or if considered most likely, angiography is warranted. At the very least, basic cardiac treatment should be commenced for such patients on the basis that they are likely to have the problem (rather than not due to its high incidence) and that waiting is not an option especially as "time is muscle".

One should not wait for the biomarkers to become positive (which can take 4-6 hours; new highly sensitive troponin tests can provide earlier results but are still not in widespread use). Remember, and I shall say it again, "time is muscle" and the longer one waits before instituting treatment, the worse the outcome in terms of morbidity and mortality.

Remember that an essential treatment in ACS is aspirin, which reduces mortality significantly. It should never be withheld unless there is a good reason e.g. acute gastrointestinal bleeding, allergic reaction. It is said that in some institutions, some cardiologists withhold aspirin initially and proceed straight for percutaneous intervention with this drug being commenced post-procedure. This method of withholding aspirin, perhaps from the misguided belief that patients will bleed excessively during PCI, is not standard treatment according to many of the world cardiology guidelines. This needlessly puts patients at risk by delaying medical treatment of ACS.

In contrast, patients with suspicion of ACS in places such as the USA and the UK are treated more aggressively and are frequently given aspirin en route to the hospital by paramedics. In some countries e.g UK, thrombolysis by tPA for ST elevation ACS is also given en route if certain inclusion and exclusion criteria are met and they are not near to a center providing urgent PCI treatment.

It is time to take Troponins elevations more seriously and be more aggressive in the management of acute coronary syndrome in Japan rather than relying on initial PCI alone and withholding life saving drug treatment prior to such procedures.......please consider

2010 American Heart Association guidelines -- see that aspirin is given early.

2011 Summary of Guidance from the European Resuscitation Council can be obtained here

Evidence is to be applied not overlooked

Dear Readers

It's been a while since I last wrote on the blog. Many of you probably thought I had forgotten about it. Quite the contrary, but I have been very busy with other things though. I will continue to write on here from time to time but with no guarantees when.....sorry :-)

I wanted to talk about the use of evidence based medical practice in every day medicine.

Many physicians talk about evidence based medicine and it's importance in modern day medicine, but when it comes to actual patient care, some do not apply it stating variously that "in A country we do x,y,z treatments instead". That is not to say that the local treatment(s) is/are wrong, but without evidence to support it's use compared to well established medicines or procedures that do have a body of evidence, how can the local treatment(s) surmount evidence based treatment?

In many instances a senior has decided the treatment based on what they were taught combined with experience based practice. Hence, "if it ain't broken then why try and fix it?" Well, the use of EBM provides the best current established methods that can support the physician to provide medical therapy in the best possible manner. Of course, such treatment may be very different from local established therapy but that does not mean it should not be utilized.

Many physicians wish to remain in a comfort zone of practice of not using a new treatment method because of fear of it causing a problem, inexperience in the use of drugs or procedures, and fear that they will not get support from their fellow colleagues who may only be practicing "eminence based medicine". The fear of the unknown is a strong emotion to stop us moving forwards as physicians to provide the best possible treatment.

For example, it is said that amiodarone use in Japan is minimal for the "fear" of the side effects, which in the acute phase of use are actually minimal and in the long term can of course cause problems, but on minimal maintenance dose, such side effects can also be limited. The fear of never having used it, for example in atrial fibrillation, instead translates into the use of class I cardiac drugs that have inherent dangerous side effects such as proarrhythmia induction or class IV calcium channel blockers that can cause worsening systolic failure in patients with existing ventricular dysfunction. These decisions may not be optimal, but it is fear of the unknown that causes such paralysis in medical decision making leading to the use of treatments that may be inferior to those used in best practise.

It is also said that in episodes of benign paroxysmal positional vertigo, patients in Japan are given intravenous bicarbonate. When challenged about the evidence for the use of such treatment, some doctors can be vague and use the standard dogma of "this is standard therapy here" without being able to provide firm evidence for the benefit of such therapy. Evidence based texts e.g. UpToDate, can provide the current standard of therapy with references that one can rely on to make clinical decisions rather than resorting to old therapies that have not been critically tested in large trials.

The fear of providing pain relief to patients is another example leading to paralysis of clinical decisions. Severe pain may not be amenable to the usual acetaminophen or NSAIDs. Sometimes the only treatment that can lead to adequate pain control can be opioids/opiates. There is again a strong fear factor that patients will become addicts or that they will stop breathing. This can sometimes translate into patients without cancer being refused adequate pain control, which may be severe, or patients with cancer being underdosed, because of physician fear.

The laws controlling the use of narcotics in Japan are very strick having been produced over 50 years ago and which need a significant overhaul for treatment of modern day patients. It is said that only patients with cancer can have opiates and even then, some physicians need a special license to prescribe it. The fact that patients in severe pain do not stop breathing with opiates is a testament that when used appropriately, they are safe. Moreover, use in the short term e.g. acute myocardial infaction and postoperatively, there is no induction of addiction. The fact that the opiate use in Japan is 1/7 that of the UK despite it having comparatively double the population, reflects the aversion of it's use in the medical community generally.

The use of EBM can help to support the physician to make difficult decisions when their experience base runs out. A physician should always recognize their limitations. If they are unable to answer the question themselves, they can ask for a specialist opinion or they can go to the books. However, the books are only as good as the time of when they were written and usually, by the time they go to print they are already out of date! Therefore, utilizing an EBM database that is updated regularly must be the best current way to answer difficult clinical questions.

One should also bear in mind that EBM texts are not just there to help with therapy. They are produced to aid the physician to consider differential diagnosis to try and prevent premature closure of diagnosis. In the early stage of an illness with few symptoms and clinical signs it can be difficult to be specific about a diagnosis. Such texts can help guide the physician about the natural history of disease and atypical manifestations and presentations. This can be very valuable as no physician can hold mountains of information in their minds ad infinitum. With the ever changing world of medicine and epidemiology of diseases over time, an updated EBM text can be a very helpful assistant.

It should never be an embarrassment to not remember something, but it is an embarrassment and sometimes negligent, if information can be checked but it is not done so because of pride of supposedly "knowing everything I need to know". From my own perspective, the more I read to keep updated, the more I realize that I know even less. I end up with more questions that when I started.

I shall no doubt be writing more on this in the future.

Essentially, there is no excuse to avoid the use of EBM at the bedside to assist in patient care. EBM can answer many of the clinical questions that come up everyday on the ward. The fear of the unknown and uncertainty is something physicians must deal with everyday. There is no escaping it by ordering more and more tests, and which "play for time", and which are unlikely to answer the questions.

As a word of warning, the use of EBM in a patient with for example, X disease, should lead to the use of that same evidence and application of it for all future patients with X disease (but by also checking to make sure the EBM recommendations are still the same or have been updated) rather than it being an isolated case or an "experimentation with EBM".

We as physicians need to keep as knowledgable as possible about the changes in medicine and by reading thoroughly we can increase our comfort zone of knowledge by applying this to patient care at the bedside rather than being fearful of the "unknown" and "personally untested". We should embrace EBM to provide the best possible patient care.

Reading EBM is good but applying it in reality is the only way to improve patient care otherwise we have a situation of "one hand clapping". Without two hands i.e. Reading and applying what was read, we will make no clapping noise and as a result, patient care will remain unchanged.

Please consider.....

Rounds around the computer are not rounds

Dear Bloggers

It's been a while since I last wrote on this blog. I'm afraid I've been very busy but I nevertheless have not forgotten about the blog.

From my experiences in Japan, patients are often discussed around computer terminals with much emphasis given to laboratory data and radiology rather than the history and examination. This is nothing new to this blog but the fact that the patients are seen for just a short time and given a cursory examination, is not what I would classify as a clinical round.

In other countries such as USA, Australia and the UK, although there is also discussion about data and scans, their emphasis is not put before the history and physical examination of the patient.

Clinical interpretations, decision making, treatments etc are based upon the combined picture of all elements including what was or was not found in the history and on the physical examination with the addition of basic tests e.g. blood tests, ECG, chest x-ray. Decisions are not based only on tests. In the emergency situation, withholding treatment while awaiting test results can end up with a dead patient. For example, a tension pneumothorax is a clinical diagnosis and sending the patient for a chest X-ray would be viewed as malpractice and even incompetence. A needle thorocotomy at the bedside is a diagnostic therapy and fully justified in such a situation.

When reviewing patients on the ward rounds, clinical signs need to be re-elicited to determine if there is a worsening or an improvement. It is not often necessary to keep repeating laboratory data daily (unless the patient is very unwell) or 'following the X-ray' or perhaps more commonly, 'following the CT'. One must remember that patient signs e.g. crackles of pneumonia, can disappear before the radiograph resolution. Hence, following a scan may prove to be less accurate than the physical examination. One must actually 'follow the patient' and not waste time with unnecessary, costly, tests when simply percussing, palpating and listening can tell you if there is an improvement or not and without cost.

On ward rounds, unwell patients need daily physical examination or even more frequently if the clinical need arises. A simple few words and a wave is not sufficient. It does not tell you what is going on with the patient. Moreover, laying on of hands is invaluable as it tells the doctor sometimes more information than a blood test or an xray. In addition, patient satisfaction is better because it shows that the medical staff are actually interested in finding the problem.

There have been situations when a full physical examination of the patient has resulted in the patient developing a 'welling look' and comments including 'I have never been examined in such detail before. Thank you.', 'I've been in hospital for many weeks and this is the first time I have been examined properly'. Family members are also highly satisfied if the medical staff show real interest and examine.

In addition, although it is not commonplace for medical staff to ask many questions as it is viewed as a kind of 'rudeness' to inquire and can be embarrassing, that kind of way will result in diagnoses being missed as the question(s) was/were never posed. Better to ask more questions by asking 'why' than be scolded by a senior doctor later with them asking you 'why not !'

Hence, ward rounds done on paper / electronically of course have their place, but they should not be the only component of a ward round. Patients need to asked more questions to help narrow down the current problems and physical examination should be performed for reassessment.

All conversation information and physical examination needs to be properly noted (under subjective and objective in the SOAP format of notation) at the time it takes place and not hours later. Remember that such information is the basis of a legal document and if not written down immediately, essential information can be and is often missed. This can lead to inaccuracies and wrong tests / treatments being ordered or not ordered at all.

Treatments need to always be re-evaluated. Antibiotics, dose, frequency, side effects, and the patient response to such therapy needs to always be considered. Moreover, rather than just starting antibiotics and forgetting about the stop-date, such treatment always needs to be revisited to decide on when to complete the course. If the patient does not respond appropriately, there can be several reasons which need to be considered:

1) The antibiotic is not covering the organism(s) e.g. anaerobic bacteria
2) The dose / frequency is too low
3) The patient has immune suppression
4) The bacteria has resistance to the antibiotic
5) A non-bacterial cause is present e.g. pulmonary embolism, vasculitis, fungal infection
6) A collection has formed e.g. lung abscess, valve ring abscess, sub-phrenic abscess
7) There may be a drug-fever; patients need to always be asked if they have ever had a reaction to drugs with antibiotics being a particularly common problem
8) There is a line infection e.g. prolonged use of central lines causing candida bacteremia

Hence, simply switching to a 'napalm-kill everything' carbapenem that kills indiscriminately is not always the answer. The bacteria may be very sensitive to the original antibiotic e.g. penicillin, but it may be one or more of the above elements that is resulting in failure of resolution. Switching to a 'penem' will of course be useless if there is candidemia, abscess formation, PE.

Carbapenem usage should not be first line except in certain situations e.g. neutropenic sepsis. Because antibiotics are strictly managed by microbiologists, pharmacists and infectious disease doctors in places such as the UK, Australia and the USA, carbapenem use is far less. In many situations, it is 3rd or 4th line but almost never first line.

Hence, evaluating where infection may be coming from rather than pumping in a 'penem' and hoping for the best is essential to ensure that the patient is receiving appropriate care.

As I have mentioned, commencing antibiotics needs deep consideration but stopping them is also a very important thing.

The usual way of stopping antibiotics is when the clinical features and (e.g. symptoms and signs), vital signs improve e.g. fever resolution, the patient feeling better, and with the hematologic parameters returning towards normal, which is sometimes not practiced in some institutions. Patients are sometimes maintained on intravenous antibiotics for weeks on end even though the patient is well, mobilising, eating and drinking for the mere fact that the C-reactive protein (CRP) is still elevated. I have heard of a case in a university hospital, whereby a patient who was well post-surgery had an elevation of the CRP and which was the sole clinical indication to re-operation. This way is not advocated. The CRP is indeed a better indicator that the laboratory is open.

When making clinical decisions, all elements must be taken into account and not a non-specific lab test.

Of course, infection causes inflammation, and even after the bacteria have been eliminated, the inflammation may persist for several days or even several weeks thereby elevating the CRP. But if the patient is feeling better, fever, signs of sepsis have resolved and other parameters are returning to normal, there is no indication to continue intravenous antibiotics. They can be switched to short-course oral treatment or even discontinued depending on the clinical situation. Exceptions are for chronic or difficult to treat infections such as osteomyelitis and endocarditis that require many weeks of antibiotics. However, for an uncomplicated pneumonia or a urinary tract infection which are exceedingly common, short course antibiotics with clinical reevaluation and early de-escalation is best to avoid prolonged hospital stay, reduce antibiotics pressure on bacteria and to reduce cost to the patient.

Remember that if a patient is on drugs that could be causing worsening of their condition e.g. ACE inhibitors, anti-psychotic drugs etc, they should be stopped to evaluate if they are the cause and to observe for resolution. An excellent resident recently keenly noted that in a patient with an FUO for 6 months, that all investigations offered up no cause. Only on instituting a 'drug holiday' of stopping all drugs, did the fever abate, inflammatory markers rapidly dropped and patient could eat and mobilize!

I can't emphasize enough the importance of bedside history taking, re-evaluation by physical examination, and re-evalautuon of drug treatments etc. Clinical examination can avoid the 'follow the CT' reflex and avoid radiation. Your patients will be much more satisfied that you've taken the time to lay hands on them to evaluate them than sending them into the 'tube of truth' to come out empty handed.

However, as a word of warning, if you do find an abnormal clinical examination e.g. unequal pulses and BPs in a patient with central tearing chest pain, the physical exam directs the physician to obtain appropriate scans and institute life saving treatment.

Without the tools of history and physical examination, we as doctors are shooting in the dark and using a sledgehammer to crack a walnut with routine CT scanning for simple pneumonias that can be diagnosed simply by traditional methods and a simple X-ray. Without the basic tools and over-reliance on the 'machine', we end up slaves to the machine and practicing defensive medicine when no such defense is necessary or warranted.

In the end, it comes down to clinical reasoning which can only be learned from experienced staff adept in managing the many conditions that medicine throws at us on a daily basis. The PC is not a patient and cannot speak or elicit signs. Better to go to the bedside. The patient will tell you more than any book or webpage.

Please consider.....

Japanese Medicine Should Use the iPad at the Bedside

Dear Bloggers

Yes, it's been 6 months since I last put finger tips to keys to write on this blog. I have been busy with many things :-)

Since I last wrote, the iPad and the iPhone 4 have come on to the market.

The iPad is a really neat device albeit somewhat heavy. The screen is a nice size but grainy unlike the new iPhone 4 retina display. But, it makes a great eBook reader, word processor, newspaper reader etc. However, I think it has many more uses including within medicine.

It can potentially be used to 'clerk' patients. That means it can be used to record the patient interview and physical findings etc. Basically, a portable electronic patients records device that can upload to the main system for synchronising data. From my experience of seeing Japanese patient record softwares, they are cumbersome and complicated. Also, you either have to have a PC desktop or a laptop. Use of a laptop even at the patient bedside is cumbersome and the battery last about 4 hours if you are lucky ! Usually, it's about an hour in reality as someone else has used the machine without plugging it in.

The iPad has a 10 hour battery after a four hour charge and it much lighter than a laptop. With the touch screen technology, you can tap boxes referring to positive or negative findings, draw diagrams, add voice notes etc This cannot be down so easily or so cheaply on the current PC technology. The iPad is cheap enough and advanced enough to take medicine into a new era where the doctor can be freed up to see the patients at the bedside rather than being tied to the nurse station where the PCs are.

In the 'good old days' the papers notes meant that you could write the patient notes directly at the bedside and define an immediate plan and decide on your tests. But, there was never a way to make that information immediately known to relevant members of the team if they were in another location. Also, it meant that in order to see something relevant in the notes everyone would have to crowd around the patient notes. With the iPad, if every member of staff had such a device, all team members could read the notes simultaneously, check the lab data and radiology on the move from patient to patient so that problems are not missed.

Taking an iPad to the bedside and clerking the patient melds the old with the new and allows immediate updates for the patient care.

Now all that is needed is for some clever software makers to liaise with what physicians need and to make a package in Japanese to allow the doctors to be freed up to practice medicine at the bedside. Such software could also include the 'Review of Systems' with check boxes that would then organise the data later on to auto generate problem lists so that the physician does not overlook the information.

Integration with other software packages that could generate a differential diagnosis would be the next step but let's get 'denshi kalte' made portable first and bring medicine into the new age of technology the way it should have always been!

Have a good week :-)

A Friday Rant On Infection

Dear Bloggers

When we do invasive procedures, we should consider whether we are doing the procedure for the right reason, that the right equipment is used, and in an aseptic manner and maintained correctly.

Should we regard urinary catheterisation as a procedure less important than let's say, central line insertion? Should we be any less careful?

Well, the UK Department of Health figures from 2001 showed that about 25% of patients end up being catheterised during their inpatient stay. The risk of developing bacteriuria is about 5% per day and of those who develop it, about 4% will develop bacteraemia. The death rate from such bacteraemia can be as high as 30%. Clearly, the numbers of patients developing infection are not insignificant at all with the knock on effects of increased morbidity, increased hospital stay, increased cost and even death.

In a review of awareness of catheterisation, the attending was the least likely to know that their patient had been catheterised and up to 22% of residents were also unaware! Unawareness led to an increase in the inappropriate use of catheters. Documentation of the reason for catheterisation was also shown to be poor. In several studies based on the appropriateness of catheterisation, up to 50% of such procedures were deemed inappropriate!

Hence, when we perform urinary catheterisation, we need to appreciate why we are doing it and is there another option. Patients should NOT be catheterised to just 'help the staff'. It is an unfortunate practice in some institutions to place a catheter in elderly patients who are otherwise continent because of mobility problems such that the staff need not toilet the patient regularly. This is not a good reason to catheterise a patient.
Even patients with low urine output do not always need to be catheterised. A bladder volume scanner can be used to estimate the amount instead of passing a catheter.

If we do decide to catheterise, the right equipment should be used including sterile gloves, a sterile sheet (with a circle cut in the middle for exposure of the genitalia) and sterile 'one use' lidocaine gel. All equipment should be prepared in advance of putting on the gloves.

There is no excuse for using non-sterile gloves or previously opened gel, as this increases the risk of transferring bacterial infection into an otherwise sterile environment and which bacteria may be potentially highly resistant to antibiotics e.g. pseudomonas.

A basic but important thing to do is Wash Your Hands before the procedure. Medical staff are not immune from carrying infection. Far from it. Use of a sterilising hand wash is ideal.

There are several instructive formats available for teaching the Global Standard of urinary catheterisation and they include the New England Journal of Medicine videos of the procedure for men and women and the new ABC of Practical Procedures, BMJ Press 2010.

• In the following explanations, the doctor has a 'clean hand' for using the sterile equipment and a 'dirty hand' for holding the penis or preparing the female labia. After placing on sterile gloves, and a sterile drape over the groin to expose only the genitalia, in men, the dirty hand pulls the penis is a vertical direction. If there is a foreskin present, it should be retracted with the dirty hand and the glans cleaned with sterile water using the clean hand. There is no reduction in bacterial infection from using a sterilising agent on the glans. Likewise, in female catheterisation, the labia should be parted with the dirty hand and the urethral area cleaned using the clean hand.
  
• Following this, 10ml of STERILE lidocaine 'one use' gel should be injected down the male urethra via a prepared syringe until all of it has been instilled. The tip of the penis is then pressed to maintain the gel inside the urethra for about 1 minute to allow the lidocaine to take its anaesthetic effect. Then, the pre-opened 12F-14F male catheter is placed down the urethra. The use of such gel is to reduce trauma, patient discomfort and infection.
  
• When the prostate is reached the patient should be told to take deep breaths which can relax the bladder neck and the catheter can be twisted slightly which can help entry of it into the bladder. In female catheterisation, as the urethral is very short, the gel can be placed on the shorter female catheter after which it can then be inserted. Once inside the bladder, the catheter is pushed in to the full extent and sterile water (usually 10ml) is injected into the balloon port and the catheter is pulled back. Urine should flow out into a prepared kidney dish and then, the collection bag can be attached. In men, the foreskin should then be return to its usual position to prevent the glans from swelling.
  
• The catheter bag should be placed on a stand by the bed and it should NOT touch the floor. It should NOT be placed above the level of the bladder to avoid reflux of urine from the bag into the bladder. The bag should be in a place which avoids the lower exit tubing coming into contact with footware e.g. when staff come to review the patient.
  

In this closed system, unless the bag needs to be drained, it should not be touched. Taking Catheter Specimens of Urine should be avoided unless necessary. Routine change of the catheter is not recommended.

The procedure should always be documented in the patient notes in addition to why it was necessary to place the catheter in the first place. Another important thing is to document the residual volume to know if the patient has outflow obstruction.

For example one can write the following in the notes, DATE / TIME: Mr Jones not passed any urine for 12 hours. Complaining of pain in the lower abdomen. Examination revealed a large distended bladder than was dull to percussion up to his umbilicus. Prostate examination: enlarged, no central sulcus, smooth and non-tender ; likely BPH. Likely urinary outflow obstruction from BPH. Need to rule out UTI. Hence, need for insertion of Foley Catheter.

Procedure explained to patient with his verbal consent to proceed. Aseptic technique carried out. 10ml of 'instillgel' inserted down the penis. A 12F Foley catheter passed with ease into the bladder. Free flow of clear urine observed. 1200ml of residual urine in the bag post-catheterisation. Sample of urine sent for MC&S [microscopy, culture and sensitivity]. Foreskin returned to usual position post-catheterisation. Collection bag placed on bedside stand. Patient now much improved with relief of pain.

The need for the patient to continue using the catheter should be reviewed on a daily basis. It should not be kept in place just for the staffs' convenience. If the patient needs to toilet at night then it is the ward staffs' job to assist the patient rather than getting the doctor to come at 2am to put in a catheter for incontinence. Moreover, a diaper can be used instead of inserting a catheter. However, there will be some occasions when placing a catheter may be necessary e.g. try to heal decubitus ulcers and avoiding urinary contamination of the sores. However, such sores should usually be covered to aid healing with water-proof dressings. The need for a 'Foley' should be assessed on an individual basis rather than carte blanche' insertion of catheters.

We should also be aware that if we decide to remove the catheter, it should be done in the morning as a Trial With Out Catheter (TWOC). Hence, if the patient goes into obstruction, it will usually be during the daylight hours when the usual team are present and a catheter can be reinserted. It is not good etiquette to expect the on-call doctor to perform a chore that the daytime team can easily do.

Condom Catheters for men who are incontinent can be used in place of a Foley catheter. There is also Intermittent Catheterisation which can be taught to competent patients, which may avoid the need for a long term catheter.

Essentially, we must try and cut down on nosocomial infection. We must take all procedures seriously and use due care and attention to maintain aseptic technique. Just because we regard good aseptic technique important for CV line insertion, it does not mean that it is unimportant for Foley catheter insertion.

Please consider.

A Flurry of Endocarditis

Dear Bloggers

There have been two recent cases of infective endocarditis in young adults -- both aged below 30 years with 3rd degree mitral valve prolpase, both growing streptococcal spp from blood cultures and both with previous valvular abnormalities. One had a 'floppy' mitral valve and suspected endocarditis several years before and the most recent patient had confirmed endocarditis in the past.

In the latter case, the patient had a history of preceding tooth extraction prior to the original onset of endocarditis. In this recurrence, the patient had lost the cap to a repaired tooth several months previously. There was no complaint about tooth pain or current problems on direct questioning.

However, on examination, using a simple spatula and a pen light to inspect the teeth, it soon became clear that the base of a previous tooth [the one that lost the cap] was fully exposed and tender to touch. This was the probable site of bacterial entry.

Inspection of the nails revealed two fresh splinter haemorrhages which had occurred since the admission and whilst using antimicrobial agents at the appropriate dose and fully sensitive for the organisms identified.

Bedside fundoscopy examination revealed no abnormalities.

In the former case, there was no evidence of tooth problems. However, in view that the patient also presented with a 'pounding' headache, despite the lack of neurological signs, a mycotic aneurysm needed to be excluded. An MRA indeed revealed an early mycotic aneurysm.

Interestingly, both patients' original chief complaint was fever. Both patients had upper respiratory tract symptoms e.g. rhinorrhoea in the former case and cough with sputum in the latter case. In both instances, the patients were misdiagnosed with conditions such as a 'common cold'. How could this be?

Making a diagnosis of a relatively uncommon infection can be difficult for the uninitiated. More often than not, such symptoms are due to a common cold. Although I do not support such practice, for convenience, it is quick and easy to prescribe 'cold' medications and antibiotics for 'fever' after a cursory look, without appreciating the importance of doing a thorough work up e.g. full history, physical examination and labs, which are time consuming in a hectic outpatient clinic where patients are lucky to get 5 minutes with the doctor. In the season of H1N1 influenza, it is easy to consider everyone has possible flu or a 'common cold'. Hence, without a full workup, endocarditis can be missed and was missed - twice.....

Learning Points and Pearls in Endocarditis

• Take a thorough history ! That includes previous medical history, medications, allergies, sexual history, travel history etc. If there is any hint of possible valvular disease, ask about dental treatment, rheumatic fever, previous murmurs etc. Don't make assumptions as you may get caught out.

• Examine the patient with focus on the potential areas that might be affected by what comes to light from the history e.g. cough and sputum = thorough chest examination; fever and previous endocarditis = look for peripheral signs and listen to the heart sounds.

• Use the modified Duke's Criteria for diagnosis of endocarditis.

• If there is a suspicion of endocarditis, ask about the patient's dental history. Even if there is no complaint of current problems, nevertheless, inspect the teeth and gums. Do not merely look. Tap them gently with a sterile instrument. A painful tooth / teeth raises the suspicion up a notch. If dentists merely looked at our teeth without touching and prodding them, they might never find the tooth decay!

• Get into the habit of doing bedside fundoscopic examination. It provides an immediate answer and saves time and money instead of sending the patient to the opthalmologist. The technique requires practice but is invaluable. It is especially important to do if the patient cannot be moved. Patients may not complain of visual loss especially if the peripheral retina is affected so again, we should not make assumptions that there are normal eyes just because the patient has no eye symptoms.
  

• Blind prescribing of antibiotics for 'common colds' is not justifiable without a firm assessment and can lead to unwanted side effects and bacterial resistance. Such treatment can result in culture-negative endocarditis thereby making treatment much more difficult to tailor later.
  

• Suspected endocarditis patients need 3 sets of blood cultures and an echocardiogram; trans-esophageal if possible. Remember that 'vegetation-negative' endocarditis exists and that trans-esophageal echo is not 100% sensitive. Newer modalities are coming to the fore such as PET-CT for identifying infected valves in 'vegetation-negative' endocarditis. If you are interested in further reading, please see A Bright Spot: Infective Endocarditis and PET/CT. Huyge et al. The American Journal of Medicine, Vol 123, No 1, January 2010

• A pulsatile headache in a patient with fever and a heart murmur or other peripheral signs suggesting endocarditis, should make one consider a mycotic aneurysm. It is reasonable to undertake further investigations e.g. contrast CT or MRI.
  

• Embolisation whilst using appropriate antibiotics is a possible indication for urgent surgery as is a vegetation >10mm. Definite indications for surgery include heart failure (moderate-severe), severe aortic or mitral valve incompetence with evidence of abnormal blood flow, fungal endocarditis or a highly resistant organism and perivalvular infection with abscess or fistula formation. UpToDate support surgical intervention after a second episode of embolisation whilst on antimicrobial agents.

• Inflammatory markers play very little role of when surgery should be undertaken. Making a decision to operate or not based on the level of CRP is nonsensical as any decision should be based on the degree of haemodynamic instability. Moreover, severe aortic or mitral valve incompetence is usually associated with some heart failure and this condition may further decompensate. Hence, aggressive treatment with early surgery should be considered in such situations. Even in asymptomatic severe valvular incompetence without heart failure, early surgery may show benefit. In a paper by Habib et al on native valve endocarditis and optimal surgical timing, it is stated that 'Patients with severe aortic leaflet destruction and congestive heart failure, patients with perivalvular extension or uncontrolled infection, and patients with high embolic risk have poor outcome under medical therapy. Early surgery is necessary in all such patients with 'complicated' endocarditis unless severe comorbidity is present'. Curr Opin Cardiol. 2007 Mar;22(2):77-83.

A Classic Bedside Physical Sign - Asterixis

Dear Bloggers


Above is the classic sign of Flapping Tremor, also termed Asterixis, commonly seen in hepatic encephalopathy and CO2 retention. It is also seen in uraemia. The clues for the cause in this patient were the obvious jaundice and palmar erythema. Smelling the breath also revealed the classic Fetor Hepaticus -- sadly there is no current technological means to purvay this smell across the internet! Abdominal palpation revealed hepatomegaly.

The technique for asterixis is performed by asking the patient to extent their arms so that they are straight at the elbow. The patient is then instructed to extend the wrists and spread the fingers wide. This will allow asterixis to be uncovered.

Pearl: When you see a jaundiced patient ask them to perform the test for asterixis. A positive test suggests encephalopathy e.g. Grade 2 Hepatic Encephalopathy. If the patient has known COPD, e.g. the archetypcal chronic bronchitic 'blue bloater' and a positive asterixis sign, checking a blood gas for rising CO2 levels is justified. Remember that Type 1 respiratory failure patients e.g. emphysematous 'pink puffers' can also develop type 2 respiratory failure on occasion!

Blue Sclera Sign

Dear Bloggers

As part of inspection of the patient, one is occasionally faced with the Blue Sclera Sign as seen below:


Often, the patient is unaware that the 'whites' of their eyes are in fact, blue.

I was first introduced to this sign as a junior doctor by a neurologist, and the patient turned out to have osteogensis imperfecta !

However, there are several causes of this unusual physical sign that are listed below:

Congential (rare)

1. Osteogenesis imperfecta type 1
2. Ehler's-Danlos Syndrome
3. Marfan's Syndrome
4. Adult type osteogenesis imperfecta
5. Pseudoxanthoma elasticum
   
6. Kabuki Make-Up Syndrome
7. Crouzon disease
8. Hallermann-Streiff-Francois Syndrome
9. Velocardiofacial Syndrome
10. Weaver (Marshall-Smith) Syndrome

Acquired (more common)

1. Any cause of severe scleritis with resulting thinning which reveals the underlying choroid tissue (scleromalacia) e.g. Rheumatoid arthritis, Relapsing polychondritis, Opthalmic Zoster infection (rare) [this can lead to rupture of the eye --> scleromalacia perforans]
   
2. Iron Deficiency Anaemia
3. Drugs: Corticosteroids (thinning of the connective tissue of the eye), Tetracyclines (chronic administration)

When one finds this sign, a hunt for the cause should be undertaken. In the newborn, children, adolescents and young adults, congenital disorders should be considered. Often, other features of the disorder present to help with the diagnosis e.g. repeated fractures (osteogenesis imperfecta), tall body habitus and high arched palate (Marfan syndrome). Moreover, there may already be a family history and hence, the diagnosis may be straightforward. In other cases, genetic testing may have to be undertaken.

In adults, other causes should be considered e.g. scleritis, drugs and iron deficiency. The history and physical examination may again be helpful to decide on the likely cause. A thorough history is required such as inquiring about symmetrical small joint problems, morning stiffness (rheumatoid arthritis), painful red ears (relapsing polychondritis), orogenital ulceration (Bechet's disease), etc... A careful history about upper GI problems, change in stool consistency and colour, medication use e.g. aspirin, weight loss, decreased appetite, dietary history, etc, should be undertaken for identifying the cause of an iron deficiency anaemia. A full drug history is essential. Steroids and long-term administration of oral tetracyclines can be an obvious cause.

Physical examination for connective tissue diseases can be straight forwards with joint swelling and deformity and nail / skin changes. Iron deficiency can be considered by finding koilonychia, glossitis, mouth ulcers and angular cheilitis. Steroid side effects may include centripetal obesity, 'Moon face', telangiectasia, proximal muscle atrophy, thin skin, subcutaneous bleeding, and striae etc. Hence, the cause of the blue sclera sign may be obvious. Last and by no means least, tetracycline administration can cause the blue sclera sign along with the 'blue nail sign'. By finding these two signs co-existent in the same patient and with a history of tetracycline administration e.g. minocycline, makes the diagnosis straightforward.

So, the next time you look at a patient's eyes, don't just look for 'jaundice' and 'conjunctival pallor', as they are signs that touch only the tip of the 'ocular iceberg'. Remember the Blue Sclera Sign as well, but only mention it to your attending physician if you find it! It is rare enough to not be mentioned as part of the 'pertinent negatives' list during oral presentation, but it will certainly prick up the ears of the attending if you find it!

The Blue Sclera Sign is one of those signs that makes one reconsider whether Hens really do have teeth, as in fact, sometimes they do! [Click on both links for some funny explanations!]

Have a nice week!

Simulated Training of Practical Procedures

Dear Bloggers

Some training institutions are instructing medical students and residents in performing medical procedures using 'simulated training' on special manikins. The aim of this kind of training is to teach the 'global standard' for such procedures with the expected outcome to make us 'better doctors' and to reduce mistakes made on the patients.

When techniques are taught on a 'see one, do one, teach one' basis, there is a tendency for the teacher to introduce their own variations or mistakes, which are not be in keeping with the global standard and may not have any evidence basis.

However, by doing such training in accordance with standardised procedure guidance, it is often possible to identify resident 'bad habits' e.g. failure to use local anaesthetic for performing lumbar punctures, and to then introduce how the standard techniques should be done.

One cause for confusion of junior residents has been the type of equipment and the inappropriate use of it. For example, although a chest tube comes with a central trochar, for years, it has been taught that the trochar should not be used for fear of puncturing internal organs. However, unless there is stipulation from 'trainer' that the trochar should not be used and that forceps introduction of the drain is safer, it is easy to see how wrong techniques and subsequent mistakes on patients can occur, especially if supervision of junior residents is not optimal. No junior doctor should ever be 'let loose' to 'Just Do It' without first training the doctor appropriately and ensuring that they are 'safe' for the patients. Many modern texts exclude the use of the trochar because it is dangerous. It should not be used. We need to diverge from the Eminence Based Instruction of 'this is how I learnt it and this is how I will teach it to you' concept and use Evidence and Benchmarking as much as possible, for attaining the best and most standardised technique for a particular procedure.

When performing simulation training, the trainer needs to be aware of the various global standards rather than teaching their own favoured technique, otherwise we fall into the 'see one, do one, teach many' concept that I see as being a problem as described above. There are many texts and videos now available to aid in procedure training.
A recent book for 2010 is the ABC of Practical Procedures from the BMJ Press - this teaches the way procedures are taught in the UK with evidence to support certain aspects of the text. I would recommend using this book because it has clear descriptions, good pictures, and an evidence basis. However, some procedures differ to those performed in the USA ! For example, in the UK, chest drains are inserted whilst the patient is leaning forwards with the arms and head supported on a table, whereas in the USA (and Japan), such drains are generally inserted with the patient recumbent. This can indeed be a challenge to the trainer to find the best 'global' technique to teach and which has the best outcome or the best evidence for its use.

The New England Journal of Medicine produces procedures on video that can be streamed or downloaded from their website. Although these are only produced in English, they are easy to understand and can aid in training with the use of manikins and patients. In fact, all the NEJM videos are demonstrated using real life subjects.

Most recently, the iPhone AppStore has started selling Procedures Consult -- a massive multi-megabyte programme and relatively inexpensive when one compares this to a regular medical textbook or video. This software has text and video demonstrations to guide you on procedures, and I would recommend it to residents and senior doctors alike to keep refreshed on how to do techniques.

The use of evidence for procedures has helped to dispel certain ideas such as:

• patients do not need iv fluid before a lumbar puncture
• they do not need to lie down for several hours after a lumbar puncture -- it may in fact make a post-LP headache worse
• purse string sutures no longer need to be used for chest tube insertion when withdrawing the tube; a Z incision, sealant and pressure dressings provide a better cosmetic result
• local anaesthetic should be used for lumbar punctures; use of a 'small' needle is still painful
  
• 5 litres of ascites can be safely removed by paracentesis in one go without the need for using fluid replacement in liver disease. Colloid can be used in place of the traditional albumin infusions if required. There is no evidence that albumin is any better. Ascites can be removed in one session so long as there is no cardiovascular compromise. Drains are removed the same day and not left in overnight or clamped for long periods.

It is important that the students / residents have an opportunity to be observed performing the techniques after their training period. This is done to ensure good technique and that they have an understanding of the complications. Moreover, sometimes, although there is no complication, the technique does not go as planned e.g. the guidewire seems to be going up rather than down when doing a subclavian vein 'central line' cannulation. Knowing that turning the head to centre, pressing on the internal jugular vein to feel if the wire is ascending and sometimes, replacing the wire completely to get better downward angulation, can sometimes overcome the 'hiccups' of this procedure. These Procedural Pearls can be extremely helpful and are rarely printed in regular texts -- it is rare that any of these 'get out of trouble' techniques have evidence to back them up, but sometimes, they do work ! :-)

The trainee also needs to understand that it is sometimes fruitless to continue with a procedure that is going wrong. It is better to start again and / or call the senior doctor to take over. As humans, we have good days and bad days, and no one is perfect. By recognising our weaknesses as doctors, this makes us safer and stronger individuals at the same time. We then know how far we are safely prepared to go and when to refer to someone with superior technique, experience and knowledge. It is better to be cautious and careful when doing procedures than being maverick. It is the latter type of way that will end up with a disastrous outcome for the patient and for the resident.

Finally, although the modern era of technology is upon us with the use of portable ultrasonography for use in procedures, we should not forget the traditional techniques. I for one, fully support the use of ultrasonography for identifying veins from arteries and fluid from solids when doing procedure training. However, we as physicians, will not always be in a situation with technology to assist us. There was a famous situation many years ago when a person developed a tension pneumothorax whilst in-flight, and two doctors ingeniously used a coat hanger and a bottle of whiskey to make an under water chest drain. There was no x-ray technology and no ultrasonography. They used their knowledge of anatomy and procedural techniques to save a life without modern technology.

Hence, when we do simulation training, although we should teach the most up-to-date technology driven procedures e.g. ultrasonography during CV line insertion, we should also consider teaching the traditional techniques too so that the residents will be fully prepared for any event whether it is first world, third world or 30,000 feet in the air.

Have a good week.

Look at the patient

Dear Bloggers

Although technology has taken medicine into a new age, we should not leave the fundamental skills of doctoring behind.

The following case is a vignette and has been anonymised to safe-guard patient confidentiality.

An elderly lady of 86 years of age had been admitted to a hospital with severe dehydration, vomiting and abdominal distension and she was tentatively diagnosed with paralytic ileus. The patient was treated with intravenous fluid and kept nil by mouth with nasogastric tube suctioning whilst undergoing investigation for the cause.

The patient had a urinary catheter placed to measure urine output and post-renal obstruction had been excluded by a normal appearance of kidneys, ureters and bladder on ultrasound scan. High doses of furosemide were also used at the same time as the intravenous fluid with the aim to 'kick start' her ailing kidneys and to avoid heart failure.

A plain CT of the abdomen had shown distal loading of the large colon with faeces and dilated small loops of bowel.

Initial blood gas on the admission revealed a severe metabolic acidosis.

Several days into the admission, the patient started to produce bloody coloured fluid from the NG tube, and upper GI bleeding was strongly suspected. Intravenous proton pump inhibitor therapy was commenced in addition to continuing fluid resuscitation whilst awaiting gastroscopy.

However, the patient's heart rate was then seen to slow on the monitor to 40/min and last the recorded blood pressure was 160/80mmHg. Initially, the physicians were looking at the monitor abnormality, but when the patient was assessed, she was found to be completely unresponsive and there was no respiratory effort. After pulse check, there was found to be no cardiac output. Pulseless Electrical Activity (PEA) was immediately considered and CPR was commenced.

In addition to the blood in the NG tube, the diaper also contained fresh pungent malaena.

This patient's circulation was initially restored with crystalloid fluids (several litres) and later with red cell transfusions, in addition to using atropine, adrenaline and high dose dobutamine support. However, the initial haemorrhagic shock and use of vasoconstrictors resulted in cardiac ischaemia. Moreover, it was unclear how long the patient had been in cardiac arrest prior to starting CPR and despite restoration of her circulation, there was no improvement in cerebral function with GCS of 3/15. Despite the resuscitation, the patient appeared inotrope-dependent, a commonly seen sequal to cardiac arrest. Unfortunately, the patient reverted to PEA and despite further attempts at CPR, she could not be revived.

An autopsy was performed which revealed an acute duodenal ulcer and distal ischaemic colitis.

The Learning Points from This Case Vignette

If there is a monitoring abnormality, look at the patient and recheck the vital signs, manually if need be, and repeat the physical examination. You should seek out the cause.

Remember to Check the Airway, Breathing and Circulation in unresponsive patients.
Focusing only on the monitor can distract you away from the patient - remember that both are important.

A bleeding patient needs rapid assessment and restoration of circulation with fluids and blood +/- clotting factors (if required).

Circulation is difficult to assess and this can be improved by placing a central venous line to monitor the central venous pressure.

Urine output needs to be measured hourly to ensure that there is no deterioration. Often, the urine output drops consistently in shocked patients before they develop cardiac arrest -- this depends on the velocity of bleeding -- it can be an early warning sign of problems to come.

Low pulse rate needs assessing just the same as high pulse rate -- this patient should have developed a tachycardia but instead had bradycardia which might reflect a severely ischaemic heart e.g. from severe bleeding on a background of coronary heart disease.

In acutely unstable GI bleeders, the endoscopy equipment can be brought to the bedside and therapeutic intervention can be done there and then. It may not be safe or practical to wait and despite the best attempts to stabilise the patient so as to get them to the endoscopy suite, it is sometimes not possible. Doing intervention at the bedside is sometimes the only viable way.

Unstable GI bleeders need to be in a monitored bed e.g. a high dependency unit, acute bleeder bed, or an ICU. They should not be managed on a general ward if they are unstable.

Group and Save blood for all bleeding patients. Those with significant losses should be cross matched and transfused rapidly. Don't rely on the haemoglobin level in acute GI bleeding as it can be falsely normal. If there is no time for the cross match then give Group O blood (universal donor) until the cross matched blood is available. Don't wait for your patient to bleed out.

Inform the surgeons in the case of a patient who is admitted with upper GI bleeding. Doctors may sometimes become over confident that 'it's just another GI bleeder' until the disaster of when the patient bleeds out. If the upper GI bleed cannot be resolved through conservative methods e.g. clipping, cautery, hypertonic saline-adrenaline, transfusions etc, the patient should be considered for surgical intervention. However, if the surgeons hear about the patient for the first time as 2 litres of malaena hit the floor, they will not be very pleased with you for telling them at the last minute. Remember, it is better to operate on a patient who is stable than on one who is unstable and which situation could have been avoided if preparations had been taken sooner. Have a low threshold for getting a surgical opinion early.

Do not be blase' about GI bleeding. It is serious and as the above vignette case demonstrates, it can lead to serious consequences. In this case, the upper GI bleeding led to unexpected and profound haemorrhagic shock and then PEA.

When you have a monitor showing unusual readings, look at it in combination with the patient. The monitor is a guide and not an absolute. Unless the patient is linked to direct arterial pressure monitoring, or transoesophageal cardiac output monitoring, it may not be possible to know that PEA has occurred. Relying on an ECG rhythm strip can be misleading especially if there is implantation of a pacemaker. Look at the patient! Check the carotid pulse. Sometimes the most simplest of things can be the most significant and helpful.

This brings me back to a previous issue of an Early Warning System -- a UK idea of several years standing, that scores patients according to their vital signs. If there is a deterioration from the normal variability, then the score rises and once a threshold is met, the doctor is called for the patient to be reassessed. Many UK hospitals utilise this system for spotting the 'deteriorating patient' with the aim to avoid problems.

The drop in pulse and an unresponsive patient would have resulted in an EWS score of 5 (>4 = call doctor as soon as possible). The low amount of urine in the catheter bag is another tell tale sign of problems. Such a low output without evidence of urinary tract obstruction makes one consider either pre-renal or intrinsic renal failure. In the event of bleeding, the former is a more likely cause.

When we look at the BUN and creatinine of a patient, don't just think dehydration if the ration of BUN-to-Creat is increased. Also think Bleeding specially if the ratio >20:1 ! This means performing a rectal examination looking for blood, passing an NG tube to check for upper GI haemorrhage, and serial haemoglobin measurements (plus renal function tests too) in addition to repeated physical examinations of the patient to look for signs of ensuing hypoperfusion e.g. cold extremities, confusion, decreased urine output etc....

Providing intravenous fluids AND diuretics to 'kick start' the kidneys is NOT the standard way to treat a hypovolaemic patient. Remember, when a patient is hypovolaemic, there is increased output of vasopressin and angiotensin II to cause the reabsorption of H2O and Na+, to try and stabilise the blood pressure and hence, renal blood flow. It is therefore no surprise that the urine is decreased and concentrated in hypovolaemia. The important thing is to replace volume to improve perfusion but NOT using diuretics as this makes matters worse by decreasing the intravascular volume yet further.

Moreover, patients can develop acute tubular necrosis which has an initial oliguric phase followed by a diuretic phase. This can be avoided if there is adequate fluid resuscitation performed early. To understand fluid status more accurately, a CV line should be placed. There is no additional benefit placing a Swan-Gantz catheter. Some physicians rely whole heartedly on the IVC compliance measurement (as assessed by echocardiogram) to make decisions, with them sometimes ignoring all other evidence of hypovolaemia when an IVC compliance appears normal, at the potential detriment to the patient. Remember, no one physical sign and/or test is always going to give the right answer, but usually a combination of signs and/or tests does. Also, the result of an echocardiogram is only as good as the practitioner performing it.

Please try and look at the overall picture of the patient and remember that it is better to give generous fluids rather than judicious fluids and catecholamines with the latter causing the potential risk of arterial ischaemia and organ failure if used inappropriately. Consider heart failure as a potential outcome of too much fluid but do not let that stop you giving adequate fluid resuscitation. Boluses of fluid to maintain circulation and re-examining for heart failure is one way to try and gauge how much fluid to infuse into the patient.

If after fluid resuscitation is performed and CVP is adequate e.g. 12cm H20, and BP still remains low, then giving catecholamines is justifiable e.g. septic shock, cardiogenic shock, adrenal failure etc, but certainly NOT diuretics as an initial therapy to try and 'kick start' kidneys or to try and avoid possible heart failure.

In summary, let's get back to basics and review the patient's status through physical examination rather than just looking at numbers and blips on a screen. The 'red flag' signs of GI bleeding e.g. haematemesis, malaena, hypotension and low urine output, are serious and require immediate assessment and intervention. No inpatient being actively treated should succumb to GI bleeding without having first, established a cause, and secondly, having attempted to abrogate the problem. Remember the H's and T's of the reversible causes of cardiac arrest of which Hypovolaemia (including haemorrhage) is one.

I hope this is food for thought. Have a good week.

End of Year Greeting

Dear Bloggers

It has been six weeks since I last updated this blog for which I am eternally sorry :-)

I hope that you have all been enjoying the end of year celebrations though.

For me, life has been rather hectic but I can assure you that I will be updating the blog with new cases and interesting matters on a more regular basis --- at least, as much as I can do in 2010.

I would like to thank you all for visiting my blog over the years and I ask that you continue to do so -- from time to time. Remember, if you have a question or comment, you can always drop me a line via the blog.

I wish you all a happy, healthy and prosperous 2010.

Answers to the November 'Spot Case'

Dear Bloggers

Thank you for waiting for the answers to the November short case which involved no history, but the sole use of observational skills.

Without further ado, here are the answers to the following questions:

Question 1: Please carefully examine the patient's arm (first photo). What physical signs can be seen here?

When we look at the picture we are immediately drawn to the skin abnormality which is diffuse, purplish and irregular. It is in fact some mild bruising rather than a melanoma, although the latter is indeed a good thought. However, this is in part, a pseudo- 'red herring'. It draws you away from the significant abnormality which is coiling of the hairs. Such a change is consistent with vitamin C deficiency (scurvy). One could indeed argue that the bruising is also caused by a vitamin C deficiency although there is not the typical peri-follicular hemorrhage that one sometimes sees in this condition.

If one increases the magnification of the picture (done by clicking on the picture) it soon becomes clear that there are whitish plug-like structures at some of the hair follicle bases which may represent lice infection.

Question 2: Please carefully examine the second photo. What physical signs can be seen here?

This photo tells a lot of information. The patient is unshaven which may signify he has not been looking after himself very well. The other clue to this is his dentition, which is very poor. There is also evidence of gingivitis, which supports the idea of poor dentition, but which may also be seen in vitamin C deficiency.

Question 3: Which ONE cause can link the main abnormalities seen below?

Vitamin C deficiency (scurvy) links both pictures.

Question 4: What is the most appropriate test(s) and subsequent treatment?

Vitamin C levels can be measured, but based on the examination findings, it would be reasonable to commence vitamin C replenishment therapy before the results are available.

The fact that this patient has a high probability of vitamin C deficiency, it should also alert the physician to consider other vitamin deficiencies and hence, replenishment of multi-vitamins would be an additional step in his treatment. The patient would also need general improvements in nutrition.

One has to also consider separate consults to dermatology, especially if there is a concern about melanoma and lice, and the dental surgeons and hygienists for optimising oral care. Lice eradication therapy would also be appropriate once confirmed by microscopic examination.

One should also consider the socioeconomic situation of the patient as well. If this patient has vitamin deficiency, possible malnutrition, and skin infestation, then he may require social help e.g. a carer for bathing and meals-on-wheels service, in addition to economic support if he has insufficient funds to cover the services required.


Both Professor Stein and Professor Dhaliwal correctly answered this month's case. Their comments are as follows:

Prof Stein:

Quesiton # 1 Problems in skin image:
1. 1) pigmented lesion of melenoma with irregular borders and 2 + different colors.And diffuse hyperkeratosis-like lesions
02)globules with tear drop forms and ? budding form suggest coiled hairs (looking like scurvy), doubt follicilitis (not looking like scurvy), yeast or parasite on skin

Question # 2
2. Front of oral cavity/lips: chronic gingivitis, candida gingivitis as seen in HIV pts, necrotizing gingivitis(trench mouth) also seen in HIV pts, and chronic periodonitis from Vit C deficiency (coiled hairs & hyperkeratosis), severe malnutrition causing necroziting periodonitis

3 & 4 For 1/1 link is CA melenoma>skin Bx; For 1/02 HIV test, ? vit C assay; For 2 xray teeth, dental consult, derm consult. Rx Vit C, multi-vit, general nutritional improvements

Prof Dhaliwal

Question 1: Please carefully examine the patient's arm (first photo). What physical signs can be seen here?

This is a wonderful exercise that asks two things of the clinician 1) observation/detection and 2) interpretation; success in #2 is intimately tied to #1. Stated otherwise, we cannot simply solve a problem (e.g., as in a presented case); we must detect and define the problem first.

The picture of the arm has a number of findings – although I cannot say with certainty which ones are decidedly abnormal. There is a dark pigmented macule that has some if not all of the ABCD characteristics of melanoma (http://www.melanomafoundation.org/prevention/abcd.htm) . One must always respect melanoma’s devastating metastatic potential when a second site of the body is being evaluated in the setting of a suspicious pigmented lesion. An alternative explanation for this skin finding would be a seborrheic keratosis, which is far more common, although typically favoring the trunk over the extremities.

The skin also seems to have punctuate yellow colored scale or buildup that is distributed throughout the skin. I regrettably don’t possess a large differential diagnosis for this finding, although things that come to mind include an exudation of excess lipid, a simple normal variant in skin pigmentation, or the accumulation of sebaceous material if regularly bathing has not been possible.

There are approximately 5-10 cystic appearing structures mostly in the middle portion of the photo. Although it is hard to tell whether they are attached to the hair shafts, I think they are at least compatible with lice. I’m hesitant to make this interpretation however, because tropism for the arm hair (in comparison to the head) would be atypical.

Finally, some of the hairs are linear, but there are a number of coiled hairs.

Question 2: Please carefully examine the second photo. What physical signs can be seen here?

This is a man, perhaps at least 30, inferred by some visible skin wrinkling, which smoking and sunexposure can accelerate. Otherwise, the external structures appear normal.

The left lower central incisor and the left lower lateral incisor are slightly discolored. The former has a grey hue, the latter, a ruddy off white appearance. Smoking may have caused a generally yellowing of the teeth. The gingival tissue associated with the lateral incisor appears to be inflamed, which may reflect a periodontal infection.

Question 3: Which ONE cause can link the main abnormalities seen below?

Since I do not recognize the dental abnormality outright, I have considered systemic diseases which may originate from periodontal disease (e.g., endocarditis) or can present as periodontal problems (drug effects like phenytoin, infiltrative processes such as leukemia, or connective tissue disturbances such as scurvy).

Given the previous observation of coiled hairs, a question I raised about hygiene (implying socioeconomic difficulties that could impair or radically modify access to food), I will hazard a guess of scurvy (vitamin C deficiency). Neither perifollicular hemorrhages nor gingival bleeding are seen however.

Question 4: What is the most appropriate test(s) and subsequent treatment?

In the case of scurvy, the diagnostic test is a serum ascorbic acid level and the treatment is the restoration of a proper diet.

Vitamin C (Ascorbic Acid) Deficiency

In developed countries the major groups affected by vitamin C deficiency include the severely malnourished, drug and alcohol misusers and the poor. In the UK, it is typically seen in the impoverished 'tea and toast' elderly.

Vitamin C deficiency (scurvy) can occur within just 3 months of deficiency resulting in various symptoms and signs largely due to impaired collagen production with impaired connective tissue organisation. Generalised symptoms include malaise, weakness, joint pain and / or swelling, depression, neuropathic symptoms, extremity swelling etc

Signs on examination include bruising of the skin, coiled hairs, bleeding gums, impaired wound healing, petechial hemorrhage, hyperkeratosis and Sjogren's syndrome.

The chronic gingivitis is thought to occur due to infection from oral bacteria in the gums of sufferers as a result of impaired neutrophil killing activity. Hemorrhage is a secondary phenomenon caused by infection disrupting fragile vessels within the gums.

Scurvy was described in the times of Hippocrates over 2,000 years ago! It was not until about 400 years ago that it was considered that 'fresh food' and if not available, citrus fruit, were the cure of the illness. About 250 years ago, the ever first medical trial took place by a Scottish doctor, James Lind, who treated sailors suffering with scurvy with various potential 'cures.' The sailors given vitamin C containing regimens recovered.

Take Home Message

• When something does not look right then it is not right. This patient had coiled hairs, ecchymosis (bruising), poor dentition and gingivitis. The diagnosis of scurvy should be considered especially in the elderly with poor nutrition and socioeconomic problems.
• When looking at clinical pictures look for the normal and the abnormal. Look at all of the anatomy rather than what you are initially drawn to, otherwise, the diagnosis may be missed entirely!
  

I would like to take the opportunity to thank Professor Stein and Professor Dhaliwal for their superb interpretations and correct answers to this difficult 'spot case'.

A Short 'Spot' Case for November

Dear Bloggers

Welcome back! I hope that you have been enjoying the recent cases.

Below is an anonymised short 'spot' case whereby the physical signs provide the diagnosis.

Question 1: Please carefully examine the patient's arm (first photo). What physical signs can be seen here?

Question 2: Please carefully examine the second photo. What physical signs can be seen here?

Question 3: Which ONE cause can link the main abnormalities seen below?

Question 4: What is the most appropriate test(s) and subsequent treatment?

Results out later this month. Good Luck !!!!

p.s. a word of advice, it may not be what you first think it is!

An interesting rash

Dear Bloggers

This 40 year old man was mending his wall when he fell and hit his chest. He was admitted to a hospital with a pneumothorax for which a chest drain was inserted. A fever developed after several days and pus started to drain from the chest tube. MRSA was cultured from the fluid and intravenous vancomycin was commenced after discontinuing initial therapy with ceftriaxone and clindamycin.

The patient developed diarrhoea during admission for which Clostridium difficile Toxin A was found to be positive. This was considered to be due to the Clindamycin, which is an infamous cause of pseudomembranous colitis. Oral vancomycin was also commenced.

The intravenous vancomycin was continued for 14 days and the patient made an excellent recovery, with resolution of the infections and pneumothorax. However, the patient noticed a red, non-painful rash develop predominantly on the back of his calf and thigh areas.

On examination the rash was as demonstrated in the pictures below. It was palpable!

A full blood count revealed a mild eosinophilia. Platelet count and coagulation screen was normal.

Vancomycin is known to cause a leukocytoclastic vasculitis, albeit rarely. It has been proposed as a cause of drug induced Henoch Scholein Purpura either directly or through a staphylococcal glycoprotein released after bacterial breakdown.

The morphology and distribution of the rash i.e. vasculitic and on the back of the lower limbs is consistent with a possible drug induced Henoch Schonlein Purpura. HSP is uncommon in adults. However, for HSP to be diagnosed, the patient should have arthritis, GI symptoms and renal glomerular involvement with IgA deposition. These latter symptoms were absent in this patient.

Unfortunately, this rash was no biopsied especially as it began to resolve after the vancomycin was discontinued.

It is highly likely that this palpable purpura was a vasculitis, perhaps of the leukocytoclastic variety. Please see the Medline references below.






Pharmacotherapy. 2009 Jul;29(7):846-51.

Vancomycin-induced leukocytoclastic vasculitis.

Felix-Getzik E, Sylvia LM.
Department of Pharmacy Practice, Massachusetts College of Pharmacy and Health Sciences, Boston, Massachusetts 02115, USA. erika.felix-getzik@mcphs.edu
Vancomycin is well recognized as causing the nonallergic skin reaction known as red man syndrome; however, it is rarely suspected as causative in the setting of an immune-mediated skin reaction. We describe a 76-year-old Caucasian woman with a history of penicillin and sulfa allergies who was transferred to our medical center while receiving vancomycin for treatment of persistent methicillin-sensitive Staphylococcus aureus (MSSA) bacteremia. After admission, the patient's pacemaker was explanted; cultures from the pacemaker grew MSSA. Based on the culture data and her allergy to penicillin, vancomycin was continued. On day 4 of therapy, the patient developed a papular rash with small blisters on her distal upper extremities. Furosemide, which she was receiving intermittently to maintain fluid balance, was initially suspected as the likely cause. Furosemide was withheld; however, the rash worsened and spread to her neck and torso. Results of skin biopsy confirmed a severe leukocytoclastic, necrotizing small-cell vasculitis that met the criteria for a hypersensitivity vasculitis associated with drug therapy. Five days after discontinuation of vancomycin, the vasculitis was resolving and continued to resolve throughout the remainder of her hospitalization. Furosemide was readministered without worsening of the vasculitis. Use of the Naranjo adverse drug reaction probability scale indicated that the likelihood of vancomycin being the cause of the vasculitis was probable (score of 5). Clinicians should be aware of vancomycin as a potential cause of small-vessel vasculitis.

Braz J Infect Dis. 2002 Aug;6(4):196-200.

Uncommon vancomycin-induced side effects.

Rocha JL, Kondo W, Baptista MI, Da Cunha CA, Martins LT.
Division of Infectious Disease, Nossa Senhora das Graças Hospital, Curitiba, Paraná, Brazil. jaimeluis@b.com.br
Vancomycin has been used with increased frequency during the past 15 years and the most common toxicity with this drug is the red man syndrome . Other adverse effects include neutropenia, fever, phlebitis, nephrotoxicity, ototoxicity, thrombocytopenia, interstitial nephritis, lacrimation, linear IgA bullous dermatosis, necrotizing cutaneous vasculitis and toxic epidermal necrolysis. Only two cases of vancomycin-induced Stevens-Johnson syndrome and one case of pancytopenia have been reported in the medical literature. The treatment for both situations is based on cessation of the vancomycin therapy; in cases of Stevens-Johnson syndrome, antihistamine and/or steroid agents can be used. This article reports a case of pancytopenia and a case of erythema major associated with neutropenia.

1: Scand J Rheumatol. 1998;27(3):233-5

Henoch-Schoenlein purpura and acute interstitial nephritis after intravenous vancomycin administration in a patient with a staphylococcal infection.

Michail S, Vaiopoulos G, Nakopoulou L, Revenas C, Aroni K, Karam P, Stathakis C, Thosios T.
Department of Nephrology, Laikon General Hospital, Athens, Greece.
We describe a case of Henoch-Schoenlein purpura, associated with oliguric acute renal failure due to acute interstitial nephritis histologically proven, in a patient with a staphylococcal chest infection. The clinical syndrome appeared twice after vancomycin administration and yielded on the withdrawal of the drug. As pathogenetic mechanism we propose an anaphylactoid reaction either to vancomycin or to a staphylococcal glycoprotein released after breakdown of the microbial cells caused by vancomycin.

The Answers to October's Case 2009

Dear Bloggers

I hope that you have had a go at trying to work out this case. This month, Prof Matsumura (Japan) and Prof Dhaliwal (USA) have kindly contributed their expert opinions to this case. A contribution was also gratefully received from a first year Japanese resident (shown below). As a reminder, here are the original questions to the case:

Question 1: From the history, physical exam, limited laboratory and radiology data, what is your differential diagnosis?

Question 2: What emergency radiology test will you do next?

Question 3: Where is the potential origin of this problem?

Question 4: What emergency treatment(s) will you consider in this patient?

From Professor Matsumura: Thank you very much for showing me a challenging case again.

This 65-year-old lady had fever and back pain. This combination is red flag sign. Back pain is very common condition (I have had this before!). However, she had fever too. I should think infection or neoplastic diseases. Moreover, she had had history of poorly controlled diabetes mellitus and bilateral renal calculi. I think these are very important information.

Question 1: From the history, physical exam, limited laboratory and radiology data, what is your differential diagnosis?

Problem list is as follows:
#1 Back pain
#2 Fever
#3 Dysuria
#4 Poorly controlled diabetes mellitus
#5 Renal calculi
#6 History of UTI
#7 Tachycardia
#8 Low blood pressure
#9 Globular distension and tender in suprapubic area
#10 Unable to grip the examiners finger with her anus.
#11 Weakness in the lower limbs
#12 Absence of knee jerks
#13 Tender spine and muscles from L1-L5 region
#14 Psoas sign
#15 Leukocytosis
#16 Septicemia, E. coli and Klebsiella pneumoniae
#17 Gas in the soft tissue in an abdominal CT scan Differential diagnoses are as follows.

Vascular: Less likely
Infection: Emphysematous pyelonephritis, Discitis, Osteomyelitis, Epidural abscess
Neoplastic: Lymphoma, Metastatic tumor
Autoimmune: Less likely
Toxic/Metabolic: Diabetes
Trauma/Degenerative: Less likely
Iatrogenic: Less likely Idiopathic: Less likely
Congenital: Less likely

#1 Back pain, #2 Fever, #3 Dysuria, #4 DM, #5 Renal calculi, #6 History of UTI, #9 Globular distension and tender in suprapubic area.
Urinary tract infection especially pyelonephritis is suspected.

#11Weakness in the lower limbs, #13 Tender spine and muscles from L1-L5 region, #14 Psoas sign. These conditions indicate inflammation spreads to retroperitoneal area including psoas muscle.

#17 Gas in the soft tissue in an abdominal CT scan. I think emphysematous pyelonephritis is most likely.

#7 Tachycardia, #8 Low blood pressure, #15 leukocytosis, #16 Septicemia, E. coli and Klebsiella pneumoniae
These findings indicated sepsis. E. coli and Klebsiella pneumoniae are major organisms in emphysematous pyelonephritis.

#10 Unable to grip the examiners finger with her anus Rule out cauda equina syndrome. #12 Absence of knee jerks. This patient had diabetes. She can have diabetic neuropathy.

Question 2: What emergency radiology test will you do next? I would perform MRI of lumbar spine to exclude cauda equina syndrome, osteomyelitis, or discitis.

Question 3: Where is the potential origin of this problem? I think urinary tract infection is likely.

Question 4: What emergency treatment(s) will you consider in this patient? If we can see typical images of emphysematous pyelonephritis, surgical resection of the involved tissue in addition to systemic antimicrobial therapy is needed.


From Dr Dhaliwal: This is a very interesting case. I have deviated from the four question format instead by “thinking aloud” as the case unfolds. My differential diagnoses are embedded throughout with diagnostic and treatment suggestions at the conclusion.

History: Fever and low back pain typically brings to mind an infectious process. The low back pain may reflect nonspecific myalgias (e.g., influenza, SBE) or can be a focus of a suppurative retroperitoneal or lumbar spine infection. The difficulty walking, standing, and urinating points to a neuraxial infection, such as epidural abscess, vertebral osteomyelitis, or discitis. Poorly controlled DM increases the susceptibility to infection in general and raises the possibility of specific complicated infections, e.g., emphysematous cystitis or pyelonephritis. The latter must be entertained with pre-existing renal calculi. She lacks the dysuria that typically accompany lower tract infection.

Exam: This is an ill patient in shock. A murmur to suggest endocarditis is not detected, but can be challenging to hear at a heart rate of 120. The tender distended suprapubic area is compatible with complicated cystitis. A pulsatile mass – which would raise suspicion of one of the most sinister fever and low back pain entities, mycotic aneurysm – is absent. The anal laxity and decreased lower extremity tone and strength collectively suggest a spinal cord syndrome, perhaps of the cauda equina variety. The areflexia is consistent with nerve root compression or early direct cord compression. Interestingly, there does not appear to be a sensory level that accompanies cord syndromes, although the sensory exam can be highly variable and subjective at times. The musculoskeletal exam appears to suggest a psoas sign of sorts, which raises the possibility of a psoas abscess, along with inflammation of any structure adjacent to the psoas.

Labs/Radiology: Gram negative bacteremia suggests GI or GU pathology. Polymicrobial bacteremia should at least trigger the thought that a connection that has been established between the GI tract and the vasculature such as an aortoenteric fistula, an ingested foreign body (e.g., toothpick), or an eroding cancer. The CT finding of soft tissue gas suggests a gas-forming organisms (like E coli and Klebsiella) and is compatible with emphysematous cystitis or pyelonephritis. Mesenteric infarction or Fourneir’s gangrene could account for soft tissue gas as well, but supporting clinical features are lacking.

Conclusion: 65 year old teacher with poorly controlled DM with E Coli and Klebsiella sepsis, low abdominal/back pain, and lower extremity weakness. One pressing question is whether there is a space occupying lesion compressing her spinal cord/roots. Numerous elements of the case suggest this, and therefore I would be most interested in a lumbosarcral spinal MRI. The next question (regardless of the MRI results) would be the origin of her gram negative bacteremia. Examination of the urine (with catheter placement) and re-examination of the CT scan would be in order. Treatment pending the above studies would include vigorous fluids and IV antibiotics.

Final diagnosis:

• Emphysematous cystitis
• GNR bacteremia
• Epidural abscess

Dr Kato (1st year Japanese resident) has kindly provided an answer to the case as follows:

Q1 DDx
Among DIET IN HIM, Infection is the most likely cause of the illness, b/c DM, B/C results, acute course of the symptoms etc. strongly suggest Infection. Also I would consider Neoplasm b/c it could be similar to infection even though it is less likely, given back pain day-to-day progressing and neurological exams. I don't have ideas of neurological and inflammation cause in this case b/c neurological exams show bilateral but motor-only impairments and her age.

Secondly, I think this patiet have DM neuropathy symptoms such as rectovesicle impairment but it does not explain bilateral pure motor weakness, maybe. In this case, I am confused by this bilateral proximal limb weakness, but it could be explained by infection such as abscess b/o the presence of poas signs. Anyway, DDx as follows.

#1 epidural abscess #2 discitis #3
lymphoma and other cancers #4 DM neuropathy #5 infection of the soft tissue it might cause the bacteremia.

Q2 Enhanced MRI of the lumbar spine if available soon. If not, enhanced CT is also a good choice of study.

Q3 Vertebra~Disc of L3-5

Q4 ABx covering at least GNR (especially E.coli and Klebsiella). But I consider broad ABx use until Dx is determined.

The Answers

Both Professors Matsumura and Dhaliwal's general diagnostic process was similar to my own so to save time, I shall not repeat another list of my own. However, the history of renal calculi and diabetes mellitus are extremely important in this case. They are risk factors for infection. As has already been alluded to, fever and back pain together are a Red Flag sign and such patients need urgent investigation. Serious diagnoses such as osteomyelitis, discitis, epidural abscess and psoas abscess should be high on the differential diagnosis list.

Moreover, with the addition of neurological signs such as an inability to pass urine, weakness of proximal musculature, and inability to grip the examiners finger during rectal examination all point to a possible cord / cauda equina syndrome as both Professors have already mentioned.

Indeed, an emergency MRI of the lumbosacral region would be warranted.

When this patient was seen by another senior doctor several days after admission, the weakness of the lower limbs had progressed more distally. The patient could only move her toes and there was no movement against gravity. Interestingly, the patient still denied sensory changes in her lower limbs.
The CT scan revealed an obstructed right kidney and a normal left kidney. There was a mild 'dirty fat' sign around the right kidney and evidence of bilateral psoas abscesses with gas formation throughout the muscle plains. This gas extended deep into the erector spinae musculature. The liver, gallbladder, pancreas, and bowel all appeared normal (no toothpicks).

The infection appeared extensive throughout the lumbar area. Emergency MRI was performed and there was no evidence spinal cord or cauda equina compression. Unfortunately, no urine analysis data was available, which in retrospect, could have been extremely useful.

The suspected diagnosis was of an emphysematous pyelonephritis.

The patient was given ceftriaxone and underwent emergency surgery which included:

• Debridement of the erector spinae muscles; the wound was left open and examined and washed daily.
• Insertion of drains into both psoas muscles to drain the abscesses, again with daily wash outs.

The right kidney was not specifically treated. No nerve conduction studies were performed.

After 6 weeks of intravenous antibiotics and surgical lavage therapy, the patient had improvement in well-being, in general blood parameters and became afebrile.

• Final Diagnosis: Emphysematous Pyelonephritis (Class 3b)
  

Emphysematous Pyelonephritis

This is an extremely serious infection. In previously described cases, most patients have been women aged over 60 years with a history of diabetes and / or urinary tract obstruction. Usual organisms include E. coli and K. pneumoniae. Candida is also a rare cause.

Causes of urinary tract obstruction can be either papillary necrosis or less commonly, renal calculi.

The symptoms of emphysematous pyelonephritis cannot be separated from those of the more usual pyelonephritis. Patients complain of nausea, vomiting, fevers, rigors, and flank or abdominal discomfort. The onset of symptoms may occur suddenly or evolve slowly over a several weeks.

Gas can sometimes be elucidated on the plain abdominal film but CT is more sensitive and specific.

The infection is managed with intravenous antibiotics. Some cases can be successfully treated with antibiotics and percutaneous drainage of pus from the kidney with relief of the obstruction. Failing that, open surgery is required with nephrectomy.

Emphysematous pyelonephritis can be classified as follows:

• Class 1: Gas in the collecting system only (ie, emphysematous pyelitis)
• Class 2: Gas in the renal parenchyma without extension to the extrarenal space
• Class 3A: Extension of gas or abscess to the perinephric space, which is defined as the area between the fibrous renal capsule and the renal fascia
• Class 3B: Extension of gas or abscess to the pararenal space, which is defined as the space beyond the renal fascia and/or extension to adjacent tissues such as the psoas muscle
• Class 4: Bilateral emphysematous pyelonephritis or a solitary functioning kidney with emphysematous pyelonephritis.

Arch Intern Med 2000 Mar 27;160(6):797-805.

Nevertheless, despite intensive treatment, the mortality from several studies can be between 7 to 19%. Not numbers to be ignored.

Neurological impairment The physical examination of hypotonia, weakness and loss of reflexes is consistent with a neurological component. Despite the apparently normal MRI scan on admission, with worsening neurology post-operatively, it would be judicious to repeat the MRI scan and perform nerve conduction studies.
Although, direct muscle damage due to infection, and as part of surgical intervention, can result in weakness, particularly of the postural muscles of the spine and flexors of the thigh (psoas) in this patient, it does not account for the distal weakness or loss of reflexes alone.

It is possible that the infection resulted in nerve damage, possibly due to diffuse radiculoneuropathy. However, a cauda equina syndrome would still need to be re-excluded by repeating an MRI. The fact that the patient stated that there was no sensory deficit is intringuing. I would agree with Prof Dhaliwal that the physical examination can be subjective on occasion although I would like to add that such an exam should be done in a standardised and methodical way to ensure that all sensory modalities are checked. Diabetic neuropathy can easily be missed unless it is specifically looked for, and the patients sometimes do not even realise that they have a loss in sensation. I would invite others to comment on this point.

The fact that she had existing diabetes can indeed account for loss of reflexes which should not be forgotten. Only with further detailed repeat neurology (in full) and repeat MRI plus nerve conduction studies can the cause and full the extent of the disease be appreciated. The cause portends the prognosis.

Learning Points from This Case

• Don't ignore Back Pain and Fever -- together they are a Red Flag Sign -- a potential medical emergency
• Make an assessment and consider the serious diagnoses that should not be missed e.g. abscess, discitis, osteomyelitis etc.
  
• If a patient complains of leg weakness then take it seriously especially when there is a history of back pain and fever. It suggests a possible cord / cauda equina compression - a neurosurgical emergency. Do not send the patient home : urgent physical examination, lab studies and radiology (CT/MRI) are required; this is especially important with neurological impairment
• Gas in the tissues is serious. Antibiotics, drainage of the kidney, percutaneously and urethral catheterisation to relieve obstruction are advised. Surgery may also be required depending on the extent of the disease - see the classification above.

I would like to thank Professors' Matsumura and Dhaliwal and Dr Kato for their very kind and informative contributions to this month's case.