The Knee Jerk Response To Urine Output

Dear Bloggers

Today I want to have a final rant for 2008!

The rant is about the sometimes observed 'knee jerk reaction' that one sees by inexperienced physicians when the patient's urine output is low and furosemide is given to 'make the patient pee'.

Low urine output means assessment of the cause rather than just pumping diuretic into the patient which may makes matters far worse.

For example, low urine output might mean the patient has a urinary tract obstruction (post-renal), hypoperfusion from hypovolaemia (pre-renal) or intrinsic renal failure from an insult (e.g. ATN).

When one assesses this problem, take further history from the patient. They may tell you that they have trouble passing urine and / or a painful lower abdomen or distension suggestive of urinary tract outflow obstruction. On the other hand, it may be more clear whereby bleeding may have already been diagnosed e.g. upper GI haemorrhage. The patient might be taking nephrotoxic drugs, have sepsis or a local glomerulonephritis. The causes of pre -, intra-, and post-renal impairment are too many to discuss on this blog.

However, in patients who have low urine output, suffice it to say that the physical examination is of prime importance in addition to looking at the sequential laboratory studies, to identify the cause and follow the progression or improvement respectively.

When one examines the patient, start generally and then focus on the individual systems.

• Does the patient look ill? Confused? Sweaty?
• Then look at the hands! Check for those splinter haemorrhages as endocarditis can cause renal failure. Assess for encephalopathy by checking for flap (asterixis) -renal failure can cause flap the same as for liver failure and CO2 retention.
• Check the pulse - is there a tachycardia?
• Assess the fingers. Are they cold suggestive of vasoconstriction?
• Check the blood pressure - is there hypotension?
• Check the skin turgor on the dorsum of the hand / arm / inner thigh? Think to yourself, could this be dehydration?
• Feel for axillary sweaty - this is lost in dehydration
• Look at the conjunctivae to assess for anaemia - patient could be in a hypovolaemic state from bleeding
  
• Check the tongue & mucosa for dryness - a sign of possible dehydration
• Check the JVP - is it raised ? (could be a sign of CHF) or is there guttering (sign of hypovolaemia).
• Check the respiratory rate and rhythm - Is there Kussmul respiration / Air hunger -- can be seen in metabolic acidosis (renal failure), bleeding etc
• Listen to the chest - is there a focus of infection? Are there effusions / crepitations of heart failure?
• Listen to the heart for murmurs, added sounds
• Inspect the abdomen - is there a focus of infection? Are there signs of liver disease ? (liver failure can result in renal failure - hepatorenal syndrome)
• Are the renal angles tender ? (pyelonephritis / pyonephrosis)
  
• Can you feel a distended bladder in the lower abdomen? It is dull to percussion and when pressed and the patient may say they want to pass urine.
• Are there any abdominal bruits? Might suggest renal artery stenosis or a dissection if there is a compatible history
• Is there pitting oedema of the lower limbs? Might suggest liver disease, nephrotic syndrome, cardiac failure, venous obstruction, lymphatic obstruction or a low protein state.
• Look at the urine in the catheter bag (if one has been placed already) - measure the total amount since it was last checked. Look at the colour - is it dark suggestive of concentrated urine (hypovolaemia) or straw coloured in the euvolaemic state. Is it orange - bilirubin or red - bloody?
• Consider a rectal examination to look for GI bleeding and / or an enlarged prostate gland and / or malignancy.
  

The above features can help you to understand whether the patient is hypovolaemic, euvolaemic or hypervolaemic and a clue of the potential cause.

A patient with a hypovolaemic state (cold hands/feet, tachycardia, decreased skin turgor, hypotension, no axillary sweating, low JVP, dry tongue, dark small volume urine) should be given fluid to replenish the circulation and NOT diuretics! The reason for the decreased urine output is a result of ADH release and upregulation of the renin-angiotensin-aldosterone (RAS) system to retain water to maintain the circulation. Using a diuretic can result in worsening renal failure at the detriment of the patient. Yes, the frusemide splurge may make the doctor and nurses feel better that the patient is passing some more urine but the worst will be yet to come with the incipient renal failure.

A patient with an hypervolaemic state e.g. CHF, can have a low urine output as a result of vasoconstriction because of low cardiac output. Frank Starling forces denote that when the myocardium is overstretched (as in systolic heart failure), the muscles contracts less. Hence, to maintain blood pressure, the peripheral resistance increases which can reduce kidney perfusion and cause reduced urine output. Moreover, such patients also can have a high RAS activity worsening matters. In this situation, blocking angiotensin 2 production or activity (ACE-I / ARB) and aldosterone (with spironolactone) plus off-loading the circulation with a loop diuretic are the mainstay of conservative therapy. In this situation, it can improve the urine output quite appropriately.
A hypervolaemic state is demonstrated by symptoms and / or signs of CHF, liver disease, nephrosis etc. One might see a raised JVP, normal skin turgor, oedema around the eyes (nephrosis usually), pitting oedema of the extremities, abdominal ascites etc.

In a euvolaemic state, none of the adverse features seen in either the hypovolaemic or hypervolaemic states should be seen. One should also consider other causes such as:

• Drugs: e.g. morphine (causes release of ADH and direct urinary retention)
• Endocrine: SIADH
• Metabolic: hypoxaemia (increases ADH secretion)
• Misc: Pain and nausea (both increase ADH secretion)
• Urological: outflow obstruction e.g. prostatic hypertrophy with acute retention, bilateral ureteric obstruction from malignancy

Please refer to a standard textbook for the extensive list of causes. The above are merely examples to consider.

Hence, when assessing a basic thing such as urine output, we come back to basics. History and physical examination.

Looking at the laboratory studies can tell us further information e.g. worsening BUN and creatinine levels. Such lab results with an examination consistent with hypovolaemia tells us that the patient needs more fluid and not diuretics.

Normal laboratory studies but an examination consistent with hypovolaemia and low urine output should still prompt us to give more fluid.

On the other hand, a hypervolaemic patient may have laboratory studies indicating liver disease, cardiac failure (raised BNP) etc. These can guide us to a more precise diagnosis. Sometimes, such patients have existing renal dysfunction and so the cautious and judicious use of loop diuretics can be considered.

Remember that in acute renal failure, a meta-analysis of 9 studies in adults with ensuing or actual acute renal failure showed no benefit with the use of frusemide and in fact, caused ototoxicity (BMJ 2006;333:420-3)

If you are concerned about causing heart failure (a topic I have touched upon several times in the past) a fluid challenge of 250ml 5% dextrose can be given stat. One can then reassess the circulation for blood pressure, rise in the JVP (or CVP), pulmonary crepitations and improvement of urine output.

If urinary retention is considered, a renal tract ultrasound is quick, non-invasive and provides valuable information. Please don't jump for the contrast CT as contrast nephropathy can ensue.

Examination of the urine may reveal white cells, red cells, casts etc, that can point you towards an intrinsic renal problem rather than pre- or post- renal cause.

So, in summary, please fully assess your patients. Don't go for the easy option of giving frusemide to increase the urine output as you may just end up with a worse problem ! Get out of the habit of knee jerk frusemide and use the grey matter you have been given instead.

Please consider.....

Can you be truly paperless? Yep!!

Dear Bloggers

As you probably have already guessed, I love technology! At the same time, I like to promote the traditional values of medicine and the basic principles and practice on which medicine was built. This seems kind of strange doesn't it; almost at the extremes of the spectrum of old and new but hey, that's me!

One thing that causes immense problems is the build up of medical papers on my desk and the inability to carry all of those papers around and to access them just when you need to.

However, I have found a way to be entirely paperless and still be able to access all of those papers!

Yep is a software package for the Apple Mac that scans your Mac hard drive for all PDF documents and organises them into a logical list for searching and viewing. It does far more than that! It allows you to scan pages and creates PDF files so that you can keep all of those medical papers with you on your laptop! It does this within the software itself. The PDFs can be tagged as well. Great!!

When displaying the files, they are projected full screen just as if you were reading the hard copy.

Of course, you also need a flatbed scanner to get the most out of the software!

The software is free to use for 21 days afterwhich, should you wish to continue using it, you must purchase it. It is inexpensive in the grand scheme of things and will make your life so much more liveable with all that extra space created with no paper getting in the way. :-)

This means having a clear desk, easier access to information, portability and organisation!

If you are interested in this software then please check out the Yep website.

With all those papers now as PDF files, they can be transferred to your PDA such as your Palm Pilot, WM5/6 smartphone, Blackberry, iPod Touch or iPhone. Another good piece of software for rendering PDF files fully viewable on the Palmpilot, WM5/6 or Blackberry devices is the Repligo software by Cerience. This reformats PDF files and allows full view or just the text to be displayed in flowed format. Moreover, it will also allow you to highlight the text in different colours. The conversion / viewing software will only work on a PC running Windows - not Mac (boo hoo).

If of course you are ultra-mobile with a smartphone having a data plan that allows cheap heavy data use, you could upload all of your PDF files to the 'internet cloud' e.g. MobileMe, GoogleDocs etc. There are several programmes availble on the iPhone that allow just this kind of access and it can save you time, smartphone memory and avoid having to lug around a laptop. The viewing experience on a smartphone is not great compared to a laptop / desktop machine but for quick access and mobility it seems to be the way that a lot of people are now choosing for access of information.

If you have any solutions to avoid the paper and killing of the world trees then please drop me a line and get published!

Christmas will soon be here and then the New Year. I will try and keep the blog articles going during this busy time, so drop in from time to time -- but I am sure you have better things to do :-)

December Case: The Long Awaited Answers

Dear Bloggers

Thank you for waiting. This case is very difficult and it would be the kind of grey-case that one would be given in the UK Membership examination (MRCP). In such exams, only the relevant data is provided with much focus on the history and physical examination with some basic radiology and salient, albeit selective laboratory data to give hints but not to lead the doctor directly to the answer. To give all the studies to you would have made the case more easy to answer but would not have been such a challenge. Nevertheless, from the information provided, it should at least have given you some clues as to what was happening in this patient.

Dr Keita Tatsuno, Department of Infectious Disease, Tokyo University, Japan has kindly sent in his answers to the case as follows:

Very interesting and difficult case. I try to answer, but please forgive me not in order. First, I guess the valve is mitral valve. Because the pansystolic murmur suggest the regurgitation. If the murmur were associated with ejection, the climax of sound would be at mid contracting phase. And the radiation to the left axilla fit in the direction from left ventricle to left atria.

Second, the subsequent loss of consciousness suggested another etiology than MSSA bacteremia. Usually, it might be typical pattern to suspect the embolic event in central nervous system, especially in acute infective endocarditis case. Of course, still there is some possibility of too early CT imaging study and need to check the MRI image. But in this case, it is not typical for emboli that the neurological abnormality ranged from loss of conscious to decreased muscle tone. I want to think such etiology as low blood glucose, hyponatremia, drug, hypothyroidism and so on, which affect all of the central nervous system including reticular activating system.

I want to check up these problems primarily, i.e. sodium, calcium, pH (arterial blood gas), glucose, serum creatinine. Especially, I am curious about sodium level. Because you mentioned she had very high urine osmolality. These sound suggesting SIADH.

Dr Stein, Florida, USA, has kindly provided answers to the case as follows:

1. Valve: Mitral-regurgitation
2. Hypoperfusion of kidneys and brain from hypovolemia and or relative hypotension [pseudo-normalization in hypertensive pt] from distributive (vasodilatation) near shock from sepsis. Cold extremities and modest tachycardia may be marker for vasoconstriction. If tent sign = extensor skin remaining up when lifted up, that is unreliable in elderly who have + sign from loss of elastic tissue. Axillary sweat absence may be indeterminate for volume status in septic patient. Another possibility is septic emboli from mitral valve to brain such as vertebral artery system to mid-brain system. Also electrolyte abnormalities such as hyponatremia may account for deterioration. She entered in hemocontrated and hypovolemia state. High urinary osmolality might indicate SIADH. However SIADH can only be diagnosed in normo-volemic state.
Another aspect is the acute IE on assumed diseased mitral valve causing acute valve perforation and acute pulmonary edema. Rarely hypothyroid and adrenal insufficiency may co-exist or exacerbate from the IE septic state. 3. Neuro involvement includes diffuse higher cortical dysfunction as found in hypoperfusion, sepsis and metabolic derangements all of which this patient had. I teach not to use the term `Dolls eyes positive.` What does this mean in simple English?: dolls eyes present(+) which is normal brain stem response or dolls eyes abnormal which is brain stem dysfunction(+sign). Hence Positive/+ has 2 opposite meaning. To avoid both inter/intra/transcultural confusion, only normal(present) or abnormal(absent) is required to avoid your Brit and US confusion. Do not depend on `tradition` to avoid this pitfall.

4. Fluid challenge/resuscitation. Follow hourly urine output increases with bolus and high DIV infusion guarding for heart failure, follow cardiac ECHO for valve perforation. Also repeat brain CT if suspect brain septic emboli.

5. See above

Hirotaka Kato, a 6th-year-student of Kumamoto University has provided an answer to the case.

Q1. Which valve is affected by the confirmed endocarditis?
Mitral valve. Radiation to axilla and becoming louder during expiration are suggestive.

Q2. What is the likely etiology of the other cardiovascular clinical signs and the loss of consciousness?
#1 hypovolemia
#2 sepsis
From the first physical exam, hypovolemia came up to my mind first. Tachycardia, slightly low blood pressure, cold fingers and dry membranes indicate that. Despite of IV fluid + antibiotics administered, the patient has been worsening, however. To me, high Hb/Ht and a high urine osmolality keep the possibility of hypovolemic state. And also, sepsis should be considered in this case, I think.

Q3. Which part of the nervous system has been affected?
Given areflexia and hypotonia, the cerebellum or neuromuscular junction or muscles can be considered.
In this patient who is likely to have the DIC state (or CNS infection possibly), the cerebellar involvement is most likely.
Neuromuscular junction (Lambert-Eaton) is also considered, but less likely now because malignancy cannot unify the symptoms.

Q4. What would be your next test?
1 physical exam. - vital sign + Is there now no edema?, cold extremities?, dry membrane?, no skin rash?
2 Blood test - Cr, BUN, Na, K, Ca, Glucose, NH3, Blood smear

Q5. What might be the cause of the neurological condition present?
Head CT and CSF analysis didn't show any abnormalities! I would like to list two as the possible causes.
1. septic or hypovolemic shock leading to hypoxia in the brain especially the cerebellum
2. shock + paraneoplastic syndrome.

Dr Yosuke Ebisu of Kameda Hospital, Chiba, also provided a reply to the case.

I read your blog. It is interesting case!! I think like that.

(Problem lists)

#1 fever

#2 obtundation

#3 Cheyne-Stokes respration

#4 oliguria

#5 splinter hemorrhage

(assessment)

# endocarditis caused by MSSA

Now you have treated it with fluoroxacillin and gentamycine. After that the patient became gradually obtundation,and her urine output decreased.

Then I think three passibilities.First,it is heart failure caused by destruction of the mitral vulve.It is because HF cause reduction of effective blood flow and then oliguria occur. Then the blood flow of medulla reduce, it cause Cheyne-stokes respiration.

Second,renal toxicity of gentamycin.It cause oliguria and if it became severe,the patient may have uremia. Then her consciousness will be impaired.

Third, septic emboli. It cause cerebral infarction. According to your blog, her extremities were flaccid and doll's eye movement was intact. So I suspect infarction of medulla.(Cheyne-Stokes respiration support this.)

(Plan)

-check heart sound(S3,S4),JVD and edema

-echo cardiogram: check the valve.(If the valve is destroyed we should think operation soon.)

-blood test,especially Cre and BUN.(If renal function decrease, we shoud change the drug or it's dose.)

-Head MRI

Here is the answer from Professor Matsumura, Kanazawa University of Medicine.

Thank you for showing me an interesting case.
I will try to make my hypothesis.

Questions: 1) From the physical examination, which valve is affected by the
confirmed endocarditis?

This case showed classic features of acute infective endocarditis. There
were several splinter haemorrhages in the nails and Janeway lesions on the
palms.
Cardiac examination disclosed Levine II/VI pansystolic murmur in the APEX
area radiating to the left axilla accentuated on expiration.
Vegetation must be on the mitral valve.

2) From the history and first physical examination, what is the likely
aetiology of the other cardiovascular clinical signs (excluding those of
endocarditis) and the subsequent loss of consciousness?

This patient had high fever. I suspect that this patient had volume
depression and pure water deficit following findings. Cold finger and toes,
Pulse 100/min regular, BP 100/80, JVP not raised, dry skin, dry mucous
membranes, tenting sign positive, no axillary sweating.

3) With the follow-up neurological examination in mind which part of the
nervous system has been affected?

This is the most difficult question of this patient.
I would make problem list.
#1 Altered mental status, deep coma
#2 Doll's Eye sign positive
#3 Tone diffusely decreased
#4 Areflexia
#5 Cheyne-Stoke respiration
#6 Anorexia
#7 Oliguria
#8 Pure water deficit and volume depression (Hb 18, haematocrit 0.5 and a
urine osmolality of 1000)

I have to differentiate the cause of #1 altered mental status first.
Mnemonic of altered mental status is AIUEOTIPS,“あいうえおちっぷす” in
Japanese.

A：Alcohol, not likely
I：Insulin（hypo/hyper‐glycemia）
U：Uremia
E：Encephalopathy（hypertensive, hepatic）, not likely, Endocrinopathy
（adrenal, thyroid）, not likely, Electrolytes（hypo/hyper‐Na, K, Ca, Mg）
O：Opiate , not likely or other Overdose, not likely，decreased O2
（hypoxia, CO intoxication
）
T：Trauma, not likely, Temperature（hypo/hyper）
I：Infection（CNS, sepsis, pulmonary）
P：Psychogenic, not likely, Porphiria, not likely
S：Seizure, not likely, Shock, Stroke, not likely, SAH, not likely

In case with endocarditis, septic emboli is the common cause of neurological
problem. But head CT disclosed no abnormalities. #2 Doll's Eye sign positive
indicates that the brain stem of this patient was intact.
#3 Tone diffusely decreased and #4 areflexia indicated PNS and/or muscle
problem, not the problem of upper motor neuron. #5 Cheyne-Stoke respiration
can indicate bilateral forebrain disease or diffuse bihemispheric disease,
Cheyne-Stokes respiration is now known to occur with unilateral hemispheric
and brainstem infarcts (UpTo Date).
It is difficult to point out the one part of neuro-anatomical problem of
this patient.
Hypo/hyper‐glycemia, uremia, or hypo/hyper‐Na, K, Ca, Mg should be
differentiated.

4) What would be your next test to confirm your suspicions?
I want to know following test.
Na, K, Cl, Ca, Mg, BUN, Cr, glucose, serum OSMO, blood gas analysis.

5) What might be the cause(s) of the neurological condition present?
My most likely diagnosis is hypernatremia, hyperosmolality. Serum sodium
must be high more than 160 meq/L. And BUN and serum creatinine must be high
level too.

Izumi Nakayama, 6th year medical student of Osaka University named the correct diagnosis below.

.... I tried this month's case on your blog. It is the first time to send you my answer.

My answer for the December case...

Questions: 1) From the physical examination, which valve is affected by the confirmed endocarditis?
1. Mitral regurgitation sound. (it is common but accentuation on expiration is unusual for the left side heart murmur, isn't it? )

2) From the history and first physical examination, what is the likely aetiology of the other cardiovascular clinical signs (excluding those of endocarditis) and the subsequent loss of consciousness?
Her dry skin, dry mucous membranes indicate she had been dehydrated.
I'm sorry but I don't know 'the tenting sign'. What is it like?
1. brain stem infarction. small thrombi from mitral vulve.(dehydration increases the risk of thromboembolism.)
2.central pontine myelinolysis (although chronic hyponatremia is not likely because she had been dehydrated. I don't know CPM can occur in rapid adjustment of dehydration or hypernatremia.).
.
3) With the follow-up neurological examination in mind which part of the nervous system has been affected?
positive Doll's sign and generalized weakness indicate the lesion either in the midbrain or in the pontine.

4) What would be your next test to confirm your suspicions?
MRI including brain stem. repeat neuro exam. plasma sodium concentration, plasma osmolarity, .
5) What might be the cause(s) of the neurological condition present?
same as question 2.

My impression is like above. First I came up with the infarction. But I think it cannot explain her gradual declining.

Many thanks for the excellent opinions sent in this month.

Now, let's go through the answers.

1) From the physical examination, which valve is affected by the confirmed endocarditis?

This patient has a pansystolic murmur in the left apex which radiated to the axilla. It is accentuated by expiration which makes it a left sided cardiac murmur. By definition, pansystolic murmur in the aforementioned location and attendant features would suggest mitral regurgitation.

2) From the history and first physical examination, what is the likely aetiology of the other cardiovascular clinical signs (excluding those of endocarditis) and the subsequent loss of consciousness?

The other cardiovascular signs include cold hands and feet (suggesting peripheral vasoconstriction), tachycardia, low blood pressure, tenting of the skin and absent axillary sweating are all consistent with hypovolaemia e.g. as a result of dehydration.

The tenting sign is procured by lifting a piece of skin with the examiners finger tips to produce what looks like an upside down V sign or what is commonly referred to as a 'tent'. In a patient with normal skin elasticity, if there is normal hydration, the skin should immediately retract to its normal flat position. In the presence of dehydration, the skin takes longer to return to the normal position producing a positive sign. However, in the elderly who have loss of elastic tissue, the sign can be falsely positive. Although the tenting sign is usually performed on the dorsum of the hand or forearm (extensor surface), the best place to check for tenting sign in the elderly is the inner thigh.

3) With the follow-up neurological examination in mind which part of the nervous system has been affected?

This patient had a completely normal nervous system examination on admission. However, the follow-up examination produced a picture that should have been interpreted as generalised flaccidity, generalised areflexia and indeterminate Babinski suggesting either an acute brainstem or diffuse cerebral injury. However, with the presence of Cheyne-Stoke respiration and positive Doll's eye sign* (abnormal), a brainstem lesion would be highly suspected. However, as we ascertain from the physical examination, the pupillary reflexes are normal suggesting that it does not completely involve the midbrain. That leaves the possibility of the medulla oblongata and pons being affected.

*note: I take heed of Dr Stein's advice and agree about positive / negative aspect that can cause confusion in respect of the Doll's Eye sign. It is probably better to describe what is seen so that everyone can understand whether the sign is present or not rather than as I originally described it. Apologies. Thank you Dr Stein for the very constructive advice.

With a normal CT brain examination, cerebral oedema would seem less likely and a significant structural brain lesion in the cerebral hemispheres would be ruled out, as would bleeding. It is unfortunate that the opening pressure of the CSF was not measured in this patient which is the usual way for understanding if raised intracranial pressure is truly present rather than just relying on a seemingly normal CT scan.

Infarction might be less easy to rule out especially in acute neurological deterioration and particularly when concerning the brainstem and cerebellum which are difficult to image accurately on CT. As this patient has confirmed endocarditis, one would naturally suspect multiple embolic infarction although other diagnoses should also be entertained such as global ischaemia, metabolic or endocrine causes as rightly mentioned by several of the above physicians and students.

4) What would be your next test to confirm your suspicions?

An MRI of the brain and brainstem with the addition of vascular views.

Although measuring the serum osmolality is useful, the physical examination tells us that this patient already has a high osmolality and moreover, it can also be calculated from the serum electrolytes. I see that formerly measuring it might be useful as a guide to know how quickly it is recovering but in reality, one follows the patient's conscious level, hydration status and basic serum electrolytes to know that.

Measuring the glucose (hypoglycaemia / hyperglycaemia) would be correct -- it was normal.

An ABG would be reasonable and in hypovolaemic states, one might see a rise in the serum lactate (lactic acidosis) and renal impairment would also contribute to a metabolic acidosis. Urine ketones would be useful to establish if there was a DKA present (not in this case) and remember that starvation can raise the ketones.

5) What might be the cause(s) of the neurological condition present?

The patient has confirmed endocarditis. Hence, an embolic source leading to brainstem infarction might realistically be the cause of the brainstem abnormality. However, we are told that the patient has history, physical examination and basic lab studies consistent with severe dehydration.
In respect of Dr Stein's comments, he is correct in saying that SIADH can only be diagnosed in a patient who is normo-volaemic. Hence, with concentrated urine being present in the context of hypovolaemia / dehydration, then this would be Appropriate ADH secretion rather than inappropriate secretion.

Severe dehydration is a risk factor for hypernatraemia and haemoconcentration. Hypernatraemia can result in brainstem abnormalities such as Central Pontine Myelinolysis (as can hyponatraemia with rapid correction) and haemoconcentration can cause cerebral vein thrombosis.

What happened next?

The MRI scan of the brain is shown below. As can be seen, the brainstem shines like a beacon as do the basal ganglia. This patient indeed had severe pre-renal failure with severe uncorrected hypernatraemia (max 170mmol/L), high BUN and creatinine for several days due to dehydration, which when corrected, was done so over 3-4 days, making the rare diagnosis of Severe Central Pontine Myelinolysis as the top diagnosis here.

The T2 'Flare' MRI pictures below demonstrate central pontine plus extra-pontine involvement in the basal ganglia, the cerebellum and its peduncles. Thank you Dr Y.


Given the fact that the CSF examination was normal goes against a CSF bound infectious aetiology for cause of the brainstem problem. Moreover, embolic phenomena were considered but the arterial views of the MRA were within normal limits. In addition, the changes of the brainstem and basal ganglia are symmetrical with no diffuse cerebral involvement making symmetrical, selective embolic impaction very unlikely. Of course, a brainstem glioma should be considered but with the over-riding history of this patient, the rapid deterioration and a previously normal CT scan makes this diagnosis somewhat remote.

Hypernatraemia is a rare cause of central pontine myelinolysis. It usually occurs in the context of hyponatraemia with the over-rapid correction of the sodium.

After a Medline Search, please see the following interesting cases below:

J Intensive Care Med. 2006 Nov-Dec;21(6):372-6. Links

Osmotic demyelination and hypertonic dehydration in a 9-year-old girl: changes in cerebrospinal fluid myelin basic protein.

Shah B, Tobias JD.

University of Missouri School of Medicine, Columbia, MO 65212, USA.

A 9-year-old girl was admitted for the treatment of hyper-natremic dehydration. Her history was significant for psychogenic polydipsia, hyponatremia, and a renal concentrating defect. She presented with a 2-day history of altered mental status, ataxia, lethargy, fever, nausea, vomiting, and diarrhea. Meningitis was ruled out. Over the course of her illness, slow rehydration was maintained with a gradual decrease (10 mEq per 24 hours) of the serum sodium. Despite this care, she developed quadriparesis, and magnetic resonance imaging performed on day 6 of her illness was consistent with osmotic demyelination (central pontine myelinolysis). To rule out an excessively rapid correction of hypernatremia as the etiology of the problem, a myelin basic protein was measured in the cerebrospinal fluid that had been obtained on hospital day 1. The myelin basic protein was 649.50 ng/mL (normal, 0.07-4.10 ng/mL). The current literature is presented regarding the postulated pathogenesis of central pontine myelinolysis and suggested therapies, previous reports of central pontine myelinolysis in children are reviewed, and the potential role of myelin basic protein in its diagnosis is discussed.

Presse Med. 1999 Jun 12;28(21):1112.Links

[Central pontine myelinolysis following correction of hypernatremia in an aged patient]

[Article in French]

Bour-Guichenez G, Savin D, Moulaire V, Lalu T, Capieu L, Jonquet O.

Rinsho Shinkeigaku. 1994 Nov;34(11):1130-5.Links

[A case of central pontine myelinolysis and extrapontine myelinolysis during rapid correction of hypernatremia]

[Article in Japanese]

Go M, Amino A, Shindo K, Tsunoda S, Shiozawa Z.

Third Department of Internal Medicine, Yamanashi Medical College.

A 69-year-old woman was admitted because of severe dehydration due to anorexia. Consciousness disturbance was found to be due to severe abnormalities of serum electrolyte balance, but recovered quickly by correcting the hyperosmolality. While the initial serum sodium value of 186 mEq/L was corrected to 139 mEq/L in 5 days, locked-in syndrome, bilateral hand tremor and tetraparesis appeared. Brain magnetic resonance imaging (MRI) revealed symmetrically high signal intensity areas on T2-weighted images and low signal intensity areas on T1-weighted images in central part of pons and bilateral middle cerebellar peduncles. One and a half month later, these neurologic symptoms were improved and the MRI abnormalities also disappeared. Auditory brain stem responses which showed prolongations of III to V wave peak to peak latency at the onset returned to normal. It is noted in this case that central pontine myelinolysis (CPM) and extrapontine myelipolysis (EPM) appeared during the period of rapid correction of hypernatremia. Although it is known CPM and EPM are caused by hypernatremia or the rapid correction of hyponatremia, there has been reported only one case of CPM and EPM after rapid correction of hypernatremia. According to the hypothesis of Norenberg, rapid rise in serum sodium may cause CPM and EPM, but if CPM and EPM are caused by the rapid correction of hypernatremia in this case, CPM and EPM may be caused by another pathogenesis of the disorder.

As can be appreciated from the above case reports, it can occur in all age groups. In its severe form, it can result in tetraparesis, pseudobulbar palsy and hence, a locked-in syndrome. There is a high risk of death in such patients; 5-10% beyond 6 months.

This problem occurs due to release of myelotoxic compounds resulting in destruction of myelin sheaths with the preservation of neurones and axons. Such patients can be found to have a raised Myelin Basic Protein in the CSF.

Hypernatraemia and Hyponatraemia

Severe hypernatraemia can be avoided- The patient presented with signs of hypovolaemia which worsened during the hospital admission, and as a result, appropriate fluid management to ensure the return of normal circulation and electrolyte balance would have gone some way to reverse this situation.

There is a commonly held view that patients should not be over-hydrated because of the fear of causing heart failure. This is an unfortunate opinion. Patients with mismanaged circulation die from renal failure and may develop problems such as coagulation abnormalities e.g. DVT, PE, cerebral and renal vein thrombosis and hypernatraemia. Signs of dehydration / hypovolaemia and pre-renal impairment suggests a generalised tissue hypo-perfusion state and therefore, it tells us that the patient needs more circulation and hence, more water and / or blood.

Of course, over vigorous hydration can in some instances result in pulmonary oedema especially if there is an impairment of cardiac or renal function. However, pulmonary oedema is much more manageable than renal failure. Fluid overload responds to drugs such as furosemide, nitroglycerine and if need be, CPAP can be used to push the fluid out of the lungs. In the worst case scenario a patient with pulmonary oedema and or renal failure can utilities haemofiltration or dialysis respectively (if necessary and if available). Of course, diuretics will only work well if the kidneys were previously normal and have a sufficient circulation and hence we come back to the use of appropriate fluid to replenish the renal blood flow.

In such a patient, central venous pressure monitoring / JVP measurement would be beneficial to help guide the fluid administration plus repeated examination of the chest for crepitations (crackles).

Conversely, if the patient has developed a severe hypernatraemia or hyponatraemia, then the correction of the sodium should be done more slowly e.g. 10-12 mmol/24 hours. However, if the patient is shocked and in pre-renal failure such fluid might have to be administered more quickly. However, the type of fluid given is very important. Opting for 5% dextrose in severe hypernatraemia can cause rapid shifts in Na-H20 and should initially be avoided. Most practitioners would start with normal saline (0.9%) which is still nevertheless hypo-osmotic when compared to the serum hyper-osmotic state. This leads to a more gradual reduction in Na level. If the serum Na does not start to correct despite the use of normal saline then half-normal saline (0.45%) can be considered but regular monitoring of Na should be ensured so that an over-rapid correction of the Na does not occur.

So remember, it is not only over-rapid correction of hyponatraemia that can cause central pontine myelinolysis, by also the development of hypernatraemia or its over-rapid correction too !

This brings me back to a salient point that I have mentioned on numerous occasions over time, examine your patients! List the problems of the history, physical examination, labs and radiology. Aim to interpret the features and group them together and try to form a hypothesis for different potential scenarios e.g. IE -> embolic infarction, brainstem signs in dehydrated/hypovolaemic patient -> ? hypernatraemia ? hypoxaemia ? cerebral vein thrombosis etc... When doing the physical examination, look for the signs of dehydration (as above), check the urine output (place a Foley catheter and measure the hourly urine production) and serum renal function and use enough fluids to correct the circulation.

Hypernatraemia with raised BUN and Creatinine usually signifies a reduced oral intake of fluid or that the patient is not producing or reacting to Vasopressin (Diabetes insipidis). The latter two are unusual causes but should be investigated if the circulation fails to improve with vigorous fluid correction. The clue that this was dehydration rather than diabetes insipidis was the highly concentrated urine suggesting appropriate ADH activity whereas in the latter disease, the urine is dilute because of failure to concentrate the urine. This could not have been consistent with SIADH as described above.

Thank you ever so much for such great contributions to this month's case. It was certainly a tough one.

Moreover, I look forwards to more challenging case to present to you into 2009 and beyond. Please keep coming back to the blog when you get the chance.

Tracheostomy in Hokkaido

Dear Bloggers

Today I want to show you some of my recent experiences in Hokkaido. I was invited by Dr K to his hospital to teach the residents.

During my visit, I rounded with the team and also lectured on a very rare complication of atrial fibrillation and on the basics of heart murmurs, added sounds and splitting of the heart sounds.

However, I was very lucky to be able to catch on camera the placement of a tracheostomy tube in a patient with COPD. The photos are obscured in such a way as to maintain the anonymity of the patient. The placement is done by the Seldinger technique (the technique is also used for CVP line and mini chest drain placement etc) which makes a hole in the trachea which is subsequently dilated up and further widened with forceps until the tracheostomy tube can be placed into the trachea proper.

The procedure went without too much problem although the patient repeatedly desaturated during inspection with the bronchoscope as a result of the severe underlying lung disease. Hence, as can be seen below, it required the presence of someone managing the airway / endotracheal tube (Dr T - 2nd year doctor in training), someone to perform the bronchoscopy to check for correct positioning of the needle and trach-tube (Professor M), and two doctors (Dr K and Dr K2 - 4th year doctor in training) to perform the actual trach placement.

The procedure was successfully completed to delight of the doctors and nurses -- and me too! :-)























I was also lucky to be able to see Dr K (above) perform mutilpe variceal ligation (banding) in a patient with previously undiagnosed portal hypertension who presented to the hospital with mild fresh upper GI bleeding but no variceal rupture.

All in all, although I went to teach on various aspects of medicine, I definitely benefited from the experience myself.

Remember, if you think you have ever stopped learning, it is time to hang up your stethoscope.

December Case - Think Carefully !

Dear Bloggers

The following case has been anonymised for the purposes of protecting patient confidentiality.

This 70 year old female patient was admitted into a distant hospital with fever which had begun several days before. The fever reached a height of 39 degrees C when at home, which prompted the patient to seek medical advice.

The patient denied respiratory, urinary, or gastrointestinal symptoms. There were no sweats, rigors or weight loss. The patient denied headache, neck stiffness and photophobia. There was no complaint of any skin, joint or muscle problems. There was no history of foreign travel, no sick contact, no insect bites and no sexual intercourse in over 10 years.

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

There was no family history of note and the patient was a non-drinker and non-smoker. She lived with her husband in a house, was fully independent and had good family support from her children and other relatives who all lived nearby.

On Examination

GENERAL - Slightly unwell; No JACCOL. Several splinter haemorrhages in the nails. Several Janeway lesions on the palms.

CARDIOVASCULAR - Cold finger and toes, Pulse 100/min regular, BP 100/80, JVP not raised, dry skin, dry mucous membranes, tenting sign positive, no axillary sweating. Heart sounds 1 + 2 + no added sounds. Levine II/VI pansystolic murmur in the apex area radiating to the left axilla accentuated on expiration. No evidence of peripheral oedema or DVT.

RESPIRATORY - Respiratory Rate 16/min, Sats 98% on room air, Trachea central, expansion normal, Percussion sound normal, auscaultation normal vesicular breath sounds.

ABDOMEN - Non-distended, Soft, No hepatosplenomegaly, No Masses, No renal angle tenderness, bowel sounds normal. Rectal examination - no masses, no posterior cervical motion tenderness, no blood.

MUSCULOSKELETAL EXAM - All joints normal range of motion and no warmth. No deformity. No Muscular problem identified.

ENDOCRINE - No tremor, no goitre or neck pain on examination.

CNS / PNS - No neck stiffness, no photophobia, Kernig Sign negative, Brudinski Sign negative. Tone - normal throughout
Power - 5/5 throughout
Reflexes - normal ++ in all limbs
Coordination - Normal
Sensations - Normal
Babinski - plantar flexion bilaterally (negative)

Pupils equal and reactive to light and consensual response. All cranial nerves seemingly normal throughout.

Fundoscopy - no Roth's spots seen. No papilloedema.

Clinical Impression: High suspicion of infective endocarditis.

Blood cultures revealed MSSA in 4 bottles and the patient was commenced on flucloxacillin and gentamicin.

Echocardiogram confirmed the existence of a small vegetation.

However, the patient was not eating or drinking during the hospital admission and intravenous fluids were subsequently commenced. Urine output began to deteriorate and mental status decreased, first with confusion, then stupor and finally with obtundation.

Laboratory studies revealed Hb 18, haematocrit 0.5 and a urine osmolality of 1000.

Repeat neurological examination after several days of admission revealed the following:

GCS - No eye opening, no response to pain, no verbal response.

Cranial nerves: Difficult to examine but pupils equal and reactive to light. Doll's Eye sign positive.

PNS: Tone diffusely decreased, unable to assess power, generalised areflexia, Babinski sign indeterminate bilaterally.

Respiration: Cheyne-Stoke respiration.

A CT brain was performed which showed no abnormality. Lumbar puncture follow-up was again normal. CSF pressure was no measured.

Questions: 1) From the physical examination, which valve is affected by the confirmed endocarditis?

2) From the history and first physical examination, what is the likely aetiology of the other cardiovascular clinical signs (excluding those of endocarditis) and the subsequent loss of consciousness?

3) With the follow-up neurological examination in mind which part of the nervous system has been affected?

4) What would be your next test to confirm your suspicions?

5) What might be the cause(s) of the neurological condition present?

Please note, this is a very difficult case. Please try your best with the limited information available to consider various diagnoses. You never know, you might just be right! Answers this month--- at some point ;-) Please feel free to send me your answers.

PRIVACY & DIGNITY UPDATE

Dear Bloggers

Professor Alan Lefor of Jichi University, Japan has kindly provided additional important comments in regards to Privacy and Dignity.

I would emphasize a few things. I don't know if all of this applies here, but it certainly does in the USA


1. Chaperons are critical, especially for male doctors examining female patients.

2. I get the history from a dressed patient, then I leave the room while they get undressed. I use that time to quickly write up the history.

3. I always have the patient remove all of their clothing (EVERYTHING!) and put on a gown, and then during the exam, I ask the patient to expose their body by pulling the gown up. I never do that to the patient. Then, when the gown is up, I quickly use a sheet to cover the patient's body except exactly where I need to examine.

4. After the physical exam I leave the room so the patient can get dressed in privacy. I use that time to collect my thoughts and write up the physical exam. Then I go back in and talk about the plan to a fully dressed patient.


Privacy & Dignity cannot be over-emphasized.

These are my additional thoughts. The comments you made are critically important!

Thank you Professor Lefor for such important advice.

Professor Lefor has provided insight into how privacy and dignity of the patient in respect of physical examination is maintained in the United States.

In the UK, most clinic rooms are 'double rooms' consisting of a consultation room and an examination room. Depending on the nature of the consultation, the patient may need to use a gown but in all cases, the patient is draped when required. The doctor enters the room after the patient has made themselves comfortable for the exam and the doctor leaves the room in order to allow them to redress and come back through to the consultation room. There is a clinic nurse present in order to assist the physician and patient and of course, to be the ever important chaperon.

However, in Japan, matters can be very different. On occasion, outpatients can consist of multiple thin-walled cubicles making privacy and confidentiality a potential problem because of acoustics. Doctors are usually rushed because of the high patient turnover in the outpatient clinic and can at best only spend 5 mins or so with each patient. In a typical morning clinic, such doctors might easily see 40 patients. One surgical friend of mine saw 120 patients in a day! No joke!!

Ultimately, history taking and physical examination are limited with most time taken up by typing into the computerised records (denshi kalte) and ordering lab tests and radiology. The turn over is very rapid, although it depends upon the specialty, and the doctor does not get the opportunity to step outside the cubicle. Privacy is maintained in some respect by pulling a curtain around the examination couch. Draping the patient should be done, but again, it depends on local practices, resources and time available. Chaperons are available on request.

In an ideal world, the patient should be given ample time for a full history, physical examination, the full consideration of all the problems at hand and step-wise assessment and plan. However, in reality, not all the elements can be carried out in such a limited and stressful situation.

In Japan, one way to reduce the flux of patients into the hospital outpatients would be to introduce a fully comprehensive community-based primary care service, as in the UK (general practitioners), who see the patients registered in their locality. They are the gatekeepers to the local hospitals and decide who needs to be seen by a particular specialist at the hospital or whether the problem can simply be managed in primary care. This system works extremely well in the UK whereby the GPs only refer sick patients who may need hospital admission. Non-acute problems are referred by letter for an appointment directly to the consultants in the local hospital (if required). Patients cannot simply turn up to the hospital outpatient clinic unannounced.

As such, patients have a longer time to spend with the consultant or registrar during their booked outpatient appointment, and a fuller understanding of the patient problems can be elicited and physical examination can be carried out in detail. Usually, a new patient will get 20-30 minutes and a follow-up patient 10 minutes. In a busy clinic in the UK, a physician might see perhaps 12-16 patients but usually no more than that.

If there were more Primary Care physicians in Japan, the stress on the hospital outpatient system would be much less. However, at present, there are not many Primary Care / Family Practise training schemes in Japan. I would hope that this will change in the future.

Please consider...

PRIVACY & DIGNITY

Dear Bloggers

Today I wanted to discuss about Dignity and Privacy for patients. By passing on helpful situational anecdotes, I would hope that you as medical students and physicians will not make the similar mistakes.

Remember, patients are human beings with as many rights in law as you. No patient should ever be examined without their expressed permission unless the patient cannot give permission and in doing so, it is in their best interests as determined by the physicians and family and pertaining to the law of the land and which should be the overriding objective of medical care.

However, despite the patient giving you as doctors permission to examine them, it does not give you free will to do what you please. You must ask the patient to reposition themselves if you want to check particular parts of the body. You must not do it for them unless they ask you, or agree for you to do so. To intervene and manipulate the patient without their consent might be construed as an assault - so be careful.

An example from the UK was when I was training for an examination. On that day, I was training with a colleague and we went to examine a male patient who was well, had clear consciousness and was very compliant with verbal requests. I examined first and following that, my colleague examined the patient's cardiovascular system. Everything was going well and the patient turned his head to the left for the JVP to be examined and then suddenly, the patient lifted his head off the pillow to answer a question. As if like a reflex, the female doctor used the palm of her hand and pushed his head back down on to the pillow. The patient appeared somewhat bemused by what had just happened.

This type of physical contact was clearly wrong and the error was pointed out to the female doctor who promptly apologised to the patient for her error and the doctor then completed her examination.

If the above had occurred in a real life examination, the doctor would have immediately failed for not considering the care and comfort of the patient and for over stepping the permission granted by the patient for the doctor to carry out the examination.

In this scenario, the patient should not be restrained from simply moving. We must ask the patient with words not to move and certainly not entertain physical restraint of any kind.

However, putting physical examination aside for just a second, if the patient is clearly confused (and unable to make a logical decision) and that restraining the patient is in their best interest and to refrain from doing so might be otherwise detrimental to the physical and mental well being of the patient i.e. self-harm, then to do so might be appropriate. In any such situation, you must be aware of the local and national laws of physical restraint to safe guard yourself as well !

If the patient is compos mentis and decides not comply then so be it. We must not take it upon ourselves to do what the patient might not want us to do. We must at all times re-examine our own decision and that of the patient whether certain parts of the physical exam can be continued because of patient compliance. Patients can revoke their decision to be examined at any time! Just remember that.

Another example was in Japan some years ago when I saw the very same 'palm-to-forehead restraining manoeuvre' to stop a patient from lifting their head up to talk. This was wrong. The junior doctor had not realised that this was an inappropriate way to treat the patient.

On the other hand, sometimes weak patients need help to be sat up in order that the chest can be properly examined, but again, patients should be treated with respect and dignity, all the time asking them if it is acceptable to continue the physical examination.

How can we learn what is right and wrong ? That comes down to ethics training at University and through our own quest to understand what is socially and ethically acceptable within our own society.

Another thing to remember when examining patients on a general ward is PULL THE CURTAINS! Patients expect privacy and again I mention it, DIGNITY. As medical staff we are used to seeing the human body every day and over time we probably become desensitized to the meaning of privacy. However, we must put ourselves in the position of the patient and think what they would want. Most patients would not want to be exposed for everyone to see across the medical bay. Pulling the curtains on a main ward is not a difficult thing to do. All it takes is to understand the patient's needs and not just your own.

Moreover, if a doctor walks into the examination area around the bedside -- RE-PULL THE CURTAINS. Don't leave gaps in the curtains for others to peer through. It is simply not the done thing.

When examining the patients remember to refasten the clothes after having exposed the patient and completing the examination. Don't leave the patient lying on the bed, clothes open for everyone to see when there is no need to. Again, it comes down to PRIVACY & DIGNITY for the patient. Only expose those areas that you are currently examining. Don't completely expose the patient in one go.

Lastly, despite medical students and junior residents being eager to learn physical examination, it does not mean that 10 people try and clamber behind the examination curtains especially around a cramped bedside. Remember, PRIVACY & DIGNITY for the patient. A patient does not want 10 freshmen gawping at their chest during auscaultation when the main problem is the cellulitis of the leg. If you are going to teach in numbers, remember that the patient must give permission first. Do not make the patient feel pressurised to accept a troop of physicians when it is not what they want. If in agreement, try to limit your examination in front of a crowd as much as possible to maintain the PRIVACY & DIGNITY of the patient.

Remember, unhappy patients complain which could mean you coming before a board of inquiry for your actions even if you thought you were right. A happy patient will not usually complain about you. If you do examine the discrete areas i.e. breasts, genitourinary system of a female patient, please have a chaperon present at all times as a means of protecting you and the patient from what could, for example, be potentially misinterpreted as a sexual assault, and please document your findings accurately and state the name of the chaperon and their seniority e.g. senior staff nurse. If a patient complains about you and the allegations are untrue, the chaperon may be the only person who can give an independent account of what happened to save your neck.

Remember, protect the patient both physically and psychologically and you therefore protect yourself. Don't overstep the mark as a doctor. Paternalist medicine went out the door many years ago in the UK and USA. These days the patient is empowered and the physician must seek agreement with the patient.

Now say after me -- PRIVACY & DIGNITY, PRIVACY & DIGNITY, PRIVACY & DIGNITY.

Thank you for reading today :-)

For further reading, there are many books available on medical ethics and such texts are well worth a perusal.

Please carefully consider....

If you have any views on the above or on medical ethics generally then drop me a line and get published! I look forwards to hearing from you.

Applied Pharmacology - time to change the way of training

Dear Bloggers

One of my significant concerns with instructing junior doctors is their paucity of knowledge and application of learned pharmacology in clinical practise.

As a medical student I learned about the in-depth aspects of the major drugs e.g. beta blockers, loop diuretics, antibiotics etc, which included their absorption, bioavailibility / distribution, detoxification and elimination in addition to drug interactions and major side effects. I learned many of the drugs in respect of their generic name which in practise makes it much easier to identify a class of drug and the potential side effect profiles.

This background provided a very good foundation before actually prescribing and using drugs in the clinical setting.

It is not simply good enough to train in basic pharmacology as we as doctors are prescribing medications everyday to our patients and we must understand the drugs with the desired and undesired effects.

In my opinion, having trained newly qualified doctors straight out of the many medical schools throughout the nation, there appears to be little requirement for detailed pharmacology knowledge. Surprising to me when I first started teaching in Japan, I found that drug names are remembered and prescribed via their trade name. Of course, using trade names of drugs is okay if everyone around knows the unique trade name, but for purposes of international communication, generic names are used predominantly in other countries. One reason for the use of generic names is to reduce the confusion over the many thousands of drugs that exist.

This current situation cannot be good for the doctors training or for the patients who rely on the doctors knowledge to prescribe the best, evidence based drugs at the least of cost.

So, what can be done to improve the knowledge of junior doctors pharmacology?

Well, it all has to do with the adequacy of training. More intensive lectures on pharmacology at medical school with focus on their clinical use and polypharmacy (use [overuse] of drugs in combination) and potential side effect profiles. Such lectures should be actually given by doctors who have used the drugs and who can truly give a ground based opinion on their use rather than regurgitating what is written in a dusty old textbook without ever having used the drug before. One such misunderstanding of drugs has resulted in the under use of amiodarone for the fear of long term side effects despite the brilliant rhythm control properties over other anti-arrhythmic drugs.

Pharmacology testing should be made a higher priority for examination purposes in the National Examination but particularly in the context of clinical use.

Moreover, the old way of senior ordering junior doctor to prescribe drugs without explanation should now be supported with evidence that such a drug works and that it is effective more than other drugs in any particular clinical scenario in order to appropriately teach the junior doctor. Evidence based practice is not just knowing a list of papers, it is knowing how and when to apply the evidence and knowing when there is a lack of evidence in support of any particular drug.

Eminence Biased Medicine has to morphologically change to become real EBM in order for medicine to be totally free from clutter of the yesteryear pseudo-leech treatments that were prescribed to treat all ailments but did little to do anything except to show the patient that the doctor was actively doing something.

At the end of the day, it comes down to training physicians to become physicians rather than training them to pass exams. Of course, we must all do standardised examinations to become doctors as there has to be a minimum basic standard, but with a change of emphasis and intensive pharmacology training, the new doctors coming through training would have a much better understanding of how to treat disease, both effectively and safely.

If you are interested in basic and advanced pharmacology, I would advocate the use of several pharmacology books which include:

• Rang and Dale's Pharmacology - Rang, Dale, Ritter and Flower, 6th Edition. Churchill-Livingstone publishers. This book is very detailed and provides a deeper background to the understanding of drugs and their actions. I used an earlier edition at medical school to supplement my lecture notes and develop a wider understanding of all the drugs I needed to know.
• Clinical Pharmacology and Therapeutics (lecture notes) - Reid, Rubin and Walters. Blackwell publishing. Again, I used an earlier edition of this book to learn the relevance of drugs to clinical practise as a medical student. It gives condensed information about the use of drugs.

I would highly recommend both books. I have no vested interest in recommending these books as it is my wish only to improve the standard of doctoring in general.

In order to be good, safe and knowledgeable physicians, we need to know our 'bread and butter' basic medicine before we can progress to the triphasic CT scan and PET scanning modalities that are looked upon so highly, yet have little to do with everyday practise. Without a good knowledge of drugs we are doing ourselves as physicians a great disservice and that of our would be patients.

Please consider....