30 July 2011 (Saturday) - Portfolio Verification

Following on from yesterday’s pre-registration portfolio verification, I’ve tweaked my website of advice. Specifically the link on the bottom left hand side “On the assessment day”.

I was thinking of adding a line “Verifiers are a mixed bag – some are overly obsequious, some are total bastards, and most are somewhere in between”, but I’m not sure this is exactly the wording I want….

29 July 2011 (Friday) - Portfolio Success

Today was rather successful at work: another of my trainees had a successful pre-registration portfolio verification.
That’s six that have passed in the last year, and twelve pre registration portfolio successes altogether. When you bear in mind the ten students who qualified via the old “Blue Book route”, that’s been quite a few trainees over the years. And today’s twenty-second was every bit as nerve wracking for me as the first was (all those years ago).

Did I get anything from today – did I learn anything? Yes: I wasn’t impressed with the examiner.
When I verify a portfolio I arrive at the candidate’s lab at 9am. And if that lab is a long way away, then I get up early. I’ve done some assessments which have had me on trains before 6am before. Today’s verifier came from London (which is forty minutes on the high speed train) and didn’t get to us until 11.30am.
He was pleasant enough on the verification process, but when delivering his verdict to us he seemed to delight in dragging out what he had to say; slowly going through pages of his report, word for word. When I’m verifying I tell them pass or fail straight away. (I did fail one student once…)
And I don’t think the bloke’s grasp of conversational English was quite what it might have been.

I might need to add some more suggestions for the link entitled “On the assessment day” over on my website of advice.

26 July 2011 (Tuesday) - E.Q.A.

I’ve been asked to take over overseeing the haematology EQA work for the Trust (as well as doing all my other stuff). It should be interesting, and I spent this morning seeing what I will actually be taking on. It looks straight forward in principle: take everyone else’s EQA returns, look at the D.I.s and mark them “Good”, “Adequate” or “Poor “ accordingly.
If I can be given some dedicated time to do the job I think I’ll enjoy doing it.

There are several areas I can see I’d like to make immediate changes. Actually getting the results in the first place. I’m told this can be problematic. I don’t see why this should be so – all I need is a few passwords and I can access the data directly from NEQAS themselves.
I suspect chiefs might be a tad reluctant to let me have passwords. We shall see…

I’m also not happy on marking a blood count as “Good”, “Adequate” or “Poor “. Given that two parameters have D.I. over two, then we have a “Poor “, as oppose to only one D.I. being over two and less than three which is classed as “Adequate”. However a red cell count or a haemoglobin or an MCV being slightly squafty could make the MCH and MCHC squafty (since they are calculated parameters) and so we’d get a ““Poor “ where really we should get the better result of “Adequate”.
Similarly coagulation investigations and haematinic assays are lumped together. I’d much rather scrutinise each measured analyte. It might be more work for me to do, but I can’t help but feel that technically it’s a much better thing to do.
I’ll squabble this one with the Head BMS and the boss consultant…

Coming on from that, despite having a degree in mathematics, I’m still rather vague about what a D.I. actually is. After six years of mathematical study I’ve only ever encountered D.I. on an NEQAS return.
I shall email NEQAS to ask them…

And it had to be said that I will need to seriously reflect on how I mark the blood film morphology. It’s easy to mark numeric assays – you can’t argue with a number. And the blood transfusion EQA already comes with (effectively) “Good”, “Adequate” or “Poor “ already. But the morphology is far more open to interpretation.
For example take a case of a megaloblastic anaemia. We are only asked to report the five most salient features. In fact we can only report five – there is no more space on the return form for more. Given the presence of right shifted neutrophils, Howell Jolly bodies, reduced platelet count, megaloblasts, anisocytosis and poikilocytosis, which one would you choose not to report? Because they would all be there, and whichever one you left off the report, you’d be criticised for missing something.
I shall discuss this with those who scrutinise blood films in the first instance…

25 July 2011 (Monday) - Cryptic Malaria

Usually the source of a malarial infestation is patently obvious. Occassionally it’s not so obvious. I found a link that gave some possible sources of malaria that might not be quite so readily apparent.

“Runway” Malaria

A plane stopping over in a malarious country might only stop for refuelling, but that delay might be enough for an infected mosquito to get aboard. Similarly there may well be infected mosquotos on a plane which, although travelling between “safe” airports, has relatively recently been in a malarious zone.
Or a patient might not realise that his holiday destination was a malarious one.

Or the unfortunate patient might never have actually been near a plane – a mosquito might be brought home in baggage and then infect someone on arrival at home.

“Late onset”

The onset of symptoms of malaria might take some time. Some eight per cent of ovale and vivax cases don’t become apparent for up to a year after patients returning home.
There would seem to be some connection with various ethnic groups and also with haemoglobinopathies in the delay of malarial symptoms.

“Person to Person contact”

Incredibly rare, but there is suspicion of this having happened in rare cases, and there has been documented cases of malarial infestation in medical staff following a needlestick injury.

“UK Malaria”

Somewhat worrying for me is the fact that the Anopheles mosquito (the one that carries malaria) lives on the Romney Marsh – an area of wetland not ten miles from my house. It is possible that an outbreak of malaria there some ninety years ago was due to local mosquitoes carrying malaria from infected ex-soldiers (who fought in the Mediterranean in World War One) to healthy individuals.

For all that unexplained malaria is incredibly rare, one needs to think outside the box – with international travel becoming more and more common, malarial infestations need to be borne in mind.

All of which brings us to today’s case: unexplained lethargy and fever turned out to be a case of P. falciparum. The G.P. assured us the patient had not holidayed anywhere recently. Was he sure? Yes. On admission the patient turned out to be a soldier who had recently been stationed in Malaria-Land. And so the patient had been true to his word – he hadn’t holidayed anywhere malarious. He’d worked there. A subtle distinction…..

22 July 2011 (Friday) - Getting a Job...


I received an email today through the “contact me” link on my website of advice for students tackling the pre-registration portfolio. In the first instance I’m pleased because this website is clearly working and being found by its target audience.
A very pleasant-sounding young lady had emailed to ask me “….I have an IBMS accredited degree and now looking to find an approved laboratory in which I can complete my training to attain the cert. of competence.  Can you recommend which laboratories to approach and how I go about contacting them, I have no idea where to start”.

My heart goes out to people like this young lady. Things were different when I was a lad: effectively we did an apprenticeship. We started in the lab having left school with “A” levels. (Or in my case having left school having failed miserably and having given up half way towards getting “A” levels).
We then did our academic qualifications on day release, with the academic subjects being taught by academic tutors at the colleges and universities, and with the specialist subjects being taught by the senior and chief biomedical scientists from the hospitals closest to the particular college or university you were studying at.
In a more enlightened era I would have been lecturing on a very regular basis at the university.
Back in the day” you therefore got a good grounding in academic/scientific theory from those best qualified to provide it, and a good grounding in the nuts and bolts of your chosen profession from those best qualified to provide it.

Nowadays you don’t seem to get that at all. It’s (mostly) all academia and very little hands-on real-life input.
Quite frankly my piss is boiling that having been on a formally accredited honours degree, no one has taken the time to explain to this young lady the logistics of getting the job for which she has been preparing herself….

19 July 2011 (Tuesday) - ADAMTS13

I was going to witter on about thrombotic thrombocytopenic purpura today seeing how we had a case recently. But on doing a little research on the subject, I kept finding reference after reference to something called ADAMTS 13.
That was new to me – it turns out that ADAMTS13 is a zinc-containing metalloprotease enzyme that cleaves von Willebrand factor and degrades large vWf multimers, thus decreasing their activity.

Deficiency of ADAMTS13 has been described in various forms of TTP – reduced levels of this enzyme (acquired or genetic) causes large multimers of vWF to accumulate, activating platelets and causing microvascular clotting.

I wonder how long it will be before ADAMTS13 assays will be available on our coagulometers? Perhaps I had better start working on it...

18 July 2011 (Monday) - Specialist Portfolio Assessment

I received the IBMS newsletter today. Some of it was interesting, some was relevant, some was dull, and one bit made me see red.
The IBMS are still advertising for Specialist Portfolio Assessors. I applied to be one back in January, and despite my regularly chasing them up I have heard nothing.
Perhaps they don’t want me….  Having said that, on reflection it took about five years to finally get accepted as a Blue Book assessor.
I had hoped they’d got more efficient over the years…..

17 July 2011 (Sunday) - Facebook


It’s a sign of the times that both the IBMS and the HPC are now on Facebook. Personally, for all that I continually spout drivel on Facebook, I feel that professional bodies such as the IBMS and the HPC should be above Facebook. Or if they must be there, then they shouldn’t be openly available as pages for all and sundry to join.
It is clear that they are not targetting their “proper” audiences as the umbrella parent organisation has two hundred followers, but the smaller subsidiary one had over two thousand.

Take the (current) most recent posting on the IBMS Facebook page from someone who clearly knows nothing of the profession: “I can't wait to be a member of this great institute. Can I join as a Master Student in Biomedical Science.” Master Student – my arse!
I suppose I should be grateful that the HPC’s page doesn’t seem to attract the crackpot element. In fact the HPC writes a blog.

14 July 2011 (Thursday) - Churg Strauss Syndrome

A new diagnosis. All sorts of allergies and asthma in someone who’s never previously had them: Churg–Strauss syndrome is a medium and small vessel autoimmune vasculitis which can lead to necrosis. It involves mainly the blood vessels of the lungs, gastrointestinal system, and peripheral nerves, but also affects the heart, skin and kidneys.
It is a rare disease that is non-inheritable and non-transmissible. Differentiation from Wegener's granulomatosis is not difficult. Wegener's is closely associated with c-ANCA, while Churg-Strauss shows elevations of p-ANCA.

The French Vasculitis Study Group has developed a five-point score that predicts the risk of death in Churg–Strauss syndrome

  • reduced renal function (creatinine >1.58 mg/dL or 140 ╬╝mol/l)
  • proteinuria (>1 g/24h)
  • gastrointestinal hemorrhage, infarction or pancreatitis
  • involvement of the central nervous system
  • cardiomyopathy.
Presence of one of these indicates severe disease (five-year mortality 26%) and two or more very severe disease (five-year mortality 46%). Clearly the blood science lab is crucial here...

13 July 2011 (Wednesday) - BCSH

I received an email from the British Committee for Standards in Haematology today. The gist of their communication was that the use of rabbit ATG in immunosuppressive therapy for aplastic anaemia hasn’t turned out to be quite the success that they had been hoping for. The full text of the article is reprinted here.

I must admit that when I joined the BCSH’s mailing list I rather expected it to be a very useful source of CPD material. This is only the second or third email I’ve had from them….

9 July 2011 (Saturday) - Near Patient Testing


Having taken up the local pharmacist on their offer of free diabetes checking, and seeing what happened, I’m wondering how reliable the concept of non-lab based blood testing is. The pharmacist who checked me out seemed to think my glucose level was high: bearing in mind the limits my lab quotes, it wasn’t (especially) high.

But at no stage did the nice lady doing the testing perform any QC whatsoever. And she seemed rather vague about the operation of the device. Rather than doing a blood test she seemed to be generating random numbers.

The problem with near-patient testing is that having generated a random number, people use that number. In my case I only wanted a ball-park figure. I haven’t got diabetes – that’s the result.
But when more accurate and precise figures are needed, why do people still believe these silly little uncontrolled hand-held devices? Here’s a worrying example of someone believing a hand-held random number generator rather than a proper laboratory result.
People died in this case….

7 July 2011 (Thursday) - Geese


Geese have haemoglobinopathies !!!
I suppose it is only logical that they would do – the mechanics and logistics of protein production are much the same for geese as they are for humans.

Bar headed geese fly over the Himalayas as they migrate. There’s not much oxygen at those altitudes, and so consequently a haemoglobinopathy has arisen: a high-affinity haemoglobin. Hb Olympia, Hb Heathrow and a hundred other high affinity variants are known in humans. It’s only logical that animals in low oxygen environments would have them too…..

I can’t help but wonder if malaria has given rise to variant haemoglobins in the animal kingdom like it has in humans (sickle cell disease and the like…)

5 July 2011 (Tuesday) - Thrombocythaemia


HIGH,PLATELETS    
DOB  04/03/1974 Sex F Pat No 996655  Source    GP
Address   HOUSE                      Clinician KILDARE
Specimen No : AW260451P    (Haematology)          


  Platelets      1228           10^9/l       (   150 to 400   ) Auth
  Potassium      5.6            mmol/L       (   3.5 to 5.3   ) Auth
  Serum Folate   1.9            ug/L         (   4.8 to 19.0  ) Auth


There are several causes of a high platelet count. However this is a case of essential thrombocythaemia. A primary condition as evidenced by the low folate indicative of the high cell turnover in a proliferative condition.

Also the potassium is raised, - this pseudohyperkalaemia is artefactual and is a feature of many haematological proliferations in which potassium leaks from the cells on storage. Potassium levels on fresh samples are normal.