Back in the day we’d just judge on what we saw down the microscope. Didn’t
I comment on that the other day?
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....
Showing posts with label case study. Show all posts
Showing posts with label case study. Show all posts
20 November 2025 (Thursday) - T.A.C.O.
Back in the day it was widely accepted
that the potential hazards of the transfusion of a single unit of blood greatly
outweighed the advantages, and so it would be at least two units of blood or
nothing.
Back in the day pretty much everyone
would be transfused until their haemoglobin level was over 10 (or 100 in new
currency).
And back in the day a lot of people
would get pneumonia whilst in hospital for no adequately explored reason.
Nowadays we are more aware of
transfusion associated circulatory overload, and today (despite being on a
day off) I tuned in to a rather interesting talk on the subject presented
over Microsoft Teams.
I listened to a couple of very interesting
case studies… and found myself wondering just what can you do for the best.
Someone’s anaemia is causing fluid retention, but trying to alleviate the
anaemia by transfusing blood is just giving more fluid…
27 July 2025 (Sunday) - Anti-U
The U antigen is part of the MNS blood
group system and is a high incidence antigen being found in approximately 99%
of Black individuals and virtually 100% of Caucasians. Consequently having a
patient with anti-U who needs blood is, as my grandson would say, a pain in the
glass.
I came in to the early shift today to
find one such case. With a haemoglobin of 45 g/L the patient was symptomatic.
Blood had been requested yesterday… we had been told that frozen blood was
available. But it was frozen and was actually in Liverpool three hundred miles
away.
There’s all sorts of talk about learning
from these incidents and there is a lot to be learned. What do you do in a
situation like this? Give blood which may well be detrimental, or wait until
the blood is available… the waiting being detrimental.
I’m glad it’s not a decision I have to
make.
22 May 2025 (Thursday) - B Platelets
From the Blood Bank Professionals group…
It has been
reported that bites from the Lone Star tick can cause the formation of
specific IgE antibodies targeting galactose-α-1,3-galactose (α-gal). This
is found in red meat and so can cause allergic reactions when you scoff any,
when hitherto you’ve been shoving it down your neck like there’s no tomorrow.
Bearing in mind that there’s loads of ticks
in the woods where I often walk the dogs perhaps I need to think about anti-tick
treatments for myself as well as the dogs. You never know – what is good for an
American tick might be good for a UK one.
Yes – I know… what has this got to do
with CPD? Well, it turns out that this galactose-α-1,3-galactose stuff isn’t chemically unlike the B-antigen.
Antibodies to galactose-α-1,3-galactose can cross-react with the B-antigen and
cause a mast cell response.
It has been suggested that this has been
seen in group B platelets which have been transfused to group O patients who’ve
been suspected of having been bitten by these ticks who have received group B
platelets.
Something which according to all the guidelines
is perfectly acceptable.
Should we restrict the use of group B
platelets?
21 March 2025 (Friday) - Reticulocytes
The nice people at Lablogatory sent
their update today – some case studies based on reticulocyte scattergrams.
In theory this sort of thing is an invaluable diagnostic tool. In practice the
computer systems of most labs aren’t up to dealing with the graphical
information the scattergrams provide.
21 January 2025 (Tuesday) - TTP
Here’s a rather good webinar on
thrombotic thrombocytopenic purpura. Admittedly it does go on a bit, but
something for nothing is never to be sniffed at.
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.
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.
22 November 2024 (Friday) - Low Platelets?
A massive drop in the platelet count…
cell fragments… in a small child with pancreatitis…
Here’s
a case study from the nice people at the American Society of Hematology.
24 October 2024 (Thursday) - Haemoglobinopathies
I’m often
grumbling about how I don’t get useful CPD… here’s
something of interest. A post to Facebook from a haemoglobinopathy laboratory
in the middle-east with the sort of cases we rarely (if ever) see here in the UK.
I used to be quite the whizz at haemoglobinopathies back in the day…
17 October 2024 (Thursday) - DIC Case Study
The nice people at Lablogatory sent a
rather good case study about DIC today. You can read it by
clicking here.
It was a rather good refresher…
2 September 2024 (Monday) - Daratumumab
I was
asked a question today. M answer was “don’t know” so I did some finding
out…
Daratumumab
is effective in cases of multiple myeloma as a monotherapy in heavily treated
patients with relapsed or refractory disease. It is a monoclonal antibody that
specifically targets human CD38, which is highly expressed on myeloma cells.
However if
a patient is on daratumumab when we do a group and save their antibody screen comes
up positive in absolutely everything which makes crossmatching problematical.
So we
send a sample to NHSBT and they send us compatible blood… what magic do they
work?
Cells are
treated with dithiothreitol (DTT) which removes the CD38. However whilst
it is at it, it also removes the K antigen, and other antigens including ones
of the Lutheran, Yt, Cromer, Dombrock, and Knops blood group systems.
Here’s
an article describing what happens. There’s no magic. It’s quite straightforward.
So why is this in the domain of the reference laboratory and not standard
practice?
10 August 2024 (Saturday) - Pre Eclampsia
The nice
people at the Medical Laboratory Observer sent me a rather good little article
about pre-eclampsia today, You can read it by
clicking here.
It was a
rather good refresher…
17 July 2024 (Wednesday) - Auer Rods
I was
mooching about on the Facebook Haematology Interest Group when I found their
archive of case studies. Here’s
an interesting one – a particularly strange case of AML with Auer rods in
the mature neutrophils.
13 March 2024 (Wednesday) - Hyperthyroidism
We had a patient today with a mild
neutropenia. The patient’s diagnosis was hyperthyroidism.
It
transpires that treatment of hyperthyroidism often causes a neutropenia
which resolves on cessation of treatment.
Something to bear in mind.
17 January 2024 (Wednesday) - Coagulation Case Study
One of our trainees was given some
questions to answer for his portfolio. The answers were circulated to all of
us, and so I’ve shamelessly blagged them.
After all, why not? This is a really
good example of where I’ve learned something…
A male patient in his 20s attends A&E after experiencing excessive bleeding during a routine dental procedure. The patient does not take any anticoagulants and has no past history of haemorrhages. In A&E, an FBC and clotting screen were requested. The results of the FBC were unremarkable.
Q1: From which derivative curve shown above would the APTT value determined?
APTT would be determined from the peak of the second derivative curve, where the rate of conversion of fibrinogen to fibrin is represented.
The patient’s APTT result resembled the plot shown above.
Q2: Which abnormal feature is present in this curve? What could this feature indicate?
A biphasic curve (or double-peak) is shown in the plot above. These are often associated with coagulation disorders such as positive lupus anticoagulant, FVIII and FIX deficiency, and Von Willebrand Disease.
The results from the patient’s clotting screen are:
| Patient’s Result | Reference Range |
PT (s) | 13.0 | 11.0-15.0 |
APTT (s) | 44.0 | 23.0-37.0 |
Fibrinogen (g/L) | 3.68 | 1.50-5.00 |
The APTT was found to prolonged. Following this, a mixing study was performed.
Q3: If the mixing study does not correct the prolonged APTT, what could this mean is causing the prolonged APTT?
If the APTT does not correct in a mixing study this means that there is no factor deficiency, and the cause of the prolonged APTT is likely the result of an inhibitor in the patient’s plasma.
Q4: Why is a lupus anticoagulant performed in cases of unexplained prolonged APTT?
Patient’s with antiphospholipid syndrome may produce lupus anticoagulant antibody. These autoantibodies target the epitopes of phospholipids bound in cell membranes. This leads prothrombotic effects in vivo but prolonged APTT results in vitro.
The mixing study corrected the APTT value therefore the sample was sent to be tested for intrinsic pathway factors: FVIII, FIX, FXI, and FXII. The results are shown below:
| Patient’s Result | Reference Range |
FVIII (IU/dL) | 52 | 50-200 |
FIX (IU/dL) | 136 | 60-150 |
FXI (IU/dL) | 144 | 70-160 |
FXII (IU/dL) | 144 | 50-200 |
Q5: Do these results explain the patient’s bleeding episode? What role does FVIII have in haemostasis?
These results show the patient’s FVIII level is borderline. FVIII is a coenzyme responsible for accelerating the generation of FXa and subsequently thrombin (which cleaves fibrinogen to fibrin). FVIII is also responsible for stabilising VWF. Reduced FVIII is associated with bleeding tendency.
Q6: Based on these results and clinical history, is Haemophilia A or Von Willebrand Disease more likely? What tests could be performed to differentiate Haemophilia A from Von Willebrand Disease?
This case may suggest VWD as patients with VWD often receive a diagnosis later in life than compared to Haemophilia A patients. This is due to most cases of VWD causing only mild disease. The following tests are often required to diagnose VWD:
FVIII:C – a measure of the functional FVIII as FVIII activity is reduced in some VWD types.
VWF Ag – the level of functional (and non-functional) VWF. VWF concentration and functionality is reduced in VWD.
VWF:GPIbB – a measure of platelet glycoprotein activity, decreased activity represents the failure of VWF to bind to glycoproteins present on platelet membranes.
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