The Fritsma Factor newsletter appeared in my inbox today. As always it is a rather useful update on all matters haemostatic…
This is (supposed to be) a reflective diary by a (not very) anonymous biomedical scientist who works somewhere in the south of England. One day this diary may well be submitted to the Health and Care Professions Council as evidence of ongoing continual professional development....
5 January 2025 (Sunday) - Transfusion Dependent
So… a group & save comes in on a
four-year-old child with a generic diagnosis on the accompanying form. I was
rather busy so I just put the thing through the analyser. The analyser wasn’t
having any of it, so as my son once told his primary school teacher, if you
want a job done, do it yourself.
Given that the child had a historical
blood group of O Rh(D) Negative I was rather surprised to see mixed field
reactions with anti-A and with anti-D. Obviously I’d stuffed something up so I
did it again and got the same result.
I then delved into the child’s history.
The child had thalassemia major. Having
had in-utero transfusions before birth he was having regular transfusions every
couple of months. Bearing in mind pedipacks are all O Rh(D) Negative that’s
what he’d been getting, as do all small children needing transfusions. And
having been started on O Rh(D) Negative, that’s what he stayed on.
It looks like the child is actually A
Rh(D) Positive – there’s no anti-A reaction in the reverse group, and where
else would the A Rh(D) Positive part of the mixed field reactions be coming
from?
BUT… how can we determine the child’s
actual group bearing in mind his condition means he will never be off of blood
transfusions long enough for his own group to come through?
I posed this question on the Facebook Blood
Bank Professionals Group. It was interesting how many people posted
responses without actually reading what I’d actually written.
4 January 2025 (Saturday) - Back in the Day
I was having a bit of a clear-out at home today when I found my old notes and exam papers for my Special exam. Back in the day after achieving professional registration we would do the IBMS Special exam. Billed as MSc equivalent you couldn’t progress at all in our line of work without having passed the Special exam, and it had a reputation for being incredibly difficult. Pretty much everyone with whom I worked when I first started told me they had failed the exam several times.
The Special exam consisted of three written papers which together accounted for fifty per cent of the mark, and a practical project accounting for the other fifty per cent.
I passed it on the first attempt, and having passed it I wasn’t obliged to do any kind of professional updating of my knowledge and skills until CPD became mandatory some twenty years later.
Looking at the old papers I took has made me realise just how vital it is that dinosaurs like me do CPD…
Paper One
- A two-hour essay. Look at the options.Is there a need for change in how we are trained? Change was to be avoided at all costs!!
- “Side Room Testing” was the devil’s work and conjured up visions of nurses playing at science. No one dreamed of the likes of us doing near patient testing.
- The future revolutionizing what we do? Pah. We thought it would. In fact we now do far less tests and send everything interesting to specialist labs… who themselves don’t actually have that much of a variety in what they do either with everyone specializing in different things.
- “Clinical Budgeting” was a management catch-phrase of the mid 1980s which has long since been superceded by other equally well forgotten terms.
Paper Two
Two one-hour essays. Again look at the options.
- Vitamin B12 deficiency. Back in the day it was radio isotopes and the Schilling test. (You’ve never heard of it, have you!)
- Erythropoetin… blah on about that for an hour?
- Laboratory investigation of myelodysplastic syndromes? Yes – we used to do that. Gets sent away now.
- Complement… don’t get me started. Back then absolutely everything that science couldn’t explain was down to complement.
- Automated diffs – that was the future. Bear in mind this was only two years after the launch of the first analyser to do a five-part differential count.
Paper Three
Three forty minute essays.
- Safety and AIDS. Bear in mind that this was only four years after HIV had been discovered, and that I was told that in 1981 the average life expectancy of people in our line of work was fifty-seven. No one ever actually said that we used to die from that which we caught in the lab, but that was implied.
- Bleeding time… don’t laugh. We used to do them. We really did cut someone and time how long they bled for.
- Rouleaux and plasma cells… string that out for forty minutes.
- Heparin monitoring… anti-Xa assays were years into the future.
- LAP – that used to be an interesting test to do. Not done one for years.
- Red cell survival rather went the way of the Schilling test. There’s only so much radiation you can inject into people.
Project
I spent an age working up a way of
identifying haemoglobinopathies by iso-electric focusing. Like everyone else
doing the Special exam I put a lot of effort into devising a technique which
would never actually be used.
It is pretty obvious that the future
expected from the mid-eighties wasn’t the future that came forty years later.
2 January 2025 (Thursday) - Missing A Trick?
I can’t pretend that I’m
really that happy with the most recent NEQAS morphology exercises. The trouble
with blood film morphology is that for the most part you operate in isolation. So
I
had this vague idea that I might like to find some form of CPD whereby I get a
blood film a day to look at which might give me immediate feedback . But I
found this web site…
It is offering blood film analysis (with
a two-week turnaround time!) for three hundred and twenty-eight quid.
Bearing in mind I can do fifty of these a day I think I’m missing a trick here…
2 January 2025 (Thursday) - NEQAS 2408BF
I got the results of NEQAS 2408BF today:
2408 BF1
I said:
Macrocytosis
Target cells (consensus 2nd)
Nucleated red cells (consensus 1st)
Howell-Jolly bodies (consensus 3rd)
Large platelets (consensus 6th)
?? Marrow infiltration
Well… The patient has
beta thalassaemia major with a previous splenectomy and was on a regular
transfusion program (2 units every 4 weeks). The latter accounts for the
normal red cells in the film, Got that wrong, didn’t I… Or did I.
I spotted the salient features, and how likely is it that we would get a sample from someone like this without a full history?
2408BF2
Macrocytosis
Basophilic stippling (consensus 6th)
Echinocytes (consensus 7th)
Target cells
Neutrophilia (consensus 3rd)
And nrbc (consensus 1st), polychromasia (consensus 4th), anisopoik,
??? post splenectomy
Again, not brilliant,
but again I spotted the salient features.
I said:
Target cells (consensus 2nd)
Nucleated red cells (consensus 1st)
Howell-Jolly bodies (consensus 3rd)
Large platelets (consensus 6th)
?? Marrow infiltration
I spotted the salient features, and how likely is it that we would get a sample from someone like this without a full history?
2408BF2
Macrocytosis
Basophilic stippling (consensus 6th)
Echinocytes (consensus 7th)
Target cells
Neutrophilia (consensus 3rd)
And nrbc (consensus 1st), polychromasia (consensus 4th), anisopoik,
??? post splenectomy
2 January 2025 (Thursday) - NEQAS 2404DF
I got the results of NEQAS 2404DF today:
Neut 37% (median 35.2% 2sd 23.3-47.0)
Lymph 50% (median 46.0% 2sd 29.7-62.3)
Mono 12% (median 11.2% 2sd 2.6-19.8)
Eos 1% (median 3.3% 2sd 0.0 – 7.7)
Baso 0% (median 1% 2sd 0.0-4.0)
I’m quite pleased with this…
Neut 37% (median 35.2% 2sd 23.3-47.0)
Lymph 50% (median 46.0% 2sd 29.7-62.3)
Mono 12% (median 11.2% 2sd 2.6-19.8)
Eos 1% (median 3.3% 2sd 0.0 – 7.7)
Baso 0% (median 1% 2sd 0.0-4.0)
I’m quite pleased with this…
31 December 2024 (Tuesday) - Partial D
Our automated grouping machine didn’t like
a particular sample and so I did a manual blood group. Look at that D rection.
A D-group is positive, or it is not. And if the patient has had a blood
transfusion from a donor of a differing D-group then there are two distinct
populations of D-positive and D-negative cells.
That’s not what is happening here…
My initial reaction was that I’d stuffed
the grouping up somehow and repeated it. And I got the same result…
A partial D
reaction occurs when someone’s red cells have altered Rh(D) proteins (and
therefore antigens) that react with some but not all anti-D typing
reagents. And that looks like what has happened here.
There are many types of
partial D, each with a unique genetic basis. Some people with partial D
have weakly expressed D epitopes and are designated "partial weak D".
Interestingly these references hint that
partial D happens in about 1% of the population… Having a degree in maths (which
I have) and knowing our workload (which I do) I should be seeing
cases like this many times a month.
But I don’t.
Presumably the anti-D we use picks up
the more common variants and only has issues with the more obscure ones?
I am looking forward to see what NHSBT
have to say about this one.
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