Answer To Recent Case

Dear Bloggers

Here are the answers to the recent case.

Question 1: Taking into account the history and examination what other feature from the CBC do you think is abnormal in this case?

The other abnormal feature is the platelet count. In fact, she had only 3,000 per microlitre of platelets hence, Severe thrombocytopaenia. Her WBC count was normal, as was her haemoglobin and other coagulation studies.

Question 2: Why are her legs most affected and what is likely to be the likely diagnosis ?

Her legs were most affected because of the effect of gravity and venous pooling. The blood being under a column of pressure and with low platelets resulted in severe petechial haemorrhage.

In view of the recent infection, and no other sinister findings being found on examination such as lymphadenopathy, the suspected diagnosis was a viral induced thrombocytopaenia. ITP was also considered strongly in view of the patient's presentation, her female gender, a normal sized spleen and absence of other symptoms.

Of course, malignancy e.g. MDS, leukaemia, other autoimmune diseases e.g. SLE, were considered, but in view of an otherwise normal blood differential and no other features consistent with these pathologies, they were not really considered to be likely as the cause.

Question 3: Why might the BUN be raised?

The BUN may have been raised because of asymptomatic gastric haemorrhage.

Question 4: Would you admit this patient into hospital even though she feels well or would you let her go home?

This patient is high risk for parenchymal haemorrhage. Initially, low platelets results in cutaneous petechiae. If the platelet count worsens, then mucosal bleeding occurs. At this point, one should be highly suspicious of potential severe bleeding ensuing e.g. intracranial haemorrhage, GI bleeding.

Hence, the patient should not be sent home and should be admitted to hospital for investigation and prompt treatment.

Question 5: What other tests would you like to perform?

• The patient should have viral titres taken e.g. Adenovirus, Parvo Virus, Hep C, CMV, EBV, Mumps, Rubella Autoimmune profile e.g. Anti-DS DNA, ANA Abs for SLE
• Blood smear to look for abnormal cell morphology
• Anti-platelet antibodies (if available)
• Bone Marrow Examination-- essential to aid in the diagnosis
• Ultrasound of the abdomen to look for splenomegaly
• Ultrasound of the knee to look for haemarthrosis-- aspiration is not safe with profoundly low platelet counts.
• Rectal examination for occult bleeding (easy to do and often avoided!!)
  
• Gastroscopy and colonoscopy
  
• Treatment here would be to transfuse platelets and treat the underlying cause (if known)

The bone marrow examination revealed: increased numbers of megakaryocytes of normal morphology. There was also a slight increase in the erythroid precursors.

The serology revealed: a normal panel autoimmune profile e.g. normal levels of ANA.

Her viral serology showed past infection with CMV and EBV and Parvovirus and HCV were negative. Other viral serology was unfortunately no performed.

Abdominal ultrasound revealed a normal spleen.

Anti-platelet antibodies were positive with a level of 75 (normal <5).

Hence, in view of the clinical history, physical examination, the bone marrow examination and positive anti-platelet antibodies, it was considered that the diagnosis was:

Immune Thrombocytopaenic Purpura.

She received prednisolone at a dose of 1mg/kg/day -- 50mg in total, and her platelet count increased to 30,000 within 3 days with no new bleeding problems. However, despite high dose steroids, the platelet count did not increase much beyond this level thereby prompting the use of other treatment modalities (see description and treatment of ITP below)

Here is a most excellent response from Professor Masami Matsumura of Kanazawa University School of Medicine with his opinion on the case.

This is interesting case for approaching the diagnosis.

ID/CC: 50-year-old woman with a diffuse skin eruption

Problem list:

1. Episodes of URTI
2. Diffuse skin eruption, suspect petechiae
3. Oral mucosal bleeding
4. Left knee acute monoarthritis without trauma history
5. Oedema of both ankles
6. Mildly raised BUN (20.1)
7. Mild monocytosis
8. Mildly raised CRP

Assessment:

After episodes of URTI, she had left knee acute monoarthritis, diffuse skin eruption, and oral mucosal bleeding. These issues are consistent with Immune Thrombocytopenic Purpura (ITP). Another differential diagnosis is Henoch-Schonlein purpura. Acute polyarthritis is observed in this disorder. However, oral mucosal bleeding is not observed in Henoch-Schonlein purpura. Moreover, palpable purpura is characteristic of this disease. I think ITP is most likely in this case.

Another differential diagnoses are follows:

• Hematologic malignancies including CLL
• MDS
• SLE
• Viral infection including hepatitis C and HIV
• Evans’s syndrome

Question 1: Taking into account the history and examination what other feature from the CBC do you think is abnormal in this case?

This patient has mucosal bleeding. I think her platelet count is under 10,000/m(micro)L.

Question 2: Why are her legs most affected and what is likely to be the likely diagnosis ?

Her physical examination revealed acute monoarthritis in left knee. When we see acute monoarthritis, Gout, Pseudogout, Infectious arthritis, Bleeding, and Trauma (PIG TB is my mnemonics) must be differentiated. She denied trauma episode. Bleeding is most likely in this case.

Question 3: Why might the BUN be raised?

I suspect GI tract bleeding. GI tract bleeding can cause elevated BUN.

Question 4: Would you admit this patient into hospital even though she feels well or would you let her go home?

This patient must be admitted into hospital for close examination and treatment!!

Question 5: What other tests would you like to perform?

• Fundoscopy for examination retinal bleeding
• Peripheral blood cell morphology for detecting large platelets
• Coagulation studies including PT and APTT
• ANA, HCV antibody assay
• Abdominal echo for evaluate spleen size
• Bone marrow aspiration

An anonymous response was received as follows:

1.? Platelets>low; stool occult blood +
2. Henoch Schoelein, Behcet [pathergy from your History], Parvo 19, R/O DVT, anti-phospholipid syndrome
3. ^ BUN from GI bleed
4. In Japan, admit; in North America follow-up in clinic
5. Skin Bx, Fiber Colon/gastro filber if stool blood +; L knee OA

Immune Thrombocytopenic Purpura (ITP)

This is a bleeding disorder resulting from low platelets not associated with another systemic disease. For the diagnosis to be made, other disorders should be excluded through other tests. Autoantibodies are usually produced against the platelet resulting in the low platelet level. In children, a viral infection can also result in ITP.

The spleen is usually normal size except if there is co-existent viral infection.

The symptoms and signs are of petechiae and mucosal bleeding e.g. in the mouth, GI tract etc. Examination of the blood reveals an isolated reduction in platelets but an other normal morphology and differential of white cells and red levels.

Bone Marrow examination reveals normal or increased numbers of megakaryocytes with other bone marrow elements being normal. Other pathologies should be excluded as described above and HIV testing should be performed in those individuals considered to be at risk because this infection can appear in an identical way to ITP.

Treatment consists of corticosteroids e.g. Prednisolone 1mg/kg/day. In those patients who respond to treatment, the platelet count should increase to normal in 2-6 weeks. The steroid dose is then tapered accordingly. In patients who do not respond to treatment and in who have a high risk of haemorrhage, splenectomy is considered.

Other immunomodulatory treatments are sometimes used such as immune globulin transfusions, cyclophosphamide, azathioprine and the anti-CD20 antibody (Rituximab).


Many thanks for all those doctors who contributed to give their opinions on this case.

There will be more great cases coming....stay tuned!!! :-)

A Case For You To Answer

Dear Bloggers

This case was provided to me by another physician and it has been anonymised for purposes of confidentiality.

A 50 year old female was seen in another hospital's out patient clinic because of a diffuse skin eruption.

She had been mildly unwell for 2 months with symptoms of an upper respiratory tract infection, the symptoms that included sore throat, mild fever, chills and nasal congestion. He was initially seen and given acetaminophen and multivitamins. Her throat examination at that time was red but with no exudate. No antibiotics were prescribed. No throat swabs were taken.

Her symptoms initially improved but there was a recrudescence of the same symptoms prompting a return to the hospital outpatient clinic. Again, medications for control of symptoms were prescribed and no antibiotics.

Two weeks before her current presentation, the URTI symptoms had completely resolved and she was feeling otherwise well.

However, after several days, her left knee began to hurt and she found it difficult to walk properly. There was no apparent swelling of the joint or preceding injury as mentioned by the patient.

A reddish-blue eruption began to emerge on her arms, legs and trunk. The eruption was composed of apparently very small areas of haemorrhage which were non-blanching and over approx 1-2m in diameter. The worse affected areas were her lower limbs. She also described other areas erupting after scratching her skin.

She denied visual disturbance, headaches, rectal bleeding or haematuria. Her other joints were non-painful.

She had described noticing blood in her mouth when cleaning her teeth and recent nose bleeds when blowing her nose hard several days before admission.

Previous medical history was nothing in particular apart from seasonal rhinitis.

She was taking no medications

She had no relevant family history and was a non-drinker and non-smoker.

On further questioning, she had no weight loss, a good appetite, no night sweats. No abdominal pains or other GI symptoms. In fact, she was otherwise feeling well.

On examination

Temp 36 C, Pulse 80 regular, BP 120/80, RR- 12, Sats 98% on RA. No Jaundice, Anaemia, Clubbing, Cyanosis, or Lymphadenopathy (JACCL)

She looked well but had a diffuse rash (as described above). Mouth- blue-black raised vesicle on the right lateral border of the tongue and on the buccal mucosa bilaterally. Elevation of the tongue revealed fresh blood in the lateral gutter at the junction of the floor of the mouth and the medial aspect of the gums.

CVS: JVP not raised. Heart sounds were normal. No evidence of DVT.

RESP: Percussion resonant, breath sounds vesicular.

ABDO: Soft, non-tender, no hepatosplenomegally. No ascites. Bowel sounds increased. Rectal examination not performed.

Left knee- mildly swollen. Not warm or tender. Bruising over infra-patella region. No patella tap. Crepitus on extending knee joint.

Oedema of both ankles.

Initial screening bloods were entirely normal except for a mild monocytosis, mildly raised CRP and BUN (20.1) but normal creatinine PLUS one other feature.

Question 1: Taking into account the history and examination what other feature from the CBC do you think is abnormal in this case?

Question 2: Why are her legs most affected and what is likely to be the likely diagnosis ?

Question 3: Why might the BUN be raised?

Question 4: Would you admit this patient into hospital even though she feels well or would you let her go home?

Question 5: What other tests would you like to perform?

PLEASE SEND IN YOUR ANSWERS BY POSTING THEM ON THIS BLOG ANONYMOUSLY AND THE CASE RESULT WILL BE AVAILABLE IN THE NEAR FUTURE.

Clinical Skills

Dear Bloggers

Now is the season when medical students visit various hospitals around Japan for a 3-day period to see what each institution has to offer for the purposes of future training in the respective residency programmes.

In Japan, most medical students do not have any clinical 'hands on' experience until the beginning of the 4th or 5th year of medical school.

From my previous interactions with several students and residents at different institutions, the general consensus is that the teaching of clinical skills at university is not optimal for what they need to examine patients. Of course, some medical schools have many sessions for teaching on real patients and there is the newly introduced OSCE system to ensure that there is a basic minimum standard. Hence, training can be variable depending on the institution in question.

Some UK medical schools have the medical students learning clinical skills from their very first year by placing them with a community general practitioner who can select for them well patients with chronic illness, who attend the clinic to have their history taken in full in addition to examination by the student. The general practitioner then listens to the history and demonstrates the examination to reinforce good practical skills and to advise on additional history which can help to make a bedside diagnosis.

My medical school was one of the first to do this in the UK and that was nearly two decades ago.

Although the basic knowledge of medicine was still to be learnt, by intercalating the learning from each system, over time it was then possible to gain deeper understanding plus having the background knowledge of how to examine for signs.

Hence, when it comes to the official clinical years, which start from the third or fourth year in the UK system, the medical student already knows the basics such as percussion, auscaultation etc...

One method that is very informative is the ward round system and listening to the consultants taking extra history and examining the patient. The UK medical system is somewhat adversarial in its way towards medical students because invariably they get picked on to be asked the various causes of XYZ disease or how to examine for ABC sign. Although this can sometimes be a stressful process, it forces the medical student to read about the patients they see. Moreover, the consultants invariably ask the medical students again at various stages of their attachment to a firm. Knowing the answer shows that medical student has taken the time to find out what the consultant wants to know.

By joining ward rounds and seeing the patients 'hands on' is the best way to learn clinical skills rather than just from a book in the class room. Patients do not write the books and there can be any number of possible combinations of acute and chronic diseases to provide a challenge to the doctor. This cannot be found in detail to any great extent in a book.

To really understand clinical medicine, you have to do clinical medicine.

Although these 3-day snap shot visits by medical students provide a mere glimpse of how hospital life operates, it is in my opinion, insufficient to learn new clinical skills.

At this hospital, there is the opportunity to do short term externships of several weeks to a month whereby the medical student can be exposed to the daily rigors of clinical medicine and how to treat the common acute problems and the difference of how to treat chronic diseases.

They get the opportunity to take histories from patients and to learn clinical examination in depth.

Such students who have done this in the past with me have learned a lot and their experiences have been very positive.

If you are interested in such an externship at this institution, then please contact me at the email address at the bottom of the blog page.

The Breast Examination

Dear Bloggers

I am a general medicine physician, not a surgeon, but it is essential to still know how to do a breast examination.

Although there are time constraints in the very busy Japanese outpatient clinics or ER departments, patients should nevertheless be asked if they have any breast problems and whether they check their breasts by themselves.

Moreover, if a female patient presents with chest pain, bone pain e.g. back pain, pneumonia or even an ovarian mass, the breasts should be examined.

There seems to be an aversion to performing breast examination especially by male junior doctors because of the age difference or even age similarity between the doctor and the patient. This should however, not prevent breast examination being performed, as it is the patient's health that is most important and not how the doctor feels. However, there are ways to make the breast examination less stressful to perform such as providing privacy by ensuring the curtains are pulled around the bedside or across the clinic examination area. Staff should be informed not to open the curtains when coming in, if indeed they actually need to come in! In fact, limit the number of people allowed to enter during the examination unless the patient has given permission. Ensure you have a nurse chaperone and that your hands are warm! Ensure that the patient is covered over whenever you are called away and when you finish the examination.

Any patient who requires a breast examination, as a doctor, you should ALWAYS take a female nurse chaperone with you so that they can observe that the examination is done correctly and that the patient and the doctor have a witness for legal purposes. Never do an examination unaccompanied.

When you eventually write your hospital notes, write down the name of the nurse chaperone as well so that you have a record of who was in attendance-- again for legal purposes.

So, how is the breast examination done?

Well, it is relatively straight forwards. First of all, GET PERMISSION FROM THE PATIENT !! You then expose the anterior chest to expose both breasts for means of comparison. Look at the skin to see if there is tethering and the classical 'peau d'orange'-- the peel of an orange, which can be a presentation of Ca breast. Look to see if there is nipple retraction. Ask the patient if the retraction, if found, is new or long standing. Some patients have naturally occurring nipple retraction, but if new, it is an ominous sign of potential malignancy.

Look at the skin colour, does the breast look inflamed? Some malignancies spreading in the surface of the breast can give a red inflamed appearance although the differential diagnosis would be an infective mastitis or even radiation exposure if there was a previous history of breast or lung cancer that had required radiotherapy.

Next, begin the palpation in the outer quadrant of the breast where the axillary tail exists. A significant number of cancers can present in this outer quadrant and can be missed by the inexperienced doctor. Palpate with both hands in each quadrant to see if the breast tissue is uniform and whether it is firm or soft. Feel to see if the breast tissue is mobile, which is normal, or fixed, the latter which is again, another sign of potential malignancy. Ask the patient if the examination is painful or not. Remember, that breast tissue changes according to the menstrual cycle with changes in female hormone levels, so tenderness may vary.

Next examine the nipple area for discharge by gently squeezing the base of the nipple. Discharge of sanguinous fluid is again another ominous sign and should alert the doctor of potential malignancy. Mucinous discharge may also be of significance.

Next, examine the axillary and cervical lymph nodes for size, consistency and mobility.

Look at the upper limbs to determine if there is any swelling of either arm and any dilatation of the veins on the arm and upper chest. Some advanced tumours can cause subclavian-axillary vein thrombosis which is a serious complication. If advanced malignancy is found, listen to the chest, palpate the bones if the patient complains of bony tenderness, perform a neurological examination e.g. brain metastases, acute cord compression, and feel the liver and other abdominal and pelvic organs. Remember that Ca breast can spread to the ovaries producing the infamous Krukenberg tumour.

If you do find anything abnormal on examination, consider asking for a surgical consultation, as such masses usually require ultrasound examination and needle aspiration or biopsy examination.

Consider checking a chest xray, and other relevant radiology depending on the examination findings plus the alkaline phosphatase, calcium and liver enzymes.

If you do not ask patients if they have breast problems then you may miss a potentially treatable problem. Some patients will not offer up that they have a breast problem unless asked. A recent patient at another hospital presented to the doctors with a breast mass that had been evolving over several years. She had not disclosed the problem to anyone and unfortunately, the malignancy was already producing end-stage problems, and hence, a curative procedure was not possible.

Just as junior doctors are not inclined to perform rectal or genital examinations, along with these, you should encourage your self to also perform breast examination whenever clinically justified because it is a part of the general physical examination that is unfortunately all to often ignored because of embarassment.

Please consider.....

Atrial Fibrillation and its Management-- the hard facts

I have talked of Atrial Fibrillation (AF) on this blog in the past, but today I think it is helpful to revisit this common disorder to discuss the correct management.

The causes of AF are well documented and I do not intend to go into any depth here, but common things being common, infection, valvular disease, ischaemic heart disease, heart failure, pulmonary embolism, thyrotoxicosis and electrolyte disturbance are what are considered the main causes.

Although treating the underlying condition may eventually ameliorate or resolve the AF e.g. Thyrotoxicosis treatment, the acute AF at the time of its presentation should be treated.

Why should AF be treated at all?

Well, AF causes disordered and rapid ventricular contraction and as a result there can be a loss of 10-20% of cardiac output (CO). In fact, this can worsened yet further in the elderly with as much as a 40% drop in CO thereby precipitating heart failure.

Moreover, studies have shown that there is a 2 x increased mortality overall from AF.

The presence of AF, especially in the elderly, can precipitate Heart Failure and ironically, heart failure can also cause AF ! It is the Chicken and the Egg phenomenon.

Fast AF can also result in rate related ischaemia and patients can develop acute coronary syndrome with rise in Troponin T, the most sensitive of the current cardiac biomarkers. I have seen this occur in many British patients.

The reduction in CO can also result in hypotension and cause patients to collapse.

Of equal importance, AF can result in thromboembolism and vascular occlusion e.g. Limb ischaemia, stroke, renal infarction.

Hence, whereas in the past AF was looked upon as some inconvenience for the patient but an otherwise benign condition, it is now recognised to be a serious cardiac disorder that requires immediate treatment.

The American Heart Association and European Resuscitation Council Guidelines ALL advocate immediate treatment for

• Control of rhythm / rate
• Anticoagulation

especially if the patient is unstable e.g. developing heart failure (please see European Guidelines above).

Moreover, AF should not just be assumed to be as a result of, for example, infection, without ruling out the other common causes e.g. MI, thyrotoxicosis, heart failure, electrolyte disturbances.

Treatment

If the patient is haemodynamically unstable (i.e. hypotensive) because of the Fast AF, then these patients should receive electrical cardioversion unless contraindicated e.g. Unfit for anaesthesia.

Haemodynamically stable patients should be treated with either rate control or rhythm control therapy although this depends on what you as physicians wish to achieve for your patients in the long term. There has been shown to be no difference in outcome between rate control or rhythm control, and in the vast majority of patients, rate control may be easier to achieve in the long term than hoping to maintain sinus rhythm.

For example, a young patient with no structural heart problem with onset of AF (Lone AF) e.g. caused by alcohol, has a greater chance of being reverted to sinus rhythm than for an old patient who may for example, have ischaemic heart disease or enlarged atria. Hence, rhythm control by chemical cardioversion, or even electrical cardioversion either within 48 hours of onset of the AF or at 4-6 weeks after combined chemical cardiovertor therapy e.g. Oral amiodarine, plus anticoagulation with warfarin can be used.

If your goal is for rate control e.g. In the elderly patient with congestive heart failure, then treatment will differ in that drugs for rate control rather than rhythm control can be used e.g. Beta blockers, digoxin, diltiazem. However, in the elderly the choice of the best drug to treat AF is also determined knowing whether the patient has heart failure, liver failure or renal failure.

In severe heart failure calcium channel blockers e.g. Verapamil can worsen CHF by reducing cardiac muscle contractility and should be avoided in patient with a low ejection fraction e.g. 40%, whereas drugs such as digoxin and amiodarone do not deterimentally affect myocardial function.

However, in liver disease, long term amiodarone therapy may cause worsening liver function.

In renal failure, digoxin levels can rise and cause toxicity which includes nausea, vomiting, colour vision changes and profound bradycardia. Digoxin toxicity can also be made worse by hypokalaemia and hence, patients need levels of digoxin performed plus monitoring of potassium. Often patients are also using diuretics that can cause hypokalaemia and hence, polypharmacy and drug interactions should always be borne in mind when prescribing such drugs.

Thus, drug therapy for AF requires a knowledge not only of the the indications and pharmacotherapeutic effects but also of the side effects and hence, the contraindications.

So, in summary, fast AF should always be treated actively.

Rate control and rhythm control have a similar overall outcome and hence, the only choice between such therapies lies in symptom control, as restoring sinus rhythm is associated with less symptomatology.

Treatment of AF consists of either electrocardioversion, or pharmacological treatment. Pharmacological therapy consists of rhythm controlling or rate controlling agents.

Anticoagulation should be commenced acutely with heparin and then converted to warfarin. Lone AF, where a structurally normal heart exists in a patient <60>

Paroxysmal AF has the same risk for thromboembolism as continuous AF and hence, anticoagulation should be provided.

Using asprin instead of warfarin is associated with a higher thromboembolic risk but this is better than no anticoagulation at all. It may sometimes be better to use aspirin in the falling elderly patient with AF instead of warfarin because there is a potential risk of head injury and hence, subdural haemorrhage. Basically, it is a trade off between reducing severe bleeding complications but achieving some form of anticoagulation.

If possible, discuss the pros and cons with the patient; they should be given the choice rather than the doctor being paternalistic and choosing for them, as anticoagulation with its many benefits does not make the patient feel better, but can cause life threatening bleeding. Remember, it is their life and they should be involved in making decisions that may affect their health.

Please refer to any of the famous texts such as Harrison's, Merck Manual, UpToDate, and of course to the American Heart Association and European Resuscitation Guidelines (above) for a more in-depth discussion of AF.

Please consider...

Professor Stein-- is back!

Dear Bloggers

Last week saw the return to our hospital of Professor Stein from Florida, USA.

Prof Stein spent 3 days going through daily cases and teaching the internal medicine residents with particular focus on history taking in order to consider the diagnosis before seeing the patients at the bedside.



Various cases were presented including a recent case of Tetanus, Miliary TB, Castleman's Disease and psoas abscesses with additional vertebral infection.

There was the excellent chance of a combined meeting with Prof Stein, the US Navy Hospital from Yokosuka and our institution. This meeting generated direct and frank discussion of the cases, the likely causes and the management.

In all, the 3 day whirlwind tour was an excellent opportunity for the residents to present their cases to a distinguished Professor of Medicine in English and to hear his words of wisdom.

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...