The Funny Things in Medicine That Turn Out to be Sad

In my time I have experienced many funny situations in my medical life.

I write this blog today because of a situation I saw just recently when I was walking in the street. I saw a female walking from one side of the road to the other wearing normal clothes and seemingly doing what a normal person would do. She made her way to the cigarette machine in the street and was looking for small change to buy the cigarettes. In the night time when this occurred, I saw something dangling from her arm which was shinning in the light from the oncoming cars headlamps. I thought that my eyes were deceiving me until I got a better look and I realised it was a drip tube. Suddenly, the patient picked up her drip bag of intravenous fluid she was having at the time. Yes, the patient was so unwell requiring intravenous fluid that she was able to get up and go out of the hospital to buy some cigarettes.

It also reminded me of when I was a first year doctor in London when I was treating a drug addict with cellulitis and anaemia. He required intravenous antibiotics and blood transfusions. However, the only available venous access was a small superficial vein in his neck to which the blood transfusion was attached. He soon went missing from the ward and despite searching for him, he had left the hospital with his blood transfusion still running!! On my way out of the hospital in the evening sunset, I saw the patient begging on the road trying to sell his blood transfusion to oncoming Londoners, no doubt so he could buy more drugs and use the intravenous access made for medical purposes as his no inlet for illicit drugs.... This was a desperate man who needed help and it showed to me just how far some people will go to try and maintain a drug habit.

At the same hospital, I was on-call one night when a patient was admitted with chest pain from a possible crises from sickle cell diseases. She was screaming for pethidine, a fast acting synthetic opioid drug that can be highly addictive. She was not from the local area and so after checking with several other hospitals to which she had been admitted with the same problem it became clear that she always asked for pethidine. At one point she grabbed hold of my arm and screamed at me to give her pethidine. I offered her other pain relief such as oral morphine as a substitute but she refused it. The reason is, oral morphine is good for pain relief but does not give a sudden "hit" that one gets from pethidine or heroin (diacetylmorphine). Hence, it became clear that the patient was after a fix of pethidine because of the unfortunate addiction that can occur from the treatment of sickle cell crises.... I felt sorry for the lady but she soon discharged herself from the ER department as she had failed to obtain the fast acting opioid she had been after.

Another example, was a man I saw when I was a medical student. He was admitted with severe pain in his loin radiating to his groin. He was writhing around in pain on the bed and was shouting for pain relief. His thermometer registered a fever and analysis of his blood revealed lots of blood. For all intents and purposes, any competent doctor would immediately investigate and treat as a renal stone plus infection. Renal stones can be very painful and sometimes NSAIDs do not take the pain away. In the end, he was given Entonox (nitrous oxide) that is also used more commonly during childbirth. He went through almost 2 large bottles of the stuff before the ER doctor decided to investigate things further.... After ringing other hospitals it soon became clear that the patient was a 'hospital hopper' and had been discharged from several other institutions with the identical same symptoms and was easily identifiable because of a unique tattoo on his arm. After being confronted, he got up as if nothing had happened and walked out the ER having succeeded in obtaining Entonox !
He had put the thermometer up to the light bulb in his cubicle to give him a fever and had pricked his finger to put blood in his urine. I had been completely fooled.....as had almost all of the ER staff !!

Lastly, but by no means least, when I was a junior doctor on-call in ER, I saw an ER senior doctor seeing to a young man having seizures. However, the patient's type of the seizures was unusual as he did not have any prolonged confusion or tiredness i.e. no post-ictal state. Moreover, there was no tongue biting and no incontinence. The patient failed the drop test which involved dropping the patients arm onto his face. If the arm hits the face, the patient is unconscious, but if the patient is faking unconsciousness, unless they know about the test, they usually avoid hitting themselves! Following this, the ER doctor was suspicious of pseudoseizures and the purpose of the patient doing this was to obtain free IV benzodiazepine-- the treatment for seizures but also an addictive drug!!!

A consultant then saw the patient at which point he said the following-- 'we take the testicle and strike it hard with the tendon hammer. If the patient is truly unconscious he will not feel pain, but if he is faking it....' He then walked away from the patient pretending to go and find the tendon hammer. Within 1 minute the patient had jumped off the ER bed, now fully conscious, and shouted a few obscene words at the consultant and ER staff before running out of the hospital.....

I hope that you have enjoyed these few examples of unusual patients. Although such cases may seem humorous initially, each case described above involves an addiction of some sort which made these patients do something that is an unacceptable thing in normal society. Whether it be going to buy cigarettes wearing a drip or selling blood transfusions, such unusual actions show us as doctors that there are many people out there in the world with problems related to addiction to chemicals or drugs. How can we help such people?

Do you have any good examples of real cases you would like to share???? Please send your comments to my blog for us all to share.

CT and Function

Although the use of CT scanning and MRI have transformed the world of doctoring for rapid diagnosis of conditions such as stroke and cancer, they do nothing to tell us how the patient is functioning.

As has been my experience in Japan, when a patient comes into hospital with some disorder that may indicate a cerebral problem, they are whisked into the waiting CT scanner for thieir cranial scan with or without contrast. Sometimes the neurological examination is bypassed as it is the belief that the scanner can give the answer to the problem.

To some extent, the use of scanning can give the answer, although not in its entirety.

A CT scan provides only pictures. Patients and their families are not interested in pictures that they bearly understand. They are interested on how the problem is going to affect them, for example, how it will affect their function.

The only way the function of a patient can be assessed is through examination.

Neurological examination is an indirect method of trying to understand what is going on in the head, spinal cord and muscles. It cannot tell us exactly what is going on, but it can tell us where a potential lesion exists and how it is affecting the function of the patient.

In fact, the use of physical examination of the neurological system and CT or MRI scanning complement eachother. However, a normal physical examination often does not require us to obtain a CT scan and a normal CT scan does not exclude an abnormality of function on examination.

Hence, physical examination is still a very much important part of a physicians armoury and it should not be skipped in favour of scanning the patient because important things can and will be missed.

For example, a patient admitted with sudden onset of speech abnormality and vomiting was found to have metastases on chest xray and hence, cerebral mets were suspected. CT was performed which indeed confirmed the mets. Great diagnosis......but the missing component was the functional ability of the patient.

When he was later examined by another doctor it was found that the patient had developed an homonymous hemianopia and unilateral upper limb weakness in addition to the speech abnormality. These differing neurological features suggest multiple areas affected. Moreover, such an examination revealed that the patient would be unsafe to drive (if feasible) because of the loss of vision and weakness of an upper limb. Following this, when one reviewed the physical findings to the CT result, it then made understanding the CT more easy as it could be understood that the patient's optic radiations to the occipital lobe had been disrupted by metastases and the speech abnormality was due to a pre-frontal lobe metastatic haemorrhage disrupting the pre-motor area in additon to the mutiple cerebellar lesions.

Acute treatment consisted of commencing dexamthasone to reduce the oedema. However, if no initial assessment of function through physical examination had been done, then there would be no way to fully know if the patient was improving or not. There needs to be a baseline admission examination.

In the UK, obtaining an emergency CT without the agreement of a radiologist is difficult. All emergency requests must be shown to the radiologist and for the decision to then be made by him or her. In my own experience, on occasions, radiologists have asked about the neurological examination and what you expect to find. If there is no physical examination or a poor physical examination performed, they will reject the request until an acceptable examination has been performed. Yes, you may think this is strict and overly controlling and to some extent it is, but it does ensure that the doctors examine their patient, think of the potential causes and what they will do if they find what they are looking for. It also reduces the unnecessary number of requests for head CT scans from anxious patients that think they have a brain tumour.

Unless a full neurological examination is performed with fundoscopy, the CT request may find itself coming back to you as rejected !! Obviously, this is case by case.

Hence, in the UK, physical examination is the mainstay of making diagnoses and in circumstances when a CT or MRI scan is needed, it will get done. In those cases where there is no clear reason for a CT but the patient wants it or the doctor wants reassurance, it is likely to be rejected by the radiologist. This cuts done on expenditure and unnecessary scanning.

The take home message is, always examine your patients neurology when such an examination is warranted and try and consider the places in the CNS or PNS which have been affected and where such problems localise to. This will then give you some idea of where you are expecting to find the problems when you eventually do scan the patient. The examination will provide you with the baseline functional status and with serial examination of the patient, it will tell you whether the patient is improving or not.

Basically, don't think that a scan is the replacement for clinical skill because it is not.

Serial ECGs and Non ST Myocardial Infarction (NSTEMI)

Today's Blog is about the simple use of ECGs to make a diagnosis of Non-ST Elevation MI (NSTEMI).

Patients with a myocardial infarction can typically give the following history:

• Sudden onset central chest pain
• Worst pain ever in their life e.g. 10/10
• The pain is described as squeezing / a tight band / like someone sitting on their chest
• Pain may be epigastric in location
• Pain may radiate to neck / jaw / shoulder or down either arm although classically on the left side
• There is usually associated nausea, vomiting, sweatiness and breathlessness.
• Patients can collapse due to sudden dysrrhythmia

However, patients can present only with sudden onset breathlessness and no chest pain. These patients are typically diabetics.

Hence, it may be impossible to obtain an MI history despite asking all the above important questions.

Examination may or may not be helpful. Acute onset heart failure is often a clue.

On admission to hospital, the cardiac enzymes may be normal. These may sometimes be of no help acutely in MI as they take several hours to rise. However, they should still be performed on admission as they provide a baseline level and if the history is more than several hours, the enzymes may have already become positive.

The, perhaps, most useful and simple non-invasive tool is the ECG. It may sometimes be initially normal only later to show changes.

Therefore, in such cases it is essential to repeat the ECGs and compare them to previous ones such as admission ECGs or even previous ECGs taken some point in the past.

Such changes are usually non-specific T wave inversion and sometimes Q waves. These signify possible myocardial damage.

As I have mentioned in a recent blog article, it is often necessary to perform a Troponin T test despite normally looking CK and CK-MB fractions especially after 6 hours.

For example, a recent case of a patient admitted with breathlessness with a background of chronic renal failure, old MI and diabetes mellitus had no chest pain or other symptoms of AMI. The patient had recently been having intake of more fluid than normal and had not had haemodialysis in several days. Hence, the heart failure that was found on examination and seen on chest X-ray was assumed to be due to fluid overload.
However, when one looked at the ECGs, the initial ones showed a tachycardia. But several hours later the T waves had inverted thoughout all the anterior and a few inferior leads suggestive of wide spread ischaemia likely due to a left main stem lesion.
Echocardiogram showed an EF% of 40% and generalised hypokinesis.

The CK level was only mildly elevated and CK MB was normal. However, after several hours the CK was further raised followed by the CK-MB and AST. A Troponin T test was then requested.

In patients with Chronic Renal Failure / Diabetes they have an increased cardiovascular risk and patients developing breathlessness should not just be assumed to have fluid overload before completely excluding AMI. In such patients checking serial ECGs and Cardiac Enzymes is essential.

Treatment for AMI (NSTEMI) in the acute phase [within 24 hours] include:

• Aspirin
• Clopidogrel (recently introduced into Japan but used for several years in Western Europe; 300mg orally followed by 75 mg daily)
• Statin Therapy e.g. Simvastatin 40mg / Atorvastatin 10mg even if the cholesterol is normal. Statins have been shown to help stabilise plaques and improve the outcome of coronary artery intervention. It is regarded as an acute treatment to be started the same day.
• Beta-blocker e.g. iv beta blocker followed by oral e.g. bisoprolol / carvedilol / metoprolol unless patient has asthma / COPD / Severe heart failure. Beta blockers have been shown to reduce mortality post-MI. They should be started the same day.
• ACE-Inhibitor e.g. Ramipril. These should alse be started the same day. They help myocardial remodelling and in heart failure reduce the readmission rate and improve survival.
• Heparin / Low Molecular Weight Heparin to be continued for 48 hours after pain has settled.

The above is the basic standard for AMI treatment (see the European Resuscitation Council Guidelines 2005)

Remember: ECG can be normal. CK and CK-MB can be normal. Troponin-T can be positive and still be an NSTEMI. You must have a high index of suspicion. Also, please use the TIMI scoring system which ranks people into High or Low Risk and such High Risk patients still require investigation and workup for coronary disease.

Please consider.

Arms and Legs

Today this blog features on how doctors examine their patients.

In the main, doctors commence their examination by starting with the Head, Ears, Eyes, Nose and Throat (HEENT). They then progress down to the chest and abdomen to complete their examination. This is the first problem...

If the arms and legs are not examined then the patient clinically has no arms or legs ! By not examining the limbs, the doctor can miss very important physical signs.

Normally, the observations are performed by nursing staff by taking the pulse, blood pressure, respiratory rate, SpO2 and temperature. These readings are normally performed on an automated machine. Here is where the next problem comes in ! By a machine taking the readings the doctor no longer takes the pulse or holds the hands and thereby misses salient clinical signs.

The pulse rate is not the only thing that one looks for when examining the pulse. The quality of the pulse is very important that a machine cannot measure so easily. When I mean quality I mean the strength and dynamics of the pulse e.g. weak pulse or strong pulse. The pulse may be slow to rise during systole or may have a brisk upstroke and then collapse, the former which may may signify Aortic stenosis and the latter Aortic regurgitation respectively. Moreover, a collapsing pulse can also be associated a hyperdynamic circulation as I have previously discussed.

An excellent example was a recent case of a patient with a fever who was being monitored. The pulse rate on the screen said 156 beats per minute. For some patients with a fever, this would not be unusual. However, when the pulse was measured, it was 84 per minute. In fact, when listening to the apex beat, it too was 84 per minute. The machine was wrong ! Yes, the machine made a mistake. Hence, relying on a machine may give you inaccurate information. You must recheck the observations by taking the pulse by hand.

Moreover, failing to check the hands you will miss clubbing, splinter haemorrhages, Janeway lesions, palmar erythema, metabolic palmar flap, so on and so forth, as just a few important examples.

Failing to examine the lower limbs and moreover, failing to remove bandages and socks, you will miss ulcers / infections / gangrene / DVT -- always take off what is covering the skin. In the UK, I saw many cases of severe medical problems being covered over by bandages, socks and even newspaper!!!!

One example was a male patient with a painful lower limb and who was vomiting. On examining his leg, which was covered in newspaper because of the leaking fluid, it was found to be critically ischaemic. The patient was vomiting from septicaemia and needed immediate surgery--which he refused. Other examples have been severe ulceration of the surface tissue down to the bone and a patient with gangrenous toes -- all covered by bandages. Bandages don't make the problem go away, it just makes us want to ignore it. However, when we see a bandage / socks, we should remove them and look at what is there !

Also, in the bed bound patient please check for decubitus ulcers. There was a case of a patient with recurrent fever at a nearby hospital who had no obvious focus. However, when the patient was rolled to the side, a decubitus ulcer was present on the sacrum and culture revealed MRSA. An isotope bone scan was advised to look for evidence of osteomyelitis. Such patients should be nursed on an airbed but failing that, pressure areas should be dressed and the patient turned regularly to offload pressure from such pressure points.

In summary, I would advise doctors to commence their examination by looking at the hands, taking the pulse, and move upwards to the head and then down the body to end at the feet. In so doing, the whole body is examined and simple diagnoses will then not be overlooked e.g. lower limb cellulitis as a cause of fever.

Please consider......

PDAs in Medicine Revisited

I have written about the use of PDAs in everyday medical practise in the past, but I would like to revisit that topic once again.

I was recently consulted by a junior doctor about the advantages of using Pocket PC devices which run Windows Mobile software-- here is a summary of my answer.....

Well, currently there has been a massive explosion of PDAs coming onto the market running various different operating systems including: Windows Mobile 6, Symbian, Blackberry, Apple (iPhone / Touch) although not the good old Palm OS [which has not changed in a long time !].

Which platform do you choose from such a wide choice?? Well, I perhaps have an answer. It really depends on what you want to use it for. If it is for lots of medical books then the Pocket PC devices are currently what I would recommend. For example, Skyscape products (www.skyscape.com) provide medical texts for Palm, PPC, Blackberry and iPhone. From my experience, the Palm version texts can cause the Palm device to crash (examples Clie NX80, TH55, Palm LifeDrive), which does not appear to happen on PPC platform.

I have no experience of the other platforms running this software so it would be inappropriate to comment further. However, Skyscape products are Excellent !! They have all the major manuals covering every area of medicine. I would highly recommend visiting the site to see for yourself.

Some good books to check out are the Oxford handbooks, Merck Manual (very good !), Harrison's Manual, MedConsult (Prof Tierney's text) and the Washington Manuals....see for yourself. They are downloadable as trial software so you can test them and see how good they really are!

UpToDate is a relatively pricey text if one compares to a standard textbook, but the fact that it is updated several times per year and that it is highly referenced with Evidence makes it a worthwhile addition for any serious physician or department. It is also available on Palm (not Clie devices) and Pocket PC. However, the other platforms are currently unsupported.

Moreover, Pocket PC can also run the Palm OS 5.0 equivalent software known as Styletap (www.styletap.com) and this enables Palm lovers to run their Palm OS software on top of a Pocket PC software structure and at the same time they have the added bonus of Multi-Tasking as Windows is running in the background, which was absent on the pure Palm-based systems.

With new machines coming with up to 8 or 16 GB as standard (HTC X7501 8GB, Apple ipod Touch) and more and more books can be stored electronically then the current Palm based devices have lost the competitive edge. By having a PDA with electronic books, it enables checking of information on the move e.g. on the ward, at the bedside, whilst travelling or even sitting at your empty desk. Yes, it will be empty as you will not longer need paper books :)

The PDAs currently running Symbian or Blackberry are gradually being catered for by medical text solutions, but it may be sometime before they can fully compete with the Windows selection of products.

The most interesting thing at the moment is the ipod Touch but it lacks a microphone (hence, no dictation ability on the ward), no bluetooth (no A2DP wireless music), no Infrared (no beaming of documents), but for multimedia purposes and of course, MP3 it is seemingly very good. It does have Wifi which means online texts such as UpToDate can be accessed---but you need to be in range of a Wifi connection !!
As the product line matures and more medical texts are produced for it, it may be the next PDA to invest in.....

Bottom Line: I would currently recommend buying a Pocket PC running Windows Mobile 6 for your daily use of electronic books, note keeping, word processing, email etc.... The higher range devices are fast, stable and are obviously compatible with the new Vista OS. The Palm and PPC devices have the largest amount of software produced although the PPC platform has edged ahead and the PPC devices are proving to be more stable.

Please consider :)

US Navy Medical Meeting

Last week was our first combined meeting with the Yokosuka US Navy doctors and their Japanese residents.

The meeting was well attended and there was a long and short case presented by the two Third year residents from this hospital.



The first case was a work-up for Fever of Unknown Origin which, in the end, was diagnosed as a lymphoma. The short case was for work-up of non-specific symptoms such as myalgia, mild fever and raised inflammatory markers which was diagnosed as a vasculitis.


The two third year residents spoke completely in English and were able to answer the excellent and direct questions from the US Navy doctors and residents, which generated very good and informative discussion.

The Third year residents did extremely well especially as it was their first time to present in another language!!

After the meeting we had a party, and for one new member of the US team who has recently come to Japan, it was his first time to see live sashimi.... unfortunately, he was not inclined to eat it, but it was delicious !! :)


These combined meetings are planned to occur on a monthly basis and I see this as a great opportunity for learning English presentation skills, how to answer medical questions in English under pressure and to discuss similarities and differences in disease presentation, investigation and treatment in an Evidenced Based Environment.

This hospital's Internal Medicine department is now probably one of the most unique facilities in Japan and it not only offers daily teaching in English from me, but it now offers a monthly American addition and it is a most exciting time to be at this institution !

Photos courtesy of Dr Shin Fukuda

Cardiac Enzymes and the TIMI Scoring System

Just how reliable are cardiac enzymes?

When working up a case of acute coronary syndrome it is usually the case that CK and CK-MB are tested.

In a typical ST elevation MI, CK and the MB fraction will rise. However, now with the more specific cardiac biomarkers of Troponin-I and Troponin-T it is now possible to identify myocardial damage even when CK and MB fractions do not indicate an MI.

Such cases can involve the Non-ST elevation MI (NSTEMI) situation in which such patients may also have a normal ECG. I have seen this on a few occasions in the UK.

Other ECG abnormalities can be shown by non-specific ST changes, such as flattening, sinusoidal ST morphology and little else on occasion.

On some occasions the CK does not rise BUT the troponin is positive >0.1 consistent with an infarction.

Hence, measuring CK-MB fraction in a patient with a suspected acute coronary syndrome would seem obsolete especially when there is a more specific cardiac marker available such as the troponin test and which remains elevated for longer.

The Troponin test is not immediately positive and can take at least 6 hours before it rises, but it can persist for up to 10 days.

Hence, if you suspect an acute coronary syndrome (ACS), in addition to checking a CK level, it would also help in assessing a troponin level after 6 hours, if that utility is available.

Troponin levels have a direct relationship with 30 day mortality and patients should be treated as high risk for further cardiac events.

Troponin levels can be raised in renal failure and the higher the level of renal failure the higher the troponin. However, renal failure is also associated with increasing cardiac risk and hence, a raised troponin in renal failure should not be ignored.

CK and Troponin can also be raised by myocarditis and pulmonary embolism and hence, in situations when patients develop chest pain diagnoses such as AMI, PE and myopericarditis should be considered if these cardiac markers are raised.

Finally, patients with chest pain can be risk stratified into low risk and high risk groups which predicts further cardiac events after either NSTEMI / Unstable Angina or following an STEMI. Such TIMI scoring systems can predict the likelihood of further cardiac events within a 14 or 30 day period respectively. High scoring patients need further and more intensive investigation and treatment. The NSTEMI / UA scoring system can produce a High Risk score even when cardiac enzyme markers are normal and hence, patients should be treated with the similar treatment intensity as those patients who do have raised cardiac markers as the risk scores can be the same.

The STEMI scoring system does not include cardiac markers as the assumption is that these are already raised because of the nature of an STEMI. However, on occasions, STEMI can be aborted with successful intervention treatment and where there is no cardiac enzyme rise although this is the exception rather than the rule.

Hence, for example, a 65 year old patient with > 3 coronary artery disease risk factors and who is taking aspirin and who develops cardiac chest pain without ST change and with no rise in cardiac enzymes scores 3 points making this a High Risk patient and with an approximate 13% 14 day risk of death or new / recurrent MI or severe recurrent ischaemia requiring urgent revascularisation. Such patients in England are very common. Typical patients are elderly angina sufferers who have cardiac risk factors and who are taking aspirin and many other medications for angina. However, they should be taken seriously as they are High Risk for further events. As a result, such patients should receive intensive medical therapy such as heparinisation, additonal anti-platelet therapy e.g. clopidogrel, anti-anginal medication, statin therapy and early percutaneous coronary intervention if available.

It is therefore safer to keep such patients in hospital rather than sending them home when the CK / CK-MB / Troponin T are negative, until their condition has stabilised on treatment and it is deemed safe for them to leave after a thorough work up and exclusion of serious pathology.

The take home message here is if the CK / CK-MB is normal, it does not exclude acute coronary syndrome. Always check a troponin at least 6 hours after an episode of chest pain-- you may be horrified to find it raised despite the normal CK.

Lastly, even if the cardiac enzymes are not raised, it does not exclude the patient from being High Risk for a future cardiac event with 14 days, as predicted with the NTSEMI / UA TIMI scoring system. Such patients should be fully assessed, investigated and treated the same as for any patient with a cardiac event with raised cardiac markers.

Please check out the NSTEMI / UA and STEMI TIMI scoring systems online by clicking on the words outlined in blue above which will link through to those internet pages respectively.

Please consider....

Hyperdynamic Circulation

The following case has been supplied by a colleague at another hospital and has been anonymised.

A patient was admitted into hospital with a three week history of intermittent malaena.

The malaena had started gradually and there was on average one stool produced per day of the typical 'tarry' black consistency.

The patient had no abdominal pain / no diarrhoea / no back pain. She was complaining of fatigue but no postural dizziness / collapse / palpitations / breathlessness.

There was no history of any use of non-steroidal anti-inflammatory drugs / steroids.

However, she was a long term alcoholic and she was drinking 3 cans of beer per day at that time and had done so for 20 years.

She had known chronic liver disease for which she was taking medication but despite this, she was still drinking regularly.

Medications included furosemide 40mg daily, spironolactone 25mg daily, and multivitamins.

There was no family history of note and the patient lived with her husband in the locality to the hospital.

She was an ex-smoker having smoked 20 pieces per day for 20 years although she stopped 5 years previously.

On examination, she appeared confused and had a poor nutritional state. Blood pressure was 100 / 40, heart rate regular at 90 beats per minute. Respiratory rate was 18 / minute, Sats 95% on room air. Temp 38.4 degrees C.

Hands: Palmar erythema, Dupytrens Contracture and Hepatic Flap.

Head and Neck: JVP was not raised. Eyes showed mild anaemia and there was scleral discolouration of jaundice. No Lymph nodes were palpable. Temporal muscles were severally wasted. Oral mucosa appeared dry. There was a smell of 'fetor' from the patient's mouth.

CVS: Pulse quality felt Bounding and Collapsing. Heart sounds were normal with No Diastolic murmur. Quinke's sign was negative but Corrigan's Sign (neck pulsations) and Waterhammer Pulse (palpation of the brachial pulse lifting the arm into the air producing bounding pulse which collapses) were positive. There was mild leg oedema.

RESP: The was diffuse wasting of the intercostal muscles and muscles around the neck. Her chest was hyperinflated. Chest percussion was resonant, and there was no evidence of wheeze or crackles.

ABDO: Soft and distended. There was dilatation of the superficial veins on the abdominal wall (caput medusae) with the blood flowing away from the umbilicus (a sign of increased portal pressure). The liver and spleen were not palpable. The abdomen was stony dull to percussion consistent with accumulation of ascites. It was not possible to perform shifting dullness as there was no evidence of bowel gas and fluid thrill test was negative. Bowel sounds were absent.
Rectal examination revealed malaena but no rectal masses.

CNS: pupils were equal and reactive to light and accommodation and the consensual reflexes were normal. Other cranial nerves appeared intact.

PNS: The patient was moving all 4 limbs, with equal power throughout. Tone was normal. Reflexes were generally depressed. Sensation was difficult to ascertain due to the patient's confusion. Babinski sign was negative.

Clinical Impression

• Decompensated Liver Disease
• Upper Gastrointestinal Bleed
• Hepatic Encephalopathy
• Spontaneous Bacterial Peritonitis
• Hyperdynamic Circulation from High Output Heart Failure
  

This is therefore quite a complicated case and to go into the depths of investigating and treating each problem here goes beyond the scope of this blog. However, the final diagnosis on the list is somewhat obscure and often missed.

The signs of Bounding and Collapsing Pulses can either be due to Aortic Regurgitation (although in this case there was no diastolic murmur) or due to a Hyperdynamic Circulation from High Output Heart Failure.

When we think of heart failure normally we consider systolic or diastolic heart dysfunction. However, in high output heart failure, the heart fails to supply the metabolically active tissues with blood and oxygen because of Shunting of Blood.

Shunting is where this is a connection or multiple connections between artery and vein thereby bypassing the capillary beds. Hence, the Cardiac Output must increase to compensate for the Shunt of blood. These patients typically have a wide pulse pressure, bounding arterial pulses that sudden collapse beneath the examining fingers which denotes the shunting of blood into the venous circulation.

There are a vast number of conditions that cause shunting to a greater or lesser degree which include:

• AV fistulae e.g. iatrogenic in renal dialysis / complication of cardiac angiography
• Acromegally
  
• Anaemia
• Anxiety
  
• Beri-beri
• Carcinoid syndrome
• Cor pulmonale
  
• Erythroderma
• Hepatic failure
• Hypercapnia
• Morbid obesity
  
• Multiple Myeloma
  
• Paget's Disease
• Polycythaemia rubra vera
  
• Pregnancy
  
• Pyrexia
• Thyrotoxicosis
• Vasodilator Drugs

In liver disease the shunting of blood occurs via the Portosystemic Anastomoses as a result of raised portal blood pressure. The raised portal pressure is as a result of damaged liver architecture. However, the splanchnic vascular bed become dilated and engorged with blood. As a result, the systemic blood pressure drops and there is an increase in peripheral vascular tone although, overall there is a total reduction in systemic vascular resistance as a consequence of the dilated splanchnic bed.

As a consequence, there is release of mediators from the kidney to increase Na+ and water retention via the Renin-Angiotensin-Aldosterone axis. This avid reabsorption of water and Na+ precipitates the ascites that is seen in decompensated liver disease.

Eventually, the increased peripheral vascular tone results in worsening renal failure and hence, hepatorenal failure can ensue. Hepatorenal failure can be precipitated by bleeding and infection, particularly spontaneous bacterial peritonitis, and portends an unfavourable outcome.

Hence, patients with Hepatic Failure develop Splanchic Steal of blood from the systemic circulation and have an increased cardiac output to try and compensate. The blood from the portal system is shunted into the venous circulation due to portosystemic anastomoses. The ascites occurs due to low systemic blood pressure despite signs of a bounding hyperdynamic circulation!

It is a very complicated process indeed !!!

Because these patients have secondary hyperaldosteronaemia, they usually require high doses of spironolactone (Aldactone). The usual starting dose is 100mg up to 400mg daily. Blocking the action of aldosterone reduces ascites but can result in hypotension becoming worse which is not unsurprising. Hence, a balance needs to be established between appropriate dose of spironolactone, renal function and blood pressure. Patients unresponsive to medication and fluid restriction require paracentesis to remove the ascitic fluid.

For an excellent description of the Splanchnic Steal in Liver Failure, please go to the following link.

So, the next time you feel a bounding and collapsing pulse think possible Aortic Regurgitation, but in the absence of an audible murmur think High Output Heart Failure causing a Hyperdynamic Circulation and refer to the above list of causes !!!

Please Consider...

The Great Cardiologist Dr Shah

Dr Shah has recently returned to Japan for the 13th consecutive year and is once again teaching our junior doctor about the importance of ECGs and echocardiography. Dr Shah's ECG lectures commenced with a refresher presentation about limb and chest leads, heart axis and vectors to name but a few items, which then progressed on to a more detailed ECG session in the afternoon, which was enlightening.

By the end of the session, the junior residents were buzzing with new knowledge on how to interpret the finer points and the intricacies of ECGs. This was a very worthwhile teaching session. The following day, Dr Shah taught the junior and senior residents about the basics of echocardiography. He then demonstrated echo such as 2D, M-mode, Doppler and Tissue echocardiography.

All in all, it was a great two-day teaching session and despite this, Dr Shah was only able to cover a fraction of his course, and he has much to be able to offer the residents in this hospital and throughout Japan today and in the future. It is hoped that Dr Shah will continue coming back to Japan for many years yet!! :)

Fever and Cancer

It is well established that the presence of malignancy itself can cause fever. Classical malignancy causing fever include lymphoma, leukaemia, renal carcinoma and so on. However, on occasion infection and hence the resulting fever, can occur because of the presence of cancer and the investigation of fever can lead to finding a sometimes unexpected malignancy.

In the following case supplied from another hospital and fully anonymised, it shows how history and physical examination gave a bedside diagnosis.

A 70 year old female was admitted with fever. The fever had started 2 days previously and was associated with appetite loss and headache. There was no associated chills, mylagia, nausea or vomiting. The headache was frontal in nature and there were no other associated symptoms of meningitis and no visual disturbance. She complained of no chest problems i.e. no dyspnoea, no cough or sputum. She had no skin or joint problems. She had no urinary symptoms. However, on direct questioning, she admitted to a long history of diarrhoea that was not painful. She denied night sweats and weight loss.

Previous medical history included hypertension and ovarian cancer that had been operated 6 years ago with chemotherapy as additional treatment, although the patient was no longer under active follow up.

She was taking no regular medication.

There was no family history of note and she lived alone and was independent.

On physical examination, she appeared relatively well. Hydration state seemed adequate although she felt hot to touch. Dentition was extremely poor.

CVS: There were no peripheral stigmata of endocarditis. Pulse 80/min and regular. BP 140/70. JVP not raised. Heart Sounds were normal with no murmurs. No peripheral oedema or evidence of DVT.

RESP: Respiratory rate 20/min. Expansion was normal and percussion was resonant. Chest sounds were normal.

ABDO: Slightly obese abdomen and soft. However, in the Right Iliac Fossa there was a smooth, tender mass arising from the pelvis. Percussion revealed dullness, but not stony dullness, making this consistent with a solid or at least a semi-solid structure. Auscultation of the mass revealed no bowel sounds. The mass was at least the size of a grapefruit from what could be elucidated from the surface examination. There was no hepatosplenomegally or ascites and bowel sounds were otherwise normal.

CNS: No evidence of meningeal signs. Neurological examination was otherwise unremarkable.

CLINICAL IMPRESSION

In view of the previous history of ovarian cancer and no regular follow up, a new fever and a tender, smooth abdominal mass, recurrent ovarian cancer had to be high on the list. However, this could have also been sepsis related to formation of an abscess although it was considered too large to be an abscess especially as the history of fever was only 2 days. In view of the poor dentition and despite the absence of a cardiac murmur and peripheral stigmata, endocarditis was also considered although this would not have accounted for the pelvic mass.

INVESTIGATIONS

Bloods revealed a raised white cell count of 20, and high CRP of almost 30, haemoglobin was normal. Renal blood result revealed mild renal failure with normal sodium and potassium. Liver tests were normal. Urine revealed blood, a high white cell count, protein 2+, bacteria 2+ and casts. Chest Xray and ECG were unremarkable. Echocardiogram revealed no vegetation.

Abdominal CT scan was grossly abnormal. The Left kidney was almost completely destroyed due to hydronephrosis and the right kidney was mildly hydronephrotic. The pelvic region revealed a very large, well circumscribed mass with internal septations and dense fluid. The mass was compressing the sigmoid colon and displacing it to the right.

DIAGNOSIS

The diagnosis was likely to be recurrent ovarian cancer and compression of pelvic structures had resulted in renal failure from hydronephrosis and as a result, bacterial infection had occurred due to urine stagnation, and probable overflow diarrhoea from colonic compression and / or invasion.

DISCUSSION

Once again, from taking a thorough and detailed history by asking questions in respect of causes of fever, it was possible to work out the likely diagnosis. In this case, the patient only had fever and few other symptoms. In such a case, the physician has to consider infective and non infective causes of fever. Direct questioning involves asking about symptoms from ALL of the body regions e.g. cardiovascular, respiratory, abdominal, genitourinary, musculoskeletal, skin, central nervous system. This is in fact part of the Review of Systems that is normally done at the end of a history taking session but when few symptoms are evident, the Review of Systems is the safety net for the physician to try and squeeze out innocuous symptoms from the patient which in this case was the diarrhoea and which the patient had not initially offered up as a worrisome symptom. Hence, the Review of Systems came in to use at the beginning of the history taking !

The shorter the history of fever, the more likely it is to be infective and yes, infection was indeed found. However, the presence of the infection led to the diagnosis of a recurrent tumour which seems to have by itself, not caused a fever at all, and only few symptoms such as diarrhoea and mild abdominal discomfort on examination. When there is a situation when one finds an obstructed and hydronephrotic kidney with fever and evidence of infection, the infection could well exist in the kidney itself and in such situations, it is necessary to insert a nephrostomy tube to try and save the kidney and drain the infection. Sometimes, a double J stent can also be inserted to drain the kidney.

In this case, the history made the physician concentrate the physical examination on the pelvic region and indeed the recurrent tumour was identified. Hence, history and examination can provide a bedside diagnosis and in this case, CT scan CONFIRMED the diagnosis rather than making the diagnosis.

Please consider.... :)

Never Ignore Chest Pain

I would like to start todays discussion with a case vignette. The case is from a colleague in another hospital and all details have been anonymised.

The patient was a 75 year old male who presented with dypsnoea and wheeze.

The patient was normally only able to walk 10 metres before becoming short of breath and needing to rest. On the day of admission, the breathlessness had got worse and wheezing had also commenced.
He had not offered up any other history and only when the doctor directly asked the patient if he had chest pain did he actually say YES!

In fact, the patient had chest pain when he was being seen by the doctor! It was described as 'heavy' and in the centre of his chest and with no radiation to jaw /neck /arms. However, the patient was breathless at rest and he had a 'cold' sweat and he was wiping his forehead with a towel. The pain was described as being similar to that as when he had a myocardial infarction several years before, although it was less painful.

He had also been apparently suffering with asthma for the last 50 years although he had never been hospitalised. Despite this, he was apparently able to lie flat in bed at night.

Previous medical history included: Old MI, Congestive Heart Failure, 'Asthma', Atrial Fibrillation (AF) and Gout.


Medications: Spironolactone, verapamil, anti-histamine, low dose steroid

On examination

The patient looked unwell. Pulse 120/min, RR= 30/min, sats 94% on room air, BP 130/82.

Skin looked atrophic due to long term steroid use. Patient used accessory respiratory muscles. Chest was hyperinflated and bilateral gynaecomastia was evident. JVP was not seen as patient was sitting at 90 degrees. Heart sounds were normal.
Chest percussion revealed a large area of dullness, reduced air entry and reduced vocal resonance consistent with an effusion.
Legs revealed bilateral pitting oedema 1/3 up the lower limbs.

Abdominal examination: Distended, no tender. No organomegally. Bowel sounds present.

An emergency ECG was performed that revealed Right Bundle Branch Block, ST depression in the septal leads and AF.

CXR revealed a large pleural effusion on the right, a large heart, upper lobe diversion and fluid in the horizontal fissure consistent with heart failure. Comparing the CXRs to a previous one taken 1 month earlier, there was evidence of worsening CHF with an enlarging right pleural effusion.

ABG revealed a Compensated Respiratory Alkalosis with hypoxaemia.

Bloods revealed mild renal impairment and slight neutrophilia. CK was normal although this was taken before the chest pain occurred.

The clinical impression was

• Worsening CHF
• COPD
• Unstable Angina

Discussion:

In this case, the physicians were able to diagnose the worsening CHF and COPD. However, it was with direct questioning about chest pain that the patient admitted to having chest pain. In fact, the patient had become so used to experiencing daily chest pain, he had considered it to be a normal occurrence and had not considered telling the doctor !!

Therefore, doctors need to ask the questions of exclusion rather than just asking questions around the area of what the patient describes. In this case, the patient had worsening CHF, but why was it getting worse???
Note that the patient has AF. The commonest cause is ischaemic heart disease and this patient has had an MI previously. Also, hyperthyroidism can worsen heart failure and cause worsening angina in patients with underlying ischaemic heart disease. Moreover, was the patient having small recurrent ischaemic events????

Despite this classic history, the patient was not using a nitrate spray, no anti-platelet agent was being used, no furosemide or ACE/ARB was being used for heart failure or any statin therapy.

This patient was clearly a high cardiovascular risk with a previous MI, hypertension, an ex-smoker and hyperuricaemia.

Moreover, his AF treatment, that being Verapamil, despite it being very effective at rate control, it can also worsen heart failure.

Treatment of Acute Coronary Syndrome

• Sit the patient up unless hypotensive
• Give oxygen by mask
• Give 300mg Aspirin immediately and then 75 mg daily thereafter or ADD Clopidogrel 300mg immediately and then 75mg daily thereafter if the patient is already taking aspirin. If patient has allergy to aspirin, then load with clopidogrel.
• Give sublingual nitrate spray / tablet
• If pain continues give morphine and anti-emetic
• Commence intravenous unfractionated heparin or low molecular weight heparin for ACS dosing until cardiac markers are found to be negative. If positive, continue the heparin until 48 hours after last episode of chest pain.
• If pain continues give intravenous nitrate infusion
• Patient should have a 12 lead ECG and placed on a cardiac monitor
• CK and Troponin T should be examined
• If pain continues then cardiologist should be contacted with the aim of emergency PCI.
• Patients should also be commenced on long term anti-anginal therapy if conservative therapy is to be continued including

- Isosorbide Monoitrate / Nitrate dermal patch
- Beta Blocker (not in severe CHF)
- Nicorandil
- Calcium channel blocker e.g. nifedipine / amlodipine

Patients should also be commenced on statin therapy even if the cholesterol level is normal as the benefits of having low cholesterol reduce cardiovascular events.

In this case, asking about chest pain revealed a major cardiovascular history and altered the emphasis on the patient's care.

Please consider....

Broad Spectrum Antibiotics and Confusion

Dear Bloggers

There seems to be some confusion on how to manage seriously ill patients will the right cover of antibiotics.

From my experience in Japan, I often hear that the patient with sepsis and no definite focus of infection is given a carbapenem antibiotic because of the various routes of coverage e.g. gram positive / negative and anaerobic.

My response is usually less than favourable because it is the last antibiotic that should be used and not the first !

I recently wrote another article on antibiotics but I feel it is necessary to reiterate the point.

Broad spectrum cover can be achieved in many ways with different combinations of antibiotics rather than with the carbapenems. For example, a second / third generation cephalosporin plus metronidazole / clindamycin has good coverage of gram +/- and anaerobes. Another good combination is the amoxicillin-clavulanate or ampicillin-sulbactam combinations which again have good broad spectrum cover. Broad spectrum cover can be enhanced by using gentamicin especially in patients with an undefined cause of sepsis and it is especially good against infections including e.g. endocarditis, pyelonephritis....

The reason I continue to push for other combinations of antibiotics for broad spectrum use is because of RESISTANCE.

From the USA, there have already been reports of bacteria producing Carbepenemases which destroy the carbapenems and if this occurs then these bacteria are resistant to all beta lactam antibiotics including penicillins and cephalosporins.

Just imagine a situation where bacteria cannot be killed by third or fourth generation cephalosporins !!! That does not leave a great choice of antimicrobials to choose from.

The UK and American physicians strongly advocate not to use the carbapenem antibiotics unless other therapies have failed. It is a hidden weapon to coin a phrase. However, if we reach a situation where the carbapenems are being used in place of other antibiotics, the latter which in combination provide a similar coverage, then resistance to this antibiotic will soon occur and then Japan will have major infectious disease problems.

Use of carbapenems should not be first line. Yes, they may be simple to give and reduce the work of the nursing staff, but that should not be the reason for their use. Resistance should always be considered and the use of such antibiotics should normally be restricted to ICU patients where all other treatments have failed.

The source /focus of infection should always be considered on initial presentation and the type of organism considered that could cause the problem. Then, a combination of antimicrobials can be chosen to cover the considered organism(s). Empiric therapy, as it is actually called, is an educated guess, but using combination drugs for broad spectrum cover will treat the vast majority of likely causes. Then as results become available, and narrow spectrum antibiotics can be used, the other antibiotics in the combination which are not necessary can simply be stopped :)

In all fields of medicine, there is always uncertainty whether the treatment is going to be the right one and especially when considering antibiotic coverage. However, uncertainty is something that we as doctors all need to accept and live with. Our medical practices should not be driven by defensive protocols but by clinical need considering history, physical, radiological and laboratory data and the likely differentials diagnoses.

If we reach a situation when all treatments are provided because the medical profession is being defensive, then we cease to be free thinking physicians.

Please consider......

Sicko and State run Healthcare Systems

Dear Bloggers

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

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

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

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

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

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

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

Does this have implications for Japan?

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

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

How can this problem be solved??

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

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

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

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

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

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

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

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

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

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

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

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

American Navy Hospital Meeting

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

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

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

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

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

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

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

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

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

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

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

Please consider.....

Depression

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Peak Flow In Asthma

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

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

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

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

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

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

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

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

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

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

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

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

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

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

ANTIBIOTICS AND LOGICAL PRESCRIBING

Today, I would like to discuss about antibiotic choice.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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