1 August 2011 (Monday) - QC Again...

Here’s an interesting dilemma. One of my IQA blood count parameters (the top one pictured above) has a bias. The results are clearly within the range of acceptability, but they are not bouncing about the expected mean – they are ever so slightly low. About two per cent low, which in practical terms is utterly insignificant, but in real terms worries me – I want to be having results on the mean, not below, no matter how slightly below.
However the weekly EQA (the lower one pictured above) is absolutely spot-on.

Should I tweak up the calibration to fix the IQA, thus forcing the EQA to be high? Should I leave it alone (bearing in mind the deviation isn’t actually significant)?

What I actually did was to increase the calibration very slightly. The IQA is still slightly biased (but not as much), and I shall see what the EQA has done when it’s EQA day next week.

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...