A Challenge For You All--- the Answers!!!

Dear Bloggers

Over week has passed since I extended the answer limit for the Challenging case I set a few weeks ago.

Following are what I regard to be the answers to the case.

In such a case it is essential to have a problem list which details the important elements of the history, examination, laboratory and radiological data in order to try and understand the problem.

Problems from History

• Vomiting and Diarrhoea
• Reduced conscious level
• Cardiac arrest
• PMH of Parkinson's disease and constipation
• Drugs- for PD, tricyclic antidpressants, senna, Aricept
  

Problems from Examination

• Hypotension, Bradycardia, small volume urine (dark colour)
• Hypopnoea, Poor chest excursion
• Distended, tympanic abdomen, absent bowel sounds
• Hypotonia, reduced reflexes

Problems From Lab Data

• Hypokalaemia, Hypophosphataemia, Hypocalcaemia (7.94 corrected)
• Normocytic anaemia
• Leucocytosis
• Elevated CK
• AST, ALT and Bilirubin elevated
• Urine - evidence of bacterial infection

Problems from radiology

• Raised Right hemi-diaphragm
• Distended loops of bowel; no mass lesion.

Assessment

1) First of all, we need to consider why this patient has developed vomiting and diarrhoea. Is it related to an infectious agent or related to a mechanical problem or even drug related? The problem appears to have started after taking a new PD drug. It is certainly possible that a drug side effect could have caused these symptoms. However, the patient stopped the drug but the symptoms persisted making the drug, whatever it is, less likely to be the cause of the problem.

The fact that the patient was taking senna and causing up to 6 episodes of diarrhoea a day is a concern. Normally, senna might cause 1 or two stools per day and therefore if copious diarrhoea is occurring, it is either over use of senna or a different pathology entirely.

Drugs known to slow the activity of the bowel include tricyclic antidepressants due to their anti-cholinergic effects and Aricept for similar reasons. Hence, they might result in a constipation-type of problem with over flow diarrhoea then occurring. However, in this case, there was no evidence of constipation on abdominal Xray which suggests that constipation was not a current problem.

Parkinson's disease can also result in constipation due to autonomic dysfunction and this is more profound in Multi-System Atrophy. Again, however, there was no evidence of constipation making the PD unlikely to be causing this problem.

In view of the high white cell count, and the dilated bowel one must consider several other diagnoses including clostridium difficile infection and inflammatory bowel disease (particularly ulcerative colitis). The former problem is a real possibility but in view of the lack of colonic haemorrhage, UC is unlikely here. Of course, a subacute mechanical obstruction might be due to an internal hernia or a malrotation of the bowel causing a volvulus.

The fact that the patient had a urinary tract infection identified is very important. This could be the cause of persistent vomiting and the leucocytosis. Moreover, UTI is a known cause of acute pseudo-obstruction of the bowel. This problem can result in electrolyte loss, vomiting, diarrhoea and constipation as well!

We must also consider why an ileus developed. Well, any of the above could result in an ileus. However, in view of the severe hypokalaemia, hypophosphataemia, it is entirely consistent that severe electrolyte depletion caused this problem although mechanical and infective causes would need to be ruled out first.

2) Then we should assess why the patient developed a reduced conscious level. Well a combination of hypovolaemia, infection, electrolyte disturbance and raised CO2 (hypercapnea) can all contribute to such a problem.

The fact that the respiratory rate dropped to 8 per minute with poor excursion of the chest in addition to skeletal muscle hypotonia and absent reflexes suggest diffuse muscle weakness. This would in turn result in respiratory failure with rising CO2 levels despite normal lungs, CO2 narcosis and unconsciousness. The muscle weakness could result from the profound hypokalaemia, hypophosphataemia and hypocalcaemia. Respiration would also be made worse by splinting the diaphragm with distended bowel.

3) Then we should assess why the patient had a bradycardia and a cardiac arrest. Well, this is multifactorial. Electrolyte disturbance e.g low K, Low Ca, can promote dysrhythmias. Hypovolaemia that this patient also experienced can cause cardiac arrest. These come from the 6 H's and 6 T's which are Reversible Causes.

H's

1. Hypothermia
2. Hyperkalaemia/hypokalaemia/electrolyte disturbance
3. Hypovolaemia
4. Hypoxia
5. Hypoglycaemia/Hyperglycaemia
6. Hydrogen ions (acidosis)

T's

1. Thromboembolism (PE)
2. Thrombosis (AMI)
3. Tension pneumothorax
4. Tamponade
5. Toxicity
6. Trauma

Moreover, one of the commonest causes of a a cardiac arrest is AMI which results from a dysrhythmia e.g. VT/VF, and should be ruled out in every patient.

4) Next we need to understand why the patient developed such severe electrolyte imbalance. Well, with a chronic history of recurrent vomiting and diarrhoea, various electrolytes can be lost. Loss of H+ ions from the stomach will cause metabolic alkalosis (and hypochloraemia) and diarrhoea can cause hypokalaemia. One should also remember that electrolytes can be lost in the urine, and so these should also be tested.

The loss of H+ ions causes the kidneys to have increased loss of K+ ions to maintain electroneutrality, and so these spill out into the urine resulting in worsening hypokalaemia! The proportional increased reuptake of bicarbonate over protons results in the metabolic alkalosis.

Thus, the arterial blood gas shows an acute respiratory acidosis (related to the CO2 retention) and a chronic metabolic alkalosis.

5) In view that the CK was raised, an MI should be ruled out and an ECG and Troponin T should be performed. In this case, the TropT was negative and the ECG revealed ST depression, T wave inversion and a prominent U wave all consistent with hypokalaemia. In view that an MI was excluded here, the cause of the CK rise could have been due to hypokalaemia associated Rhabdomyolysis or due to chest compression from the Cardiopulmonary rescuscitation.

In order to consider the kidneys, a urinary myoglobin level would be necessary. However, in such cases of renal failure following rhabdomyolysis, the CK is usually very high (several thousands) to result in renal impairment.

SUMMARY OF ANSWERS TO QUESTIONS

1) Why did the patient develop CO2 retention?

• Muscle weakness from combined Hypokalaemia, Hypophosphataemia , Hypocalcaemia
• Splitting of the diaphragm

2) Which two simple cardiac tests would you perform and why?

• ECG and Troponin T to look for dysrhythmias and rule out an MI.

3) Identify as many possible reasons why this patient developed a cardiac arrest?

• Multiple electrolyte disturbances particularly hypokalemia.
• Hypovolaemia
• Acidosis
  
• Possible AMI.

4) Which one urine test would you perform to investigate the cause of the possible renal failure in a patient with this clinical history?

• Urinary myoglobin level

5) Taking into account the entire history, list as many causes as possible for this patient developing an ileus. Is there a Syndrome that encompasses all of these features??

• Mechanical cause
• Infective Cause
• Inflammatory Cause
• Neoplastic (mass lesion; not seen on CT scan though)
• Electrolyte Imbalance
• Drugs
• Parkinson's disease

• Syndrome of Acute Pseudo-Obstruction is known as Ogilvie's Syndrome.

6) What does the arterial blood gas show and why do you think it occurred?

• Acute respiratory acidosis and a chronic metabolic acidosis.
• Acute changes due to respiratory failure from muscle weakness and reduced consciousness, chronic changes due to electrolyte loss resulting in raised level of HCO3.

• The liver function here was also abnormal- however with fluid and antibiotics, the levels improved quickly and may have resulted from sepsis, hepatic hypoperfusion amongst several causes.
• The chronic normocytic anaemia is also a problem here and a haematinics work up, blood smear and autoimmune profile to exclude autoimmune haemolysis (raised bilirubin and AST) plus a reticulocyte count would be warranted.

In this case, the patient was treated with intravenous K at a rate of 20mmol/hour as a continuous intravenous infusion plus a phosphate infusion whilst on an HCU being cardiac monitored. He was provided with 3 litres of intravenous fluid per day.

The patient was reviewed by the surgeons who agreed that this was indeed an acute pseudo-obstruction (Ogilvie's Syndrome) and a flatus tube was passed per rectum to reduce the bowel distension. Over several days, the distension decreased and bowel sounds could be heard suggesting bowel recovery. This was aided by the use of intravenous Erythromycin which has evidence to cause increased bowel motility.

The ECG returned to normal.

The patient was able to breath by himself without the aid of assisted non-invasive ventilation. The Blood gas also began to reverse towards normal.

However, the patient developed a polyuria of up to 6 litres per day. The serum osmolality was normal and the urine osmolality was dilute at about 380 mOsm/L. The patient still required large amounts of fluid daily to maintain his blood pressure in addition to dopamine catecholamine support.

During the illness, the patient revealed no evidence of renal failure, in part, because aggressive fluid management was commenced on admission to maintain renal perfusion. Therefore, this makes an acute tubular necrosis unlikely. Moreover, the patient did not have any profound oliguria or anuria suggestive of renal failure.

The polyuria suggested an insensitivity to ADH (nephrogenic diabetes insipidus) which can be caused by---- hypokalaemia !!! Patients who are well and who have polyuria and polydipsia can usually undergo a water deprivation test once diabetes mellitus has been excluded. However, in view that this patient was bed-bound and reliant on intravenous fluid to maintain blood pressure in addition to catecholamine support, it was considered unsafe to perform such a test. Therefore, an ADH level was attained which showed a mildly elevated level. In view that most causes of nephrogenic DI result in a partial insensitivity to ADH rather than a complete insensitivity, the use of supraphysiological doses of ADH (e.g. nasal desmopressin) can sometimes reverse such problems.


There are many causes of nephrogenic DI including congenital and acquired. These include:

• sickle cell disease
• medullary sponge kidney
• release of periureteral fibrosis
• pyelonephritis
• hypokalaemia
• hypercalcaemia
• amyloidosis
• Sjogren's syndrome
• myeloma
• lithium
• demeclocycline (used to treat SIADH)

Another potential cause was Fanconi Syndrome which in some patients is related to chronic hypokalaemia, the treatment of which is fluid replacement until there is spontaneous recovery of the kidneys.

So, this case was extremely complex related mostly to electrolyte disturbance!!

I hope that you enjoyed the case!

Please let me know your comments.

Have a great weekend!!

History Can Be Better Than CT !!

Dear Bloggers

I want to tell you about another real patient case that has been anonymised to show you how history can give the diagnosis better than a CT scan !

An elderly patient was admitted into hospital with a 3-day history of increasing dyspnoea and cough. The patient was normally wheelchair bound following an episode of Stevens-Johnson Syndrome several years before although she was able to walk a few steps to visit the toilet. However, in the 3-day period, because of breathlessness the patient was unable to walk at all.

The cough was productive and the sputum was said to be clear and there was no apparent bloody tinge to the sputum or any haemoptysis.

However, prior to admission, the patient developed a high fever of over 39 degrees which prompted the admission into the hospital.

The patient admitted that she had been losing weight and had a reduced appetite for at least 6 months.

The patient was a heavy smoker and had been so for many years.

The patient denied any chest pain (pleuritic) or bone pain.
There were no shaking chills or night sweats.
There were no upper or lower gastrointestinal symptoms, no joint or muscle pains, no genitourinary problems and no cardiac symptoms such as palpitations.

Previous Medical History included the above in addition to type 2 diabetes and hypertension.

The patient was being treated with glimepiride, metformin, enalapril and aspirin.

The was no family history of note and the patient lived with her husband in an apartment block and the elevator was working and they had good family support.

On examination

The patient looked slightly unwell and was sweaty (perspiration on the forehead and a drenched hospital gown) but was conscious and alert. The patient was hot to the touch.

Hands revealed tar staining of the fingers on the right hand consistent with heavy, prolonged cigarette smoking but there was no finger clubbing. There was some mild palmar erythema but no CO2 retention flap.

The pulse was regular, bounding in nature and tachycardic at 110/min. Skin turgor was reduced.
BP was 110/60 supine- a sitting blood pressure to assess for hypovolaemia was not performed.

JVP was not elevated and there were no palpable lymph nodes in the neck or axillae.

Eyes were normal and there was no anaemia, jaundice and no Horner's Syndrome.

Mouth examination revealed a bone-dry tongue and coagulated blood around the gums.

CVS: heart sounds were normal 1 + 2 and no murmurs or added sounds. There was no peripheral oedema.

RESP: respiratory rate was 14 per minute, the chest was hyper-expanded and the trachea revealed the 'tug'-sign consistent with chronic lung disease but it was not deviated.
Percussion was resonant throughout anteriorly and posteriorly.
Auscaultation in fact revealed coarse, wet crackles at the left base and reduced air entry on that side.

ABDO: Abdominal examinaion was soft, non-tender, no hepatosplenomegaly, no renal angle tenderness. A 4-5 cm abdominal aortic aneurysm was identified in the epigastric region- there was an added bruit. The bowel sounds were normal.

Peripheral pulses were normal.

CNS examination was grossly normal.

PNS examination revealed proximal muscle wasting although there was some wasting of the small muscles on the dorsum of both hands.
Tone was within normal limits.
Power was approximately 4/5 throughout.
Reflexes were present in the upper limbs but absent in the lower limbs. There was no muscle fasculation.
Coordination and sensation testing had not been performed.
Babinski examination was normal on the right and equivocal on the left.

Impression

From the history and examination it was clear that this patient had an acute illness and a bacterial pneumonia was highly likely.

However, the preceding 6 months of weight loss and reduced appetite plus the evidence of a proximal myopathy made a bronchogenic carcinoma also likely. Ca lung is well established to result in paraneoplastic proximal myopathy.

Examination of the chest Xray on the PACS (electronic radiology) was unrevealing.

Bloods revealed a raised WBC and inflammatory markers plus a raised BUN and normal creatinine which respectively indicated infection and dehydration that were already found through the history and examination.

A senior doctor was not content with the PACS radiograph and asked to see the hard copy plain film because experience showed that more can be seen on the plain film.

Indeed, on looking a the hard copy CXR it was clear that there were several ununited rib fractures, an odd shadow at the hilum on the left side around the area of the aortic knuckle and looking behind the heart shadow there was consolidation.

To the senior physician, it made the suspicion of a bronchogenic carcinoma even more likely.

Review of the CT earlier by the junior doctor had suggested only a consolidation was evident but on review by the senior doctor, with the idea that a malignancy was likely, indeed a malignant neoplasm was identified around the region of the aortic arch.

The moral of the story is that there were two process in play here. Firstly, the acute deterioration with symptoms and signs of a pneumonia. Yes, pneumonia is very common in the elderly but in a chronic smoker, one must always think about malignancy. With the more chronic component of weight loss and appetite loss, a hunt for the malignancy was imperative.

Using a PACS system is excellent as it can be used throughout the hospital and films almost never get lost! However, it depends upon which type of computer screen and resolution whether you can see the problems. If it is a high-tec radiologist high resolution screen then there is usually no problem to identify changes. However, if it is an old LCD screen with poor resolution, covered in dust and finger print marks then I would suggest looking at the plain film every time because otherwise, you will miss important problems.

In this case, the patient had a pneumonia secondary to a malignant tumour that had metastasized to bone. This malignancy had been initially missed, although later picked up by the senior doctor, because the CXR could not be adequately read on the PACS system and moreover, because the history of weight and appetite loss had not been fully appreciated by the junior physician.

The clinical suspicion came from the history and physical examination and the odd shadow around the aortic knuckle confirmed the suspicion. CT gave nicer pictures but did nothing to aid in the diagnosis.

A bit of advice is, try to hold the plain xray film at an angle when looking at the heart shadow because you can sometimes see areas of consolidation show up that had previously been unseen when looking head on. Also, try not to stand so close to the Xray. Sometimes, standing back, you will see the consolidated area literally jump out at you and you will wonder how you missed it in the first place. Lastly, remember that the lungs extend below the upper level of the diaphragm shadows on the CXR-- hence, pneumonia can sometimes be hiding below the diaphragm. CXR reading is an art and it is not simply done before doing a CT !! If you can read the CXR properly, in most cases, you don't need to do a CT especially for pneumonia.

Repeating tests to give you the same answer makes little logical sense and increases radiation exposure and cost.

Please consider not using CT scans when they are not clinically necessary. It should be enough with taking a thorough history, physical examination and a plain Xray film unless there are unusual features that cannot be easily determined or that require more detailed examination.

So, next time you see a smoker with pneumonia, find out if they have symptoms of malignancy e.g. bone pain, weight / appetite loss, symptoms of hypercalcaemia etc and bear that in mind when you look at the CXR !

Have a great weekend!!!

How to make the transition from medical student to doctor?

Dear Bloggers

Today's discussion is slightly different. I would like to discuss my opinion on the transition from medical student to becoming a doctor.

I remember being a medical student and attending lectures to learn about diseases, pharmacology, anatomy, biochemistry and so on and so forth. The information in those lectures was excellent and provided the foundation of my knowledge of common diseases.

In part, I was also allowed to go to different locations for training outside the university for specialties such as surgery, paediatrics, obstetrics and gynaecology, general medicine, general (family) practice to name but a few.

In so doing, I was able to learn as a student how the information in the lectures and in the books bore relevance in the hospital system. As such, I soon learnt that the rare diagnoses such as Zollinger-Ellison Syndrome from gastrinoma are very rare, but of course, such rare diagnoses are what everyone remembers. However, the common things such as heart failure, its presentation, investigation and therapy may have only been covered in a single lecture with no emphasis on this being an important thing to know.

Hence, using the basic knowledge from medical school and seeing how it is applied in the real life scenario of the hospital system is really essential how to understand and make the transition from medical student to doctor.

One thing I always say is Common Things Are Common, and I often hear from medical students and junior doctors alike, rare diagnoses, which albeit are correct, are not the commonest presenting illness for the symptoms and signs.

How did I make the transition from medical student to doctor??

Well, I was always advised by my mentor, a famous Professor in Infectious Disease medicine, to see the patient and obtain the history and physical examination and then read about the problems in the textbooks, thereby reinforcing the medical problems with literature. This indeed was useful and I use such a method to this day. In fact, the patients are the best teachers. Going to the bedside and going through a detailed history in the correct order of how things occurred will in fact teach you a lot about the illness by itself. In so doing, the information obtained can then allow you to concentrate on areas of the physical examination that cause concern.

Then, by drawing together the positive elements of the clinical picture along with the pertinent negative symptoms e.g. no chest pain, no sputum, in a body systems review, allowed me to understand which diseases were not likely to be causing the problem.

By having a problem list from history and physical examination alone, I was then taught to consider the likeliest diagnoses from these problems e.g. central crushing chest pain, dyspnoea, diaphoresis, nausea and vomiting are more likely to be an AMI or unstable angina rather than Bornholm's disease from coxsackie virus.

It is all very good to use a medical list of causes, the one which I constructed is DIET IN HIM, an example case that I published last year maps out the different causes from the DIET IN HIM list for a particular patient problem. However, this is just the start!! One has to know the epidemiology of disease such as the age of onset, the likelihood in female or males e.g. SLE, how the disease usually presents and the salient features for diagnosis. Then one has to produce the differential diagnosis based on which is the best diagnosis to fit all the features and with less common ones below this.

Remember, this is based solely on history and physical examination alone.

In the UK, most patients admitted will been seen by the junior doctors who takes the history and physical at the bedside. There may be an ECG available and rarely have any blood tests been taken except if it is a referral from the Accident and Emergency (ER) department or another team. Then the junior doctor takes the blood tests and orders the radiological tests.

However, in the interim, whilst awaiting the results, treatment is usually commenced in anticipation of the results. Hence, treatment is not delayed waiting to see if you are right or wrong. How can this be done??

Well, it comes back to interpreting the history and physical examination. Patients with signs of heart failure get furosemide before the chest xray is performed with oxygen therapy. Patients with chest pain consistent with an ST elevation MI on ECG get the aspirin, heparin, oxygen, morphine, and thrombolysis before the CK and Troponins are available. Patients with signs of a tension pneumothorax get the needle inserted into the 2nd intercostal space in the mid-clavicular line before the CXR is taken. The patient with a good history of PE e.g. sudden onset pleuritic chest pain, cough, dyspnoea, hypoxaemia and a clear chest examination and Xray get heparin before the D-Dimer or spiral CT are performed.

The fact is, making a diagnosis based on history and physical examination is imperative. Without the proper history and poor physical examination skills, the ability to make a diagnosis can be delayed and then the reliance on machines to make the diagnosis for you increases and treatment for severe illnesses can be delayed resulting in adverse outcomes.

Problem Based Learning (PBL) using common presenting illnesses to teach how to understand differential diagnoses and which common diagnoses to consider is very important. This type of teaching is used for the famous MRCP exams in which limited data is provided and the likeliest diagnosis needs to be selected. The USMLE exams are similar in format as well. You see, patients do not present to you and say I have all of these symptoms and my diagnosis can only be X disease. There are many diseases that have overlap of symptoms and signs and the only thing that can separate them can be the timing of onset, epidemiology, sex predominance, location in the world, sexual history, so on and so on.

However, PBL is a classroom based idea and sets the mental framework about how to go about thinking of the patient problems. It is an entirely different scenario being tired and on-call at 4am and to be called to the ER to see a sick patient. This is where the use of bedside teaching comes in to play. By knowing which salient questions to ask as a discriminator to quickly get to the likely diagnosis can speed up the history taking and allows the doctor to already consider what treatments the patient is likely to require.

For example, the patient with the classical history of ischaemic chest pain is going to be questioned about the elements of the pain, its severity, its radiation, to ascertain if it is truly ischaemic or related to for example a dissecting aortic aneurysm because the treatments are different, the former being medical in most cases and the latter being emergency surgery!!

It is my opinion that training as a doctor is a vocation. When you become a doctor for the first time, you have just started on the long road to learning about diseases, their diagnosis and treatment. Medical school does not adequately prepare you for real life medicine. It neither prepares students about how to talk to patients or their families.

The best way to really make the transition is to see as many patients as possible as a student and really try and take a decent and comprehensive history including the Body Systems Review. The teaching of physical examination is really very much reliant on your teachers but you can also learn from some very good books that are available these days.

Try and practise Problem Based Learning. One UK book I would recommend is Rapid Review of Clinical Medicine (for MRCP) by Sharma and Kaushal and published by Manson Publishers. This book is available from Amazon.

Then, with this background of patients cases from real examples plus PBL examples, when you see a similar patient case in future, you should go through a similar process for the differential diagnosis and scale according to likelihood the most likely diagnosis and consider what further tests you would do and more importantly, what emergency treatments you will start.

Learn, learn, learn your medical emergencies e.g. treatment of AMI, PE, COPD, Asthma, Seizure etc.... There are many books available to do this, but I would strongly suggest you use one based on current evidence rather than on opinion.....

The ability to solve medical problems come from many years of experience and even senior doctors get it wrong on occasion because patients don't write the textbooks and doctors are human.

Good luck with your quests!

Extension for Case Result

Dear Bloggers

As you are aware, I posted a case for you to attempt to answer last week. In view that there have yet to be any replies to the case, as a consequence, I will therefore extend revealing the answers for a further week to allow you more time.

Please feel free to send in your answers anonymously.

Have a great day!

A Challenge For You All

Dear Bloggers

I have in the past presented cases and posed questions for you to answer. Today's challenge is very interesting and I would like you to post your answers on my blog for all to see and so everyone can learn.

The case has been anonymised for confidentiality as always.

A man was admitted with reduced conscious level.

He had been transferred from another hospital following a cardiac arrest on their ward. The reason for the initial admission had been vomiting and the patient was being investigated for the underlying cause. The vomiting had been occurring for several weeks following the commencement of a new Parkison's disease drug, the name of which was unknown, although that drug was eventually stopped. However the vomiting continued and the patient was developing regular vomiting of stomach contents each lunch time. The patient had never complained of much even when he had been ill in the past, so the family were unaware if he had any body pains.

The patient had a long history of constipation and had been taking medication for some time resulting in 5-6 episodes of diarrhoea daily.
The patient had not complained of any chest or abdominal pain. There was no haematemesis, malaena or haematochezia (fresh rectal bleeding). There was no complaint of any visual disturbance e.g. blurred vision, or headache (consideration of raised ICP). It is unknown whether there were any symptoms of gastroesophageal reflux (GERD).

Previous medical history included Parkinson's Disease, Constipation, Dementia, Depression and a Cerebral Infarction.

He was receiving anti-PD drugs (names unknown), Sennoside (for constipation), a tricyclic anti-depressant and Aricept.

He was a non-smoker and had previously drunk alcohol in moderation. The patient's ADLs were impaired because of the severity of the PD and he was limited to walking a few yards. However, he was nevertheless able to feed and wash himself.

The examination at the other hospital is unknown but they were investigating the suspected cause of an ileus.
The patient underwent a gastroscopy which revealed undigested food but no other abnormalities. A CT abdominal scan was also performed which revealed dilated loops of bowel but no mass lesion.

On the day of the cardiac arrest, the patient had been initially alert but soon became increasingly unconscious and then stopped breathing. A cardiac arrest ensued and he was found to be in an asystolic rhythm. He was effectively resuscitated and transferred to the current hospital. Arterial blood gas prior to the cardiac arrest revealed the following: PaO2 132mmHg, PCO2 105 mmHg, pH 7.33, HCO3 53.3, BE 23.5 (after 10L O2).

On transfer to the new hospital, his physical examination revealed the following:

JCS 300, Afebrile, pulse 50 beats per minute and regular, BP 80/60mmHg, SpO2 95% on 10L O2. Reduced skin turgor and dry mouth. No anaemia. Dark coloured, low volume urine in the catheter bag.

CVS: regular rhythm, good volume pulse, JVP not raised. Heart Sounds 1 + 2. No murmurs or added sounds.

RESP: RR 8/min, no tracheal tug or use of accessory muscles. Trachea central. Poor excursion of chest. Percussion resonant and reduced air entry throughout. No wheeze or crepitations (crackles).

ABDO: Distended, non-tender. No bowel sounds. No obvious masses. No rebound or guarding. Tympanic sound throughout on percussion. No renal angle tenderness. No abdominal hernia seen. Rectal examination-- no stool present, no mass lesion.

CNS/PNS: Pupils equal and reactive to light. Unable to perform other movements.
Moving upper and lower limbs spontaneously. Reduced muscle tone and reduced reflexes. Babinski sign negative bilaterally. Unable to test sensory or cerebellar function. Fundoscopy was not performed.

Lab Data revealed the following:

BUN 16, Creat 1.2, K 1.1, Na 134, Mg2+ 2.3, Ca 6.9, Alb 2.7, PO4 0.6, CK 850, ALT 102, AST 103, Bil 1.5, ALP 320, gamma GT 24.
WBC 38.2, Hb 9.0, MCV 82, Plt 20.0, INR 1.2

Urine revealed >100 WCC/hpf, 30-49 RBCs/hpf, 1+ protein, negative ketones, negative to glucose, 4+ bacteria.

CXR was normal apart from a raised right hemidiaphragm due to dilated bowel pushing up from below. AXR was abnormal showing loops of bowel distended with gas. No stool could be visualised on the Xray.

Questions:

1) Why did this patient develop CO2 retention?

2) Which two simple cardiac tests would you perform and why?

3) Identify as many possible reasons why this patient developed a cardiac arrest?

4) Which one urine test would you perform to investigate the cause of possible ensuing renal failure in a patient with this clinical history?

5) Taking into account the entire history, list as many causes as possible for this patient developing an ileus. Is there a Syndrome that encompasses all of these features??

6) What does the arterial blood gas show and why do you think it occurred?

Please send in your answers and in 1 week, I will publish the answers! This is not an easy case but please try and have a go-- you might just be right!

Happy sleuthing.

History is Everything-- yet again :-) !!!

Dear Bloggers

This is a case from another hospital and has been anonymised as usual for patient confidentiality.

A 45 year old lady had been playing tennis following which she had eaten lunch which included several glasses of wine. Following this, she went back to play tennis.

She developed sudden onset of lower abdominal pain which was crampy in nature. This was associated with watery diarrhoea followed by the passing of fresh per rectal bleeding only one time. The patient was so concerned that she presented to the hospital.

She had had several previous episodes of the same fresh rectal bleeding in the past and had been admitted to hospital on those occasions, and it always followed consumption of alcohol.

There was no associated nausea or vomiting.

Previous medical history included renal failure due to type 1 diabetes requiring 3x weekly haemodialysis, hypertension and paroxysmal atrial fibrillation that was refractory to recent ablative intervention.

Drugs included Valsartan, Warfarin, Flecainide, Verapamil and insulin.

She was a non-smoker and had full activities of daily living.

When she was examined on the admission day, she was afebrile, looked well, and all observations were stable.

Cardiovascular, respiratory and abdominal examinations were unrevealing except for the rectal examination. The rectal exam showed normal brown stool but occult blood was positive. There was no evidence of fresh blood !!!

Blood tests revealed normal levels of white cells, haemoglobin, MCV and platelets. INR was subtherapeutic at 1.76.
BUN and Creatinine were consistent with severe renal failure and the K was 6.5
Liver function was normal.

ECG showed sinus rhythm. No acute changes were evident.

Ultrasound scan of the abdomen was unrevealing.

Flexible sigmoidoscopy was subsequently performed which showed slight redness of the rectosigmoid mucosa but no fresh bleeding.

What was the diagnosis linking all the elements together?

Well, history here was everything.
It was clear from the drug history that the paroxysmal AF was poorly controlled as the patient, despite cardiac ablation therapy, was still using two kinds of antiarrhythmic agents. Moreover, the use of alcohol is a known precipitant of AF. The patient had suffered from this rectal bleeding problem on a total of 3 episodes and all were associated with alcohol consumption.
The INR was subtherapeutic and with PAF, the patient would be at risk of atrial thrombosis and embolism.

From the symptoms of lower abdominal pain and GI symptoms, the problem was affecting the territory of the latter transverse colon, descending colon and rectosigmoid region. The rectal exam showing normal stool with a previous bleed indicated that the bleeding must have come from an origin close to the rectosigmoid area as defecation had resulted in clearage of the blood to leave normal brown stool decending from above. Indeed, the flexible sigmoidoscopy confirmed these thoughts.

The previous flexi-sig pictures from other admissions, showed an ischaemic element to these episodes and biopsies comfirmed ischaemic colitis.

So, putting the elements of the history together with the examination, it was postulated that the patient was most likely having recurrent paroxysmal AF with resulting thromboembolism as a result of a subtherapeutic INR or ischaemia due to ensuing hypotension from fast PAF. The PAF was probably being caused by a combination of alcohol, hyperkalaemia and silent ischaemic heart disease.

However, the resident doctor thought that the patient had not had a recent episode of PAF during the tennis match. The patient was however prone to PAF during haemodialysis.

It was time to go to the bedside to take more history and then examine!

The patient was comfortable and speaking normally. On direct questioning, the patient admitted that the PAF episodes were occurring frequently and had occurred on the day that she had played tennis. In fact, this chain of questions from the senior doctor led to very interesting answers from the patient. It turned out that the patient counted her heart rate and it was irregular running at 120/min and was associated with a heavy chest feeling, radiation to the jaw and worsening paraesthesia in her fingers. The episode prior to admission also made her breathless. Following this, the patient developed the abdominal pain and bloody diarrhoea.

Examination of the heart revealed a soft systolic murmur but the patient was in sinus rhythm. Chest and abdomen were unrevealing.

In this case, it became clear that the PAF was a big problem. In fact, it was causing ischaemic symptoms to the heart and it was very possible that there was underlying coronary artery disease unmasked by the tachyarrhythmia from hypoperfusion. The PAF and subtherapeutic INR could have resulted in thromboembolism and ischaemic bowel and resulting in haemorrhage. The same would be true for an episode of hypotension resulting in bowel ischaemia from fast PAF.

On the other hand, the patient had been playing tennis. Physical activity tends to divert blood away from the gut to muscle, heart and brain etc. The patient had then eaten food requiring more blood flow to the gut after which, she went back to play tennis thereby again requiring blood flow away from the gut. With an onset of the PAF and reduction in potential blood flow, it is possible that ischaemic bowel resulted especially if there was a partial obstruction to the inferior mesenteric artery in the first place e.g. from a previous thromboembolic event or atherosclerosis.

In this case, a combination of factors were promoting frequent episodes of PAF. The potassium level was a major concern especially as she continued to be prescribed an angiotension receptor blocker to control blood pressure. Flecainide is a Class 1c agent and is can make ischaemic heart disease worse and hence, it is contraindicated in IHD!!

Using a beta-blocker to control AF and hypertension would be one option, but without knowing the cause of the bowel ischaemia could make the situation worse by exacerbating ischaemic bowel. Moreover, in diabetes, use of beta-blockers can result in loss of hypoglycaemic warning signs and hence, it would not be a first choice of most physicians.

In view of the renal failure, digoxin would not be a option as toxicity would be a real problem.

Using a calcium channel blocker (cardiac specific) at a higher dose regularly would be a option and verapamil was already being used.

In my experience, Amiodarone is the most effective anti-arrhythmic agent for AF per se. Despite its famous side-effect profile and the fear of most Japanese physicians to prescribe it, it nevertheless saves lives!
It is widely used in the UK for such difficult to treat patients and has little adverse effect on myocardial contractility. This is the drug I would have advocated in this case.

Remember that Warfarin and Amiodarone have an interaction and can cause the INR to rise.

As for investigating the ischaemic bowel, perhaps the most sensitive way would have been to do an angiogram of the mesenteric vessels. The procedure is however invasive and the patient was warfarinized and would require conversion to heparin before doing the procedure. On the other hand, a contrast abdominal CT scan might also have provided the answer.

Cardiac echo would have been essential here to rule out thrombus and if negative, a Bruce Protocol stress test to assess coronary artery disease would have been justified although failing that, a myoview scan could provide a similar answer. The gold standard of course would be a coronary angiogram.

In summary, a thorough history provided very essential clues. Simply relying on what the patient tells you is not enough. You must ask detailed and structured questions about each of the presenting complaints and previous medical history. In this case, the previous medical history of PAF was in fact, current medical history !!!!

Don't let a normal ECG fool you to exclude PAF. PAF means it is paroxysmal (intermittent) and hence, it is not always detectable !! Have a high suspicion of recurrent PAF and ask about palpitations, dyspnoea, ischaemic chest pain, and other ischaemic pains.

Always examine the drugs !! In this case, despite the history of ablation, it was clear that the PAF was uncontrolled as by definition, the patient was still taking anti-arrhythmic drugs!

Remember, STOP dangerous drugs. Examine the side effects and contra-indications. As new information becomes available you must decide which drugs should be stopped or continued or which ones to begin-- not an easy task at all.

When you think of Gastrointestinal bleeding, don't just think of localised disease such as ulcerative colitis, Crohn's or diverticular disease. Also think of system disease as well e.g. thromboembolism, systemic hypotension induced ischaemia e.g. in patients with peripheral vascular disease (ASO), endocarditis, vasculitis, congenital e.g. Aortic stenosis with bowel telangiectasia. This list of causes is wide and beyond the scope of today's discussion.

Please consider...

Congratulations Dr Aoki

Dear Bloggers

Saturday night was the celebratory party for the great Dr Aoki in respect of the publication of his revised second edition book on infectious diseases. Dr Aoki is the sole author of the book, which in itself, is a major achievement in today's medical publication era. As Prof Tierney alluded to in his speech, in modern times, the production of most major textbooks has 25-30 authors, and so a single author in a medical sub-specialty is a rarity and should be congratulated and respected. I second that.

A number of other notable business people and physicians were in attendance including Mr Matsumoto (Sakura), Professor Kurokawa and Dr Tokuda who also all made wonderful speeches.

Professor Stein sent a special telegram to celebrate the occasion and stated how Dr Aoki has contributed to the improvement of medical care in Japan especially in respect of the logical prescribing of antibiotics.

In all, about 80 people were in attendance at the party and it was wonderful to see how many friends and supporters Dr Aoki has formed over the years of hard work in promoting infectious disease medicine in Japan.

The night finished all too soon and with snow falling heavily outside, it was certainly a night to remember! :-)

I for one am hoping for the English translation of the second edition !!! :-) Now that would be fun!!

Congratulations Makoto!!!

Drugs Revisited...

Dear Bloggers

I have previously discussed drugs on this blog.

I must again reiterate the importance of not just starting drugs, but also Stopping Drugs.

There are many thousands of drugs available to use as physicians that allow us to treat a whole array of medical problems. However, on a daily basis, we perhaps use a small number to treat the most common conditions such as heart failure, angina, diabetes, infections etc...

However, although drugs have defined therapeutic effects, they may also cause adverse effects resulting in physical and psychiatric manifestations. As part of our work up of patient conditions, it is our duty to examine the list of drugs to look to see if the problem relates to a known side effect of the drug or drug combination.

Merely represcribing the drug is not enough. Knowing the drug class, knowing the common side effects and drug-drug interactions is essential. Moreover, knowing the correct dose of drugs is also necessary and to know that drug levels become altered in other diseases such as renal failure.

Carrying a drug book with you either in paper or electronic format can provide a wealth of information and help you decide whether to continue a drug or stop it either permanently or temporarily.

As real examples, a patient was admitted into hospital for work up of a skin rash. He was a known hypertensive patient for many years and had recently had the introduction of a thiazide diuretic. One month later the rash appeared which was non-painful, non-itchy, flat and purpuric-like. There were no adverse symptoms such as neck stiffness or photophobia, no diarrhoea etc.. The blood results were entirely normal with no renal failure and no rise in the inflammatory markers. The urine revealed 1+ blood only and no renal casts and no protein. The admitting resident considered this to be Henoch-Schonlein Purpura because of the distribution of the rash on the patient's arms and legs. There was also the consideration of Amyloidosis and a rectal biopsy was being planned.

The temporal sequence of commencing a thiazide diuretic and then developing a rash caused me to examine the side-effects of the drug which revealed the very top dermatological manifestation as 'purpura'!!

Hence, a trial of stopping the thiazide diuretic would have been advantageous. In the UK, a GP or hospital physician would simply stop the drug and observe and if failure occurred in resolution of the rash occurred, then further workup would be warranted.

Of course, consideration of HSP and Amyloidosis was appropriate and excluding these more serious pathologies was correct.

However, common things present commonly (drug side effects in this case) and the history was of salient importance. A common medical saying in the UK goes something like this "When you hear hooves think of horses rather than zebras."

Another case, was of an asymptomatic elderly female who was found to have a iron deficiency anaemia on her annual medical check. She had normal food intake and had not complained of malaena or urogenital tract haemorrhage.

She had a history of hypertension and amongst other drugs, she was taking aspirin. She was not taking any PPI therapy.

Her haemoglobin was 6g/dl with a low MCV of 69. Her iron levels were low with a high TIBC.

It was clear that the aspirin may have been causing asymptomatic gastritis or even peptic ulceration, which are known to occur painlessly in the elderly and which I have seen several times in the past. Moreover, she could have also had a malignancy or one of many causes of gastrointestinal bleeding. Having a negative rectal examination does not rule out chronic GI bleeding.

The resident had mistakenly overlooked stopping the aspirin when it was clearly a potential risk factor. There were more risks for continuing the aspirin than stopping it and hence, stopping the drug, either temporarily or permanently, would have been the best way forwards. That is not to say that aspirin was the actual cause of the problem, but with chronic haemorrhage, anti-platelet therapy can worsen the problem.

These two examples show that side-effects of drugs can be important even for very straight forward problems. It is important to recognise these problems and decide whether to stop drugs that can be harmful.

My advice would be to examine each and every drug on every patient you see to understand if the drug or drugs are causing the problem or at least contributing to it.

Reading about the side-effects and putting that knowledge into practise is essential.

Drug interactions are also important and carrying a software on package on a PDA e.g. epocrates (which is free www.epocrates.com) can help you decide whether there is a potential drug problem.

Please do not overlook drugs as just names on an admission sheet. Take time to look at them and the patient. It will make your workup of the patient more logical and easier to perform e.g. stopping a thiazide diuretic and observing, stopping the aspirin and arranging a gastroscopy and colonoscopy rather than performing a CT abdominal scan which might be premature or even unnecessary.

Please consider....:-)

UpDates in Diabetes Care with Potential Application To Japanese Medical Practise

The 2008 Guidelines for the Standards of Medical Care in Diabetes have been released by the American Diabetes Association.

I have endeavoured to summarize the important elements of the current ADA guidelines in addition to adding my opinion on their application to clinical practise in Japan plus any other recent evidence in support or contradicting these current guidelines to try and give an overall view of things.

Interestingly, the guidance refers to several interesting areas in particular which include:

1) HbA1c: aiming to get the HbA1c (DCCT-aligned value) as near to 7% is the goal with the aim to avoid hypoglycaemia. However, there is now the goal to get the HbA1c into the normal range if possible. The thought behind this is likely to maximise the advantage of avoiding the microscopic and macroscopic changes associated with diabetes. The HbA1c value that the ADA are advocating is to reduce it to less than 6%, if possible ,with the avoidance of hypoglycaemia.

This may of course be possible in proportionately more type 2 patients than type 1 patients as the severity of disease may be different and the former have relative insulin resistance rather than deficiency. The problem with attaining an HbA1c of <7%>

The downside to the application of such guidelines in Japan is the inability for type 2 patients taking oral hypoglycaemic agents to check their daily blood glucose levels because such monitoring therapy is not currently covered by the medical insurance system and therefore, patients are unable to know if their blood glucose levels are being well maintained on therapy or not. HbA1c measurement every 3 months is insufficient to really know if the patient is having good control. I say this because patients can have a seemingly good HbA1c result but still have frequent hypoglycaemic episodes and hyperglycaemic episodes alike.

Diabetes control can be imagined to be something like the climate and daily weather. The climate is the gradual change in temperature that beig like the HbA1c whereas the daily weather is the blood glucose level. We all know that one day there can be sun and the next there can be rain. The climate does not tell us what has happened on a day to day basis. Hence, measuring the HbA1c only tells us of an average of the glucose control over the last 2-3 months and particularly the last 1 month prior to testing. Therefore, in Japan, the clinic doctors need to ask particularly about hypoglycaemic episodes and encourage at least urine testing for glucose. However, if patients can afford to buy their own glucose monitoring kits and to manage their diabetes through empowerment and better understanding, then in my opinion, they should be encouraged to do so.

2) Carbohydrate monitoring: There is advice on carbohydrate counting and glycemic index which is of course part of the famous DAFNE thinking (Diabetes Adjustment for Normal Eating), which allows patients to adjust their insulin doses according to the amount of carbohydrate they consume. This is opposed to the traditional way of doing things where the person eats similar amounts of food every day and fixes their insulin doses. The latter can certainly work in those individuals who have a strict daily regimen, but is inflexible for young patients with hectic lives and who eat infrequently. I have seen such treatment used in the UK to good effect.

The usual regimen of insulin is the fast acting novorapid/humalog isulin for every time food is consumed and a long acting insulin at night to prevent hyperglycaemia e.g. detemir / glargine. However, such a carbohydrate monitoring regimen may not be possible in Japan because Lantus (glargine) was discontuned due to a problem of administration and as far as I am currently aware, detemir has yet to reach these shores. Hence, older regimens of longer acting insulins might be required instead e.g. insulatard, which have a shorter period of activity and can result in severe nocturnal hypoglycaemia.

Currently, some institutions are using mixed combinations of insulins e.g. novomix, three times a day with interesting results in HbA1c, in view of the lack of longer acting insulin availability, but this in my opinion, still does not provide the flexibility in insulin-food control that the DAFNE style of therapy can do. Moreover, I have yet to see any patient thus far being treated with combination of oral hypoglycaemic agent with insulin in Japan, which is standard practise in the USA and UK, with good results in HbA1c levels and reduced weight gain and lower amounts of insulin being required e.g. metformin with insulin.

3) Immunisation: The ADA guidelines suggests that all DM patients should be vaccinated for influenza on an annual basis of more than 6 months of age. Patients should also receive pneumococcal vaccination if more than 65 years of age. The pneumococcal vaccine is available in Japan and should be used in such high risk patients. I am aware though that stocks of the vaccine were previously low and hence, again, it may or may not be possible to administer such therapy depending on your local resources.

4) Lipid Management: Statin therapy should be added to lifestyle therapy (dieting and weight loss) REGARDLESS OF BASELINE LIPID LEVELS for diabetic patients:
i) with overt cardiovascular disease (CVD)
ii) without CVD who are over the age of 40 and have ONE or more CVD risk factors (e.g. hypertension, family history)

The above guidance is also in line with the International Diabetes Federation guidance (IDF) of 2005.

Statin therapy should be considered in patients with low risk if the LDL cholesterol remains > 100mg/dl or in those with multiple CVD risk factors. Aim for LDL cholesterol in those patients with low risk is less than 100mg/dl.
In patients with overt CVD, a lower LDL cholesterol level of less than 70mg/dl, using high dose statin, is an option.
In the event that LDL-cholesterol levels do not reach these targets, a reduction of LDL-cholesterol of about 40% from baseline is an alternative therapeutic goal.

5) Antiplatelet Agents:Aspirin should be used in patients with a history of CVD as secondary prevention. Aspirin should also be used as Primary prevention in type 1 or type 2 patients at increased cardiovascular risk including all patients over 40 years of age or who have additional risk factors (family history of CVD, hypertension, smoking, dyslipidemia, or albuminuria).

Aspirin is not recommended under 30 years of age due to lack of evidence of benefit in this age group and certainly not to those aged less than 21 years because of the risk of Reye's Syndrome.

Combination with other anti-platelet agents e.g. clopidogrel (Plavix) should be used in patients with severe and progressive CVD.

6) Glucose Goals: There are also guidelines for use of tight control in patients with severe illness. There have been previous trials of use of insulin in critical care patients and the overall outcome has been a benefit in survival. However, a recent German study using insulin in such patients saw a detriment in using tight insulin control.
However, when one reads the methods of the study, they measured blood glucose levels every 1-4 hours. This is a major downfall with the study leaving a potential cause for the increased mortality. In fact, when tight control is required in such patients, hourly blood sugars should be done, and a four hour delay is dangerous, in my opinion. This study was published in a famous journal and the monitoring delay, which I see as a flaw in the study design, was not addressed in the conclusions by the Authors, which is disappointing. I would not advocate a change to the current advice of tight control in critically ill patients unless there are future studies with more rigorous designs showing similar adverse outcomes.

There are many other areas of advice in the current ADA guidelines but are too much for today's blog. If you want to read more please go to Diabetes Care, Volume 31, Supplement 1, Jan 2008.

Probe Your Patients For History

Dear Bloggers

I have written about history and its importance many times on this blog and here is yet another example of why it is so important.

This case has been anonymised as usual to maintain patient confidentiality.

An elderly male was admitted into another hospital following a two-day history of chills, lower abdominal discomfort and frequency.

He had attended a local hospital in the vicinity and a UTI was diagnosed for which intravenous antibiotics were prescribed to be continued as an outpatient.

However, the chills continued and urinary incontinence occurred as a new problem prompting admission to another hospital.

At the current hospital it was elucidated that he had a long history of Benign Prostatic Hypertrophy. He had no recent sexual contacts and no change in bowel habit and no weight loss.

He otherwise had a history of ischaemic heart disease with an AMI several years before for which he had a Coronary Artery Bypass Graft (CABG), hyperlipidemia and hypertension. He had no known history of diabetes mellitus.

Medications included

• Aspirin
• Atorvastatin
• Amlodipine
• Medication for BPH (name unknown)

He was an ex-smoker and drank no alcohol. He was other wise normally fit and well.

When he was examined by the admitting resident, he was apyrexial and had normal vital sign. His cardiovascular, respiratory and abdominal examinations were within normal limits apart from evidence of a previous sternotomy scar for his CABG operation and a loud aortic systolic murmur. Rectal examination revealed a large smooth prostate which was non-tender.

Clinically the patient was admitted with a simple UTI secondary to obstruction to urinary outflow.

A catheter was inserted to drain the excess urine (residual volume unknown) and antibiotics were continued.

Up to this point, things seemed relatively straight forwards.

However, a Senior doctor reviewed the history, physical and lab data as things seemed not quite right.

There was no history about the severity of the urinary outflow symptoms. Moreover, the lab data revealed evidence of a raised CK of about 350 (normal CK-MB) and some mild renal impairment BUN 25, Creat 1.4. Previous blood tests several years ago also revealed a mildly raised HbA1c of 6.4% and a follow-up was normal.

The ECG had T wave inversion from V3-V6 inclusive and it had been initially considered to be old except when it was compared to a recent ECG within the last few weeks, and the current tracing showed NEW T wave inversion in V3 and V4 inclusive.

There was a high suspicion of an Acute MI. However, the resident clearly stated that the patient had not complained of any other problems.

The Senior doctor nevertheless went back to the bedside and asked the questions again. On this occasion, the patient had said that he had become breathless, with central heavy chest and leg pains, with him almost having lost consciousness. The pain was described in severity as 10/10 and lasted for up to 1 hour. There was no radiation to the neck, jaw, arms, back, or abdomen and no sweating or vomiting.

Asking about the urinary symptoms, the patient mentioned that he only passed very small amounts of urine, had frequency and felt he never had completely voided his urine in some time despite treatment for BPH.

Hence, from the history, it would appear that the patient was experiencing an Acute Coronary Syndrome several days prior to admission which might account for the new ischaemic ECG changes and raised CK.

Most people will now think, hey, the CK-MB was normal, so not an acute coronary syndrome! No! The serum levels of CK drop rapidly within 24-48 hours of an MI with other markers such as LDH and Troponin T remaining raised for much longer periods, the latter for up to 10 days post-infarct. Hence, it is of no surprise that the CK-MB fraction might be normal at the time of presentation to hospital.

In view of the previously raised HbA1c, it is also plausible that the patient had undiagnosed diabetes. In fact, the American Diabetes Association states that HbA1c should not be used to diagnose diabetes as a significant number of people even with normal HbA1c can still have diabetes-- it is not a fool proof test for diagnosing diabetes.

Also, having DM might also put the patient at increased risk for development of a UTI on a background of urinary outflow obstruction.

On examination the patient indeed had a loud Aortic Ejection systolic murmur with radiation to the carotid arteries in addition to left renal angle tenderness on bimanual palpation.

PROBLEM LIST

1) Outflow obstruction from BPH
2) UTI due to 1 above with complication of pyelonephritis
3) Likely Acute Coronary Syndrome ? Aortic Stenosis
4) Possible undiagnosed Type 2 DM

SUGGESTION

The senior doctor suggested the following;

• Obtain Troponin-T level
• Add Clopidogrel ( this is advocated for use in NSTEMI and was proven to be more effective when combined with aspirin than just aspirin alone in the CURE trial; a newer analogue is being trialled at present in the USA with even better anti-platelet effects when combined with aspirin)
• Increase the Statin dose (a recent meta-analysis of 14 Statin trials in Lancet 2008 has suggested that benefit from statin therapy occurs in diabetic and non-diabetic patients to the same level with the most benefit derived from patients with high LDL-cholesterol levels; however, all patients benefit with cholesterol lowering therapy independent of starting level of cholesterol. The meta-analysis suggests that for every reduction of 1mmol/L LDL-cholesterol there is a 20% reduction in cardiovascular events. Moreover, there is no lower level of cholesterol which to attain. The ADA guidelines of 2008 suggest that statin dose should be used to the maximum tolerated dose to reduce cholsterol as low a possible e.g. below 70mg/dl in patients with known cardiovascular disease.
  
• In Japan, I have often heard doctors stating that the cholesterol has reached normal levels or is normal to start with, and that they do not need to start or increase the statin dose despite the patient having had a new coronary event with them being at high risk. The international medical data and current guidelines suggests that a normal cholesterol can still be a risk, and hence, statins should be commenced or increased in 'at risk' patients. Moreover, use of statins is an acute treatment in AMI and not only helps to stabilise atherosclerotic plaques, there is also some data that it can increase the success rate of delayed PCI therapy.
• Consider switching the calcium-channel blocker (amlodipine) to a beta-blocker. The thought behind this was, firstly, the blood pressure systolic value was about 100mmHg and further anti-hypertensive therapy on top of the calcium blocker might result in hypotension and cause worsening angina. Moreover, the pulse rate was about 80 per minute. This is not ideal in patients with ischaemic heart disease. Use of beta-blockers reduced heart rate (improving blood flow time) and vasodilates the coronary arteries. They also have the effect of reducing ventricular rupture and can treat dysrrhythmias unlike a peripherally acting calcium blocker that has little chronotropic effect. A beta-blocker with both alpha and beta effects might also be useful in that it might help with the prostatic hypertrophy too.
• Obtain an echocardiogram
• Discuss with the cardiologists about a coronary angiogram
• Discuss with the urologists about a long term catheter or an operation (TURP); but to remember that an immediate operation would be contra-indicated in light of a possible ACS.
• Screen patient for diabetes with fasting blood sugar and perform an oral glucose tolerance test (the Gold Standard test for diagnosing DM).

Additional Results

The Troponin was positive at 0.72 thereby confirming an Acute Coronary Syndrome in this patient and this therefore was a contra-indication to any planned urological interventional surgery that might have been considered.

Indeed, the echocardiogram confirmed a good systolic wall motion. However, it also revealed an Aortic Valve gradient of 0.6cm2, and a maximum ejection pressure of 78mmHg with an average of 49mmHg consistent with Severe Aortic Stenosis.

It is usual for testing of DM to be performed several weeks after an AMI, unless the hyperglycaemia is obviously present and with DM then easy to diagnose, because of the phenomenon of stress hyperglycaemia. As AMI is a strong stressor, hyperglycaemia can occur but when patients recover, a significant number return to normoglycaemia in the post-infarct period.

Summary

In this case, the patient had symptoms of an obstructive uropathy with infection. The admitting medical doctors had failed to obtain a thorough history of ischaemic heart disease despite a previous history of the problem and with the patient having had a CABG. Moreover, the ECG and raised CK had not been fully appreciated.
With a thorough history retaken at the bedside with focused questions to rule in or rule out ischaemic chest pain, it was possible to elicit salient information from the patient to thereby determine that there was a likely ACS.
Indeed, with a positive Troponin T and with severe aortic stenosis being found, it is likely that the stress from the infection resulted in coronary ischaemia by means of cardiac outflow obstruction and atherosclerosis as the demand for increased blood flow could not be met.

In patients >70 years of age, the usual cause of AS is due to atherosclerotic-like changes of the tri-leaflet valve itself. Many features affecting the valve are similar to atherosclerosis but use of statin therapy does not reverse the changes, which can otherwise occur with atherosclerotic plaques in main blood vessels. Moreover, analysis of excised valves can also show bone and cartilage formation too !!
In the younger age group <70>40mmHg is consistent with severe AS (please see UpToDate 15.3).

Patients with severe aortic stenosis tend to suffer with the following problems:

1. Ischaemic chest pain e.g. angina, AMI
2. Syncope / Dizziness e.g. fall in cardiac output under stress
3. Heart Failure, as an end-stage complication

This patient had already suffered the first two symptoms in addition to echocardiographic proof of severe AS. In view that the patient was otherwise in good health, he was referred to the cardiothoracic surgeons for workup of an aortic valve replacement.

In view of the patient's advanced age and the antecedent risks of anticoagulation with mechanical valves, it was felt that a bioprosthetic valve would best suit this patient and he underwent successful valve replacement.

Moral Of The Story

The moral of this story is, don't ignore ECG changes and always compare ECGs to old ones for new changes when possible.
Never accept a raised Creatinine Kinase (CK) as trivial and always try to elicit a cardiac history in such circumstances especially when there is a previous history of such problems. Even if there is no obvious history but the suspicion of an acute coronary syndrome is high, a Troponin T should be always measured (at a minimum of 6-12 hours after the onset of any cardiac sounding chest pain).
I am afraid that using CK-MB to rule out MI is simply too unreliable and if you just use this, you WILL MISS Acute Coronary Syndromes. Troponin-T is cardiac specific but moreover, it is more sensitive a test than CK-MB and remains elevated for longer than CK.

In the presence of an aortic systolic murmur, dizziness, ischaemic chest pain, and new ECG changes consistent with an ACS, severe aortic stenosis should be considered, as it was in this case.

Hence, an apparent simple UTI turned out to be a blessing in disguise for this patient because a life-threatening cardiac condition was identified, investigated and effectively treated.

Lastly, do not expect your patients to simply tell you every aspect of their history and health. Many patients forget things and do not think unrelated events are important. It is up to you as doctors to ask the questions. The questions can be asked as part of a Body Systems Review which I have discussed at length on this blog already. For information on the Body Systems Review, please search under this topic at the top of this blog page. I would also recommend the book 'The Patient History- Evidence Based Approach' by Professor Lawrence Tierney, Lange Publishers.

Please consider....

A Benkyokai Bonanza

Dear Bloggers

Yesterday afternoon saw two acclaimed speakers attend our institution to teach the residents their wisdom.

Firstly, Professor Alan Lefor, Professor of Surgery, Jichi University presented talks on Trauma followed by Surgical Site Infections.



Professor Lefor's strident and direct approach were refreshing and it was interesting to see evidence based practise at work.

There was the presentation of several cases from the United States which showed trauma surgery at work.

There was emphasis on ATLS, including the elements of ABC, reassessment, D, E an so on.

The residents were very receptive to this different approach to teaching.

The talk on Surgical Site Infections presented the current evidence for use of antibiotics, warming the patient, not shaving patients, etc...

The two-hour set of talks were very interesting and Professor Lefor's talks are certainly well worth it!

Next was Dr Kitahara of Keio University who is also American trained with specialist interests in Infection and Haematology.

He was presented several difficult and unusual cases by the Department of General Internal Medicine and it was interesting to hear his view on the cases.



All in all, the two speakers provided an excellent opportunity for the residents of our institution to get up-to-date training on both surgery and medicine alike.

It was a really good day of teaching and it was enjoyed by the residents and myself alike.

TropT or Not To Be- That is the Question

Dear Bloggers

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

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

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

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

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

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

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

Family and social history were unknown.

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

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

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

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

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

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

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

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

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

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

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

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

IMPRESSION

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

Moral Of The Story

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

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

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

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

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

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

Have a great weekend !!!

Should Medicine Become Protocol Driven??

Dear Bloggers

What are medical protocols and should we be using them?

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

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

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

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

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

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

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

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

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

Please consider... :-)