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.

Meningococcus

Dear Bloggers

Sorry for the lack of new articles but I have been busy with teaching plus nursing my recent head cold which has left me feeling unwell....

A recent case was passed to me about a patient from another hospital who was admitted with an alteration in consciousness. The patient could not speak very well following a sub-arachnoid haemorrhage some years ago that left the patient with paresis and required a VP shunt to be placed in vivo.

The patient had developed a drop in consciousness and vomiting. There was no fever or other symptoms from the patient.

The salient clinical signs included a high blood pressure (systolic >200) and a disseminated haemorrhagic rash on both forearms (patient was not taking warfarin).

CSF examination revealed a high WCC, High protein and low Glucose but no visible bacteria.

These findings were consistent with a Meningococcial Meningitis and Septicaemia.

However, the high blood pressure concerned me that there may have been a blockage in the VP shunt due to infection causing a Hydrocephalus.

CT film showed an old infarction area, the VP shunt but evidence of a dilated anterior horn on the contralateral side to the shunt. There was no midline shift.

The patient was started on Vancomycin, Ampicillin and Ceftriaxone which is the standard therapy for meningitis when the organism is unknown.

Patients with meningococcus infection can develop complications including:

1) Disseminated Intravascular Coagulation (DIC)
2) Adrenal Failure (Friederichson-Waterhouse Syndrome) from DIC
3) Haemorrhagic rash (from DIC)
4) Renal Failure
5) Death

The rash may intially present a small areas of non-blanching haemorrhage around or within the white of the eye (sclera) or it may progress to diffuse ecchymosis.

Blood cultures should always be done!! Don't ever delay using the antibiotics for fear of a negative CSF gram stain / culture because the longer you wait the greater chance of death.

In fact, in the UK, GPs routinely will give Benzylpenicillin intravenously / intramuscularly if they suspect meningitis in order to start treating the disease before they reach the hospital. They will not delay treatment.

Apparently, CSF can still yield a positive culture up to 4 hours after antibiotic use (CMDT 2007, Tierney, L. Lange press). If such CSF exams reveal no bacteria and suspicion of meningococcus is high, then consider checking the CSF for meningococcal PCR. Also consider nasal and throat swabs for the organism as it is in these two places where meningococcus can be found and where it is considered to invade in the later location.

REMEMBER all close contacts e.g. family members / nursing home residents / kissing contacts / and RARELY medical staff need TREATING WITH RIFAMPICIN as prophylaxis (600mg twice daily for two days) to prevent them from developing meningitis or spreading the organism they may harbour derived from the sick patient.

This treatment can be done as an outpatient, but it should not be forgotten or delayed.

Patients with meningococcal sepsis / meningitis should ideally be treated on an ICU / HCU ward until stable.

Please consider....

Medical Student Visits and Ways of Thinking

This week and last week has seen the usual influx of medical students from throughout Japan coming to see how this hospital works.

I have as a result been very busy with my daily rounds teaching history and physical examination to the students so that they can also understand the patient problems.

When I am asked by Residents what the problem is, I naturally produce a differential diagnosis but I then throw the question back to the Medical students. I usually get but only a few answers.

I am aware that in Japan, because of the hierachical structure of the senior doctor to the junior that in some cases what the senior doctor says is final and with little or no questions from the juniors / medical students as it might be seen as embarrassing or insulting.

Well, I do not mind questions. I think questioning seniors is good. In fact, fresh medical students / junior doctors fresh from medical school can sometimes have the right answer as they know the most uptodate information.

Sharing of ideas and challenging why a diagnosis has been made allows all the members on the round to understand the thought process behind diagnosis. By questioning the senior doctor allows everyone to understand and to find out the evidence / experience of the senior doctor and hence, all can learn from this type of interaction.

I had a discussion just yesterday with several medical students and I advised them that they should always read about the patients that they see. In doing so, they truly learn about the conditions and the associated problems, workup and treatments.

As a medical student / doctor you need to read to fill in the gaps in knowledge that everyone has. No doctor is perfect-- except perhaps Prof Tierney ! :)

By reading, one can learn about the evidence base of current diagnostics and therapeutic measures and why old treatments lose or regain favour etc...

Never just rely on the notes taken at university as they soon become out dated and moreover, they are sometimes opinion of the lecturer rather than based on evidence and fact.

The take home message today is always question in your own mind what is being said to you and never just accept that it is correct. Go away and read about it and decide for yourself if that is correct or not. In so doing, you will grow as a physician and become better diagnostitians.

Let's Get Physical-- Let's Get Training

During my time in Japan I have been able to assess the medical students way of examining patients and to some extent the skills that have been taught are sometimes inadequate for finding common clinical signs.

This is a concern for me because some of the students are soon to become junior doctors.

For example, I have recently seen several medical students miss a basal pneumonia that was identifiable from loud wet crackles. The reason was the students only examined half the lungs ! Each made the same mistake.

They only placed their stethoscopes half way down the chest at the back and said they could hear no problem. Only when demonstrating the surface anatomy of where the lungs commence (at the apex) and where they finish (12th ribs posteriorly) were they able to then understand that the lungs fill the entire space and hence, they should listen at the lung bases as well.

Even after doing this, only one student was able to identify the sounds suggesting that the practical, 'hands on' ability to detect through physical examination was previously not taught to them optimally.

Moreover, one medical student started examining with his stethoscope through the patient's clothes, which must not be done as it is not possible to always differentiate the rubbing of the clothes from the sounds in the patient's chest.

So, why are some Japanese medical students unable to identify pathology / diseases through physical examination? The problem may be when they start learning physical and how they learn it.

In the UK, modern medical school teaching starts with physical examination right from the first year. This is not the case in Japan where physical only starts from 3rd/4th year onwards. Moreover, some medical students have also said to me that the opportunities to examine patients at medical school in Japan are too few.

Hence, by the time some medical students start to visit other hospitals to decide where to do their two-year residency, it becomes clear to me that some institutions training in physical examination is not optimal. Of course, this is a generalisation and on a case-by-case basis, but a final year medical student in the UK would be expected to be able to examine the three main systems (e.g. cardiovascular / respiratory / abdominal) and to pick up straight forward diagnoses such as pneumonia, pleural effusions etc...

The utility of percussion of the chest for signs of consolidation or effusion is not universally taught in Japan as some medical students have never seen this done before until they visit me at my hospital. They have been reliant on the chest xray / CT to make the diagnosis for them. Even if some students have seen percussion done, they have not fully appreciated its significance or the great utility that it has to offer until they come to this institution.

Examining simple things such as the hands and the quality of the pulse are, in my experience, not considered by medical students as important, and hence, if one were to start from the eyes, as is done in Japan, the patient's physical examination misses a vital area. Essentially, the patient has no arms as no parts of the upper limb are examined !

Things such as clubbing, splinter haemorrhages, Beau's lines, Janeway lesions, Osler's nodes, Dupytren's contracture, nerve palsies, metabolic flap, collapsing / slow rising pulses are MISSED because they are not examined for. Serious diagnoses can therefore be missed.

I also did a local seminar last weekend where I presented a case of a dissection of the aorta. I was asked whether Review of Systems questioning was necessary and worthwhile because it took so much time. I am glad that such a question was asked and of course, it is indeed very important because it is a safety net for the patient and the doctor to pick up additional information that might help with the diagnosis / diagnoses that may have been overlooked by the patient and the doctor.

Taking a little bit of extra time at the beginning might save the doctor time in the future by cutting down on unnecessary tests / scans.

Communication with the patient and thorough history taking is Essential. I am somewhat concerned that medical students do not find that this might be useful because of time constraints. This may also be because of the reliance on laboratory data, xrays and other advanced radiological studies rather than the basics of a good story of the problem and then having the appropriate skills to find the problem(s) by physical examination.

Whilst medical students come to visit here for three days only on their tour of different institutions, it is never possible to show just how the basics of being a doctor can provide quick and straight forward answers that might otherwise not be obtainable by any scan ! However, they are able to see how classical physical examination should be and how it is possible to dissect and rebuild a junior doctor's patient history so that the problem(s) can be elucidated and hence, following that, how appropriate investigations and treatment should be considered.

For those interested in improving 'level up' on history and physical, they should consider coming here for more than 3 days as it is otherwise insufficient time to obtain the true nature of what is on to offer to the medical students.

Essentially, with an ever growing elderly population and few doctors and with a large medical expenditure in Japan, I believe it will become evermore important for doctors to take more time on history and physical so that instead of doing 'blanket' blood testing and scanning otherwise referred to as the 'pan-man' scanning, the doctor will order tests related only to their considered differential diagnosis rather than doing lots of tests without really knowing what to look for and hoping to find something, as this is not efficient or cost effective.

If you are interested in an externship or a longer period than three days then please let me know on skghjpn@gmail.com

Trip to Hokkaido

For tyhe past few days I have been in Hokkaido for purposes of teaching junior residents.

There are several medical residents working under General Internal Medicine and they get to see some interesting cases in addition to the everyday 'bread and butter' cases.

I was presented several cases of unusual general medical conditions. One case required for examination of the Central Nervous System wherein I was able to determine both old and acute neurological dysfunction because of history and examination only.

The scans presented to me after the physical exam confirmed my suspicions.

I was also there to teach opthalmoscopic examination with the handheld opthalmoscope. The doctors were able to identify the optic disc of the patient which is perhaps one of the most important tests as it is necessary to check the optic disc in patients with suspected raised intracranial pressure e.g. meningitis and hence, I hope the doctors were able to gain some valuable experience from this practise.

Following this, I went on a 3 hour sightseeing trip and the pictures of that experience are below:

Type 2 Respiratory Failure and Therapy

In my years as a doctor I have seen many patients come to hospital with worsening respiratory failure due to all sorts of underlying diseases.

The classic example is with the patient with underlying heart failure who gradually gets breathless with worsening oedema who then is so breathless at rest eventually calls for an ambulance.

Of course, in some instances, the paramedics are unaware of the underlying problem and give high flow oxygen.

When the patient reaches the hospital, they can sometimes have a low conscious level which in some instances makes the doctor think of an intracerebral cause and the patient gets sent for a CT head scan which comes back as normal.

In this case, the patient has CO2 Narcosis and hypoxaemia causing the reduced conscious level.

A history from relatives or even the patient plus a detailed examination can provide a wealth of data that can quickly narrow down the cause and differential diagnosis to provide swift treatment.

When examining the patient-- START WITH THE HANDS. Assess for warmth and sweatiness that one can get with CO2 retention. In addition, red palms can also be due to this problem. However, the Gold Standard test is to look for a CO2 retention flap of the hands.

This can quickly tell you if there is a major problem and the likely cause. It is referred to as a Metabolic Flap as it can be caused by CO2 retention, Liver and Renal Failure in the main.

Pulse is an excellent measure. Not checking just the rate, but the QUALITY too. CO2 retention gives a Bounding Pulse that is easy to find. The blood pressure may also be high.

Check the JVP to see if it is raised. There are several causes of raised JVP such as heart failure, cor pulmonale of Type 2 respiratory failure, dysrhythmia, valvular dysfunction, tamponade, superior vena cava obstruction, pulmonary embolism, severe respiratory failure etc...

However, this is where a good history will be of help to try and make some discrimination as to the cause such as being a heavy smoker, previous evidence of myocardial infarction, thromboembolic events in the past, being on oral contraceptives.

Listening to the heart sounds may provide an answer such as obvious heart murmur or reduction in heart sounds as in tamponade. Feeling the apex to assess if has shifted laterally can reveal the chronicity of the problem as in chronic heart failure.

Listening to the chest may reveal the dullness and reduced air entry associated with a pleural effusion plus the classical sounds of bronchial breathing. Moreover, in heart failure, the appearance of widespread wet crackles aids the doctor to make the diagnosis at the bedside. Wheeze is not so easy, as it may signify asthma, COPD or even heart failure. That is why a history helps to refine the mental diagnosis along the way.

Feeling the abdomen for ascites and organomegally can provide further clues about heart failure and lastly, checking the legs, buttocks and abdominal wall for oedema and of course, around the face can also provide salient clues about the extent of heart failure.

Hence, a basic clinical diagnosis can be made at the bedside without a chest xray or blood results. However, these tests DO need to be done, but that should not stop you as doctors from providing emergency treatment whilst awaiting such results.

Basic life saving treatments include:

• Appropriate oxygen therapy. For example, in the patient with hypoxaemia and a high respiratory rate, high flow high percentage oxygen is likely to be appropriate. However, in the patient with heart failure / COPD and a low respiratory rate, hypoxaemia and reduced conscious level, low percentage oxygen may be more appropriate. The percentage oxygen provided should be guided by arterial blood gas analysis, not just by saturation probe monitoring.

• Percentage oxygen should be given throw a Venturi Mask and not nasal cannulae. I have seen in the past doctors trying to put 4 litres through nasal cannulae. The idea is flawed because the maximum effective amount of oxygen that can be put through nasal cannulae is only 2 litres. Moreover, if the patient is mouth breathing, there is no way that even 2 litres will give the desired effect. The only way to really ensure an adequate percentage of oxygen is via the Venturi system of facial mask.

• Normally oxygen starts at 24% and increases upwards to maintain an oxygen saturation of about 92%. In patients with Type 2 respiratory failure, such patients rely on hypoxic drive for respiration. If the drive is abolished by high flow oxygen, the CO2 rises and the patients respiratory status worsens. Patients need to have careful oxygen replacement in order to maintain this hypoxic drive. Of course, when the patient is established on the right percentage of oxygen, a repeat blood gas needs to be obtained to ensure that the oxygen saturation is adequate and that the CO2 is beginning to fall. Additionally, acidosis, should it be present, should be seen to improve.

• If the Venturi oxygen mask fail to ameliorate the problem of Type 2 Respiratory failure such as persistent hypoxaemia, rising CO2 and acidosis e.g. pH < style="font-weight: bold;">BIPAP. Such therapy is very effective to reduce CO2 and improve acidosis and at the same time raise the oxygen saturation. This can be used in COPD and heart failure, and in the latter condition, the positive pressure helps to push fluid out of the lung tissue and into the vasculature. In such events, reducing the fluid inside the lung alveoli improves compliance of the tissue and reduces the alveolar-capillary barrier thickness and thereby improves oxygenation.

• Again, once established on BIPAP, blood gases need to be taken to ensure the patient is improving.

• However, intubation and ventilation is sometimes the eventual progression of these disorders, but instituting such therapy should be the last option as in doing so you put the patient at risk of not being able to be weaned off the machine. Only after a few days of ventilation by a ventilator, the intercostal muscles start to waste and hence, this makes the patient ventilation capability worse if they were to come off the ventilator.

Other measures to improve respiratory outcome:

• If heart failure is the main problem then using nitroglycerine and furosemide are standard therapies. Nitroglycerine reduces venous return and hence, preload of the heart is decreased. Furosemide has a similar effect and also cause diuresis and reduces afterload. These therapies are relatively safe as long as the patient has a sustainable blood pressure. If the clinical opinion is heart failure, giving such therapies is unlikely to do harm.

• If wheeze is the predominant problem, giving steroids and beta-stimulant nebulisers may help. Even if the cause of the wheeze is not clear, such as a suspicion of heart failure, but a smoker and previous history of COPD, such therapies should not be withheld. Sometimes, it is not clear which condition predominates and so as a result, treatment for heart failure and COPD/Asthma are given until more information is available to refine the diagnosis. Withholding such life saving therapies to ascertain the true nature of the problem which could take several hours is not good practise because the patient suffers. It is better to sometimes treat several suspected problems at the same time on admission to the hospital as an inpatient and with further test / scans the treatments can be stopped or continued depending on the outcome. Hence, the patient has the life saving therapies from the start and comes to no harm from the disorder as treatment was not withheld. This way of practising medicine is common place in the UK and USA.

1. Sit your patients up!!! Yes, it is a simple thing to do but very rarely done in Japanese hospitals. I have been to several hospitals in Japan, and in almost every one, patients with COPD and heart failure are nursed flat. This is not standard treatment. Patients who have cardiorespiratory diseases often find it easier to breath when sat up. For example, in COPD, such patients rely on diaphragmatic contraction for breathing as their hyperinflated 'barrel' chests poorly expand. If the patient is sat upright, the use of gravity is enhanced and patients can also sit forwards to fix their chest to enable deeper breathing. By lying COPD patients flat abolishes this advantage and worsening respiratory function can ensue. Heart failure patient rely on gravity so that the pressure in the upper lungs is less than the higher pressure in the lower lobes. This can help with respiratory function. Lying such patients flat equalises the pressure and breathless gets worse. This is why one sees the phenomena of orthopnoea in COPD and CHF and Paroxysmal Nocturnal Dyspnoea in CHF when lying flat. Just by sitting you patients up may improve their oxygen saturations !!!! However, please let your nursing staff know that the patient must be nursed in that position because failure of you as doctors to communicate such orders will find the patient put flat and situation repeats itself.
   

• Dysrhythmias should be treated if pathological. For example, fast atrial fibrillation should be treated. It should not be left as a mere matter to observe. AF can lead to worsening heart failure and cardiorespiratory function can worsen as a result. Such patients need to have a echocardiogram to exclude thrombus formation, thyroid function tests and cardiac enzyme level measurement to ensure cardiac damage has not occurred.
  

• Patients with renal failure and fluid overload can develop respiratory failure. Such patients may have a metabolic acidosis and poor urine output. Consideration for dialysis / haemoflitration to reduce circulatory volume should be considered on an urgent basis.

The above is by no means an exhaustive guide, but basic patient management with oxygen, positioning and standard basic drugs can make a world of difference to your patients care and hopefully prevent them from progressing to a worsening state.

Remember, the patient comes first. Please consider......

Electrolyte Disturbance, Spasm and ECG Disturbance

A case presented to a hospital and has been anonymised for patient confidentiality.

An elderly male was brought to the hospital with a reduced conscious level and evidence of respiratory distress.

No history was obtained from the patient, but there was the possibility that the patient had developed aspiration from poor swallowing.

The patient had known dementia and had previously undergone a thyroidectomy some years before.

Drug history was unknown as was the family history.

The patient apparently lived alone prior to admission to the hospital.

Physical examination on admission confirmed a right basal pneumonia and the patient underwent intubation, ventilation and antibiotic therapy was initiated.

The laboratory data revealed a low K of 2.7 and a low Ca of 4.7 in addition to evidence of infection with raised white cells and inflammatory markers.

A senior doctor suggested that the patient might have tetany to account for the breathing difficulty, and also for a potential swallowing disturbance. Moreover, the tentany may have resulted from the thyroidectomy in the past and hence, the patient probably had hypoparathyroidism and hypothyroidism.

On examining the patient, there was a loss of the outer 1/3 of the eye brows and a swollen face with pale skin consistent with hypothyroidism. There was a necklace scar confirming a thyroidectomy had occurred in the past. The reflexes were generally absent.
Applying a blood pressure cuff to the left arm provoked CarpoPedal Spasm (Trousseau's Sign) and Chvosteck's Sign was negative.

These physical features indeed suggested tetany and hypothyroidism.

ECG revealed atrial fibrillation and T wave inversion in the lateral leads.

It was suggested that a magnesium levelshould also be obtained in addition to thyroid hormone tests and a troponin T level.

The resident gave intravenous calcium gluconate and started K replacement whilst awaiting the results of the other tests.

However, the K level dropped further despite replacement. This was because the Mg proved to be half the normal level. The K cannot be corrected if the Mg level is Low.

Hence, the resident then gave an infusion of magnesium and within a few days, the K level had normalised and the Ca level was also increasing towards normal.

The ECG improved with normalisation of the T wave to the upright position and the patient was in sinus rhythm.

The thryoid tests came back with a TSH of 14 and low T3 and T4 confirming hypothyroidism. The Troponin T test was negative.

Thyroid hormone was commenced at low dose of 25 micrograms/day in view that the patient was elderly and might have underlying ischaemic heart disease.

Diagnosis in this case include:

• Tetany due to combined Hypocalcaemia dn Hypomagnesaemia
• Hypokalaemia due to Hypomagnesaemia
• Iatrogenic Hypothyroidism
  
• Iatrogenic Hypoparathyroidism
• Aspiration pneumonia
  

It was considered that the dementia-like state might improve with thyroid replacement as such problems can occur in profound hypothyroid states.

Moreover, this was a great example of how tetany can present. Tetany can be due to low Calcium or Magnesium, and in this patient, both were present.

The low Magnesium would have precipitated low potassium and the combined electrolyte and thyroid hormone dysequlibrium would have caused muscle weakness which could have lead to problems with swallowing and hence, aspiration pneumonia.

The lessons to be learnt hear are:

1. Always go back to the patient to test a hypothesis. In this case, the low calcium prompted the search for physical signs of Tetany. The positive physical sign and low K, lead to the thought of low magnesium that might otherwise have been missed.
2. If the patient has dangerously low electrolytes, they must be corrected on an urgent basis
3. Thyroid hormone replacement should be started at low dose in the elderly and gradually titrated up until the TSH and T4/T3 are normalised.
4. Electrolyte disturbance can cause ECG abnormalities that can resemble an ischaemic ECG. Moreover, low Ca and K can each precipitate a Long QT syndrome and hence, such patients are at risk of Torsade de Pointes. Thus, reversing such electrolyte abnormalities is required urgently.
   
5. Thyroid deficiency can cause reduced conscious level and even a dementia type picture. When starting replacement, always start at low dose in the elderly.

For a more detailed description, please see an appropriate textbook.

Please Consider......