May 31, 2011 (Tuesday) - Yuk-o-cytes

Another on-line morphology exercise. I think it’s fair to say I stuffed this one up. Or not so much “stuffed up” as “hadn’t got a clue”.
In practice having seen a blood film of which I could not make head or tail, I’d refer it to a consultant. But in the on-line exercise “haven’t a clue” isn’t an option….

May 26, 2011 (Thursday) - Low Platelets

Another on-line morphology exercise. The salient feature of this one was that the platelet count was only 5. I spotted that, and wanted to give ITP as the most likely diagnosis, but couldn’t find it in the list. The actual diagnosis was autoimmune thrombocytopenic purpura. Had I actually seen that on the list, I would have chosen it. I simply didn’t see it as an option, even though I looked for ten minutes.
Some of my further testing suggestions were a tad awry, but the suggested further testing was microbiological in nature, and that’s not my forte.
However, my differential white cell count was perfect!

May 25, 2011 (Wednesday) - The BBTC Certificate

Today’s lunchtime talk was on the BBTS Specialist Certificate in Transfusion Science Practice. I for one have heard a lot of misinformation and disinformation about this qualification, and so it was good to get first hand information about it.

Whilst I don’t think that the qualification is one I would undertake myself, it strikes me that there is a lot of common ground between it and the blood transfusion sections of the IBMS specialist portfolio. Maybe I could revisit my website of advice for the IBMS specialist portfolio with that in mind…?

May 24, 2011 (Tuesday) - VBAC

An anaemic lady who has just given birth. The diagnosis was a new one to me – “VBAC”. This stands for “vaginal birth after caesarean”.

                             Specimen Results Entry

Bleeding, Profusely                              
DOB  18/08/1983 Sex F Pat No 222333       Received  11:04
Address   Her house                       24/05/2011
Diagnosis VBAC
Specimen No   :  AW172400M               Selected Auth Level : S

 HB     8.7    F000 |MONO   0.9    F000
 WBC    13.2   F000 |EOS    0.0    F000
 PLT    157    F000 |BASO   0.0    F000
 RBC    3.37   F000 |~F1   ^FILMW  F008
 HCT    0.270  F000 |                  
 MCV    79.2   F000 |                  
 MCH    25.8   F000 |                  
 MCHC   32.6   F000 |                  
 NEUH   10.5   F000 |                  
 LYMPH  1.8    F000 |                  

I naively assumed that having had a caesarean section for one birth rather forced the patient into having caesarean sections for subsequent pregnancies. I was wrong.

It would seem that this was the general opinion for much of the twentieth century, but in the 1980s and 1990s there was a move away from that school of thought, and normal deliveries would be attempted. More recently opinion has changed, and normal deliveries in such cases are only attempted given the availability of immediate surgical intervention. Having said that, some 60-80% of attempted VBAC are successful, therefore reducing the amount of caesarean sections that would have been performed in such cases.

Having said that, sometimes things are not as simple as this might seem – this case had a pre-delivery Hb of 12.4g/dl. Clearly there has been post-partum haemorrhage.

May 23, 2011 (Monday) - A Disciplinary Offence...?

Because the HPC’s disciplinary and competence hearings are a matter of pubic record, we can reflect on them. I do this quite often, but because this one involved what I do on a daily basis I find I’m taking the outcome rather personally.

A biomedical scientist in Devon was working on a late shift. There was an “incident, and now she’s been disciplined and given strict conditions of practice. From what I can determine from the public record it looks like she’s been sacked, but this is not stated explicitly.

Ms “X” (I’ll cell her Ms “X”, even though her name is openly available) was doing blood counts on the late shift. She found one of the blood count samples was clotted, and reported it as such on the hospital’s I.T. system. However she did not phone the fact. It transpired that the patient in question had a massively high white cell count which went undetected until a subsequent blood count was performed a day later. The white cell count was so high that it was judged that Ms “X” ‘s actions (or lack of)  “were serious and had a potential of causing patient harm”.

I have grave reservations about this decision.

If the late shifts Ms “X” works are anything like mine, they are not easy shifts. Telephoning results to a busy A&E department is not an easy task – they are often too busy to answer the phone, and when they do, results are often mislaid. Also patients have often moved on to other wards by the time lab results are available. Lab staff also do not have the luxury of time to spend hunting down patients. In the time it takes to phone one result, a biomedical scientist can generate another twenty sets of results. Far better to make results available (on a computer system) to people who will act on those results.

I honestly think that Ms “X” did the right thing in putting the result of “clotted” onto the computer. When the clinicians reviewing the case were in a position to consider the blood count, then they would realise the need for a repeat sample. Let us look at the facts of the case: the sample had been clotted and had not been noticed by any ward staff. Surely the fact that a patient had been in hospital for a day with a white cell count of 80 was far more “serious and had a potential of causing patient harm”?
Let us look at the causes of high white cell counts:

  • Chronic leukaemia: May not be clinical symptoms evident. A Wbc of 80 could be left overnight
  • Acute leukaemia: Patient would (most likely) have symptoms of anaemia and thrombocytopenia
  • Acute infection: Patient would (most likely) have symptoms: fever and rigors.
I honestly believe that either the patient could have been left overnight with no untoward effect, or if harm would have been done by leaving the patient, then clinical symptoms would have been evident to those looking after the patient regardless of the results of the blood count. After all, in this case she was on a hospital ward.
The fact that the first person to become aware of the report of “clotted” was another member of lab staff, and that that was a day later speaks volumes.

But Ms “X” remains with restrictions on her clinical practice, has to undergo a period of re-training, and has the only consolation that her ex-employer would “employ her in a clinical role as a Biomedical Scientist once her training is completed”.
All of which for doing what I feel I would have done in the same situation.

I can’t help but feel I’m missing something here….

May 20, 2011 (Friday) - Neutrophil Drumsticks

Whilst looking at some blood films today I found a case with rather prominent neutrophil drumsticks. I used to know what they are. I refreshed my memory. Neutrophil drumsticks are evident in females – they are the inactive X-chromosome. Women do not have two active X-chromosomes. One is randomly deactivated. (It’s not so random in marsupials, however!)
To be honest I’m not sure than much of the Lyon Hypothesis is particularly relevant to my daily round. It somehow explains tortoiseshell cats, but for my point of view, women’s neutrophils have a protruberence. For the purposes of a blood film, that’s good enough for me….

May 18, 2011 (Wednesday) - Neonatal Lupus

A lunchtime presentation: neonatal lupus erythromatosis - a rare condition in 1% of children born to mothers suffering form SLE. It's caused by the trans-placental passage of the IgG antibodies that cause SLE.

Apparently in the case discussed the mother was known to have SLE, but it wasn't considered to be a cause for concern to the baby. My initial reaction was that this is typical of modern medicine - people tend not to think out of their specialities. But then I'm guilty of this - it came as a major revelation that antibodies other than blood group antibodies can cross the placenta....

May 17, 2011 (Tuesday) - Night Work: 2011-Style

The first night shift I ever did was Wednesday 14 August 1985. Back then we had very strict instructions as to what work we could and couldn’t do during night shifts when there was only one person in the lab. That night I was called into the lab on four separate occasions. I did three emergency crossmatches, seven emergency blood counts, one emergency clotting screen, and I was finished and in bed by 12.30am.

Nowadays we have very different instructions as to what work we can and can’t do during night shifts when there is one person in the lab. Our instructions are that we do absolutely bloody everything and anything. And between the emergency work we do the routine work. And when that’s done we do the admin.
So last night I went into work at the start of my shift at 7.45pm. I worked constantly until I made a conscious decision to stop. At that point (at 2.30am) I walked out for a cup of coffee (leaving chaos and mayhem for ten minutes), and I finally got myself straight at 5.30am. During that time I did not stop at all. To be honest I didn’t stop after 5.30am either, but from 5.30am onwards I had a sense of being in control; that had been lacking earlier.

During that time I did (about) eighty urgent blood counts, forty urgent coagulation investigations and one malarial screening. I did clerical data entry work on several hundred requests, and once the data entry was done I started on the routine work. I went through (about) one thousand routine blood counts, several hundred ESRs (I lost count), and screened about seventy five blood films. And I then produced hard copy reports on all the work that I’d done.
I then set up and performed daily maintenance on eight assorted analysers, and did the daily chuck-out, produced and circulated the minutes of the staff meeting, and reviewed one of my student’s homework.
And seeing how it was me on last night, someone else did all the blood transfusion work. Heaven only knows how anyone could do both the haematology and the blood transfusion.

And from a purely mercenary point of view, the change in the rate of remuneration over the years is interesting. In August 1985 I was paid (about) ten hours money for the night work I did then. Last night I got four hours extra money, but was graciously allowed to take the day off either side of the night as paid leave.

But this isn’t just a rant about how crappy my night shift was. This is CPD – intended to “contribute to the quality of the author's practice and service delivery” and to “benefit the author's service users
Having had to get off my butt and do some work (for a change), I’d like to reflect on night work. How can we change practice to benefit the service users. I am well aware that some of my turnaround times for the urgent work last night weren’t quite what they might have been.

Back in 1985 the system was hopelessly wrong; blood counts would only be done under conditions agreed by consultant medical staff, and requests were often vetted by senior medics. Which was no help to the junior medics who needed the guidance that a blood test can give.
Is the system any better today? Clearly not. Having removed any restriction on what blood tests can be done at night has led to staff being swamped with an unmanageable workload.

So what is the answer? Back to a system in which blood tests are performed under only certain circumstances? More staff to cope with the workload? Not doing one thousand routine blood counts single handed?
I don’t know what the answer is, but I do know what the answer isn’t….

May 16, 2011 (Monday) - Night Work: A Historical Perspective

A day off work today? Not really… When I first started working in blood test-ology back in 1981 we worked from 9am to 5pm on Monday to Friday. We did 9am to midday on a Saturday once a month, and the rest of the time was “on-call”. When I first started as a trainee it was standard practice that on the night when a person was on-call, that person would start work on (say) Monday at 9am and work through to 5pm. They would then stay at work to deal with any emergencies and come home. Should any dire emergency happen during the evening or night, then that person would then go back into work, deal with the emergency and come home again. Back in the day there was a very strict definition of what constituted an emergency (as far as our involvement was concerned), and it was unusual for there to be more than five call-outs during the night. In between call-outs, the person on call could sleep, and it was rare to get called out more than once after midnight. The person who had been on-call would be expected in at work at 9am the next day, and would be expected to do a full day’s work (unless the worst had happened – and that was very rare).
So in theory a person had been on duty for thirty two hours. In practice it was two eight hour shifts separated by a sixteen hour period when they might be called, but otherwise they would do as they pleased. For which they received a full wage for the standard working hours, and (about) two hour’s money for each call into work which lasted less than two hours, after which time a second call’s payment was made. Given that no blood transfusion work was required (that took longer to do!), one could be in and out in less than an hour, and get two hour’s money for less than one hour’s work. And they paid your petrol money and phone rental too.

By the time I started night work it was busier. So much so that I didn’t bother driving home between calls: as soon as I got home I had to go back anyway. So I stayed at work and by a strict application of the rules I found the night work could be quite lucrative. By not wasting time travelling to and fro I could get more calls in the same time period. It wasn’t unusual to get up to eight calls in one night. Which would be about sixteen hour’s money for sixteen hours time given up (if not sixteen hours work). And so by doing regular night shifts one could increase one’s salary by up to fifty per cent.
As time went on, the night and weekend work got busier and busier, and in order to budget effectively, management fixed the rate of pay at eight calls per night. And as we got more and more work after midnight so management allowed us (firstly) to take the afternoon off after a night shift (paid), and then the whole day off. And eventually the whole day before a night session as well. But I for one still managed to sleep most of the night when I was on-call.

At first sight it would seem that we were on a gravy train; two days’ pay for doing nothing at all, and more than a day’s money for doing the night. However, from the point of view of those paying our wages, one got what one paid for. Back in the day we had a robust system. We were able to confidently provide cover twenty four hours a day, every day of the year. People wanted to work because it was good money. People wanted to work on Bank Holidays and at Xmas. People rarely went sick because the money was good. And if they did go sick we were able to cover the sickness, sometimes at only a few hours’ notice.
In retrospect I did far too much work back in those years – sometime doing seventy hours a week; missing family birthday parties and events because the money was so good. In fact we all ran ourselves ragged doing on call because it paid to do so.

Eventually a bean-counting management realised how much money was being spent on out-of-hours provision of cover. I saw the changes coming, cut my hours considerably and I got out. Instead of a lucrative overtime system, people now work a standard thirty seven and a half hour working week. The payments have been slashed, and night work is a contractual obligation for those who were doing night work when the new system came in and for all new staff.
Nowadays when one works a night shift one is not expected in at work on the working days either side of the night shift, but is paid for those hours. And the twelve and a half hours of the night shift are paid at a rate of one-third one’s normal rate. So one gets twelve and a half hours at time and a third. This is sixteen and a quarter hours money.
The bean-counters are happy, but those charged with providing a robust system of cover are not. Personally I’d rather not do the night shift; I’d rather do two day shifts and get fifteen hours’ money. One and a quarter hour’s money is no incentive to do a night shift.
Especially when one bears in mind that it is not on-call work any more; one is expected to work constantly during that shift. And to add insult to injury, those who are on the night work rota have their hours adjusted to be a weekly average of exactly thirty seven and a half hours. Should one offer to cover a night shift (due to unexpected unavailability of staff) one gives up fifteen hours day shift time (two seven and a half hour days) but only does twelve and a half hours at night. One effectively does the firm a favour and ends up owing the firm two and a half hours.

I gave up night work seven years ago, but I still do the occasional one when there is literally no one else available to do it; on average about once every eighteen months. As a special one-off favour to management I’ve offered to help them out of a problem situation tonight.

I’ve not worked all night since 24 March 2009. Let’s see how tonight night goes….

May 11, 2011 (Wednesday) - Haemoglobinopathies Revisited

Two days ago I revisited my presentations on haemoglobinopathies, and today I combined them into one big talk for the Wednesday lunchtime CPD seminar.
Every Wednesday we have lunchtime seminars which are for the benefit of all staff. Admittedly staff have to attend in their own time, and so attendance is voluntary and not compulsory. Having said that, the attendance today was rather low. Am I that bad a speaker?

But I shall not be discouraged….. If only I could persuade management to take the subject of CPD more seriously and allow staff time to attend. If only I could persuade more of my colleagues to give presentations.
The current program has only a few weeks left to run. Maybe next year’s sessions might be different….

May 10, 2011 (Tuesday) - Pre Reg Portfolio (an introduction)

Another trainee is embarking on the pre-registration portfolio, so today I sat with her and told her what she's letting herself in for. In preparation for this I revisited the PowerPoint presentation I have on the subject. And since the presentation was originally compiled, things have changed:

  • It had the old address for the website of advice, so that had to be changed
  • The assessor no longer has the certificate of competence to award. This is now posted on at a later date.
  • The assessor is now called a verifier.
  • And I added another example to the presentation.
I spent a little while revising the presentation which is now downloadable from the website of advice for the pre-reg portfolio.
So much for thinking I could compile the presentation once and just keep re-using it: these things need constant updating...

May 9, 2011 (Monday) - Haemoglobinopathies

This month's topic for the specialist portfolio students is sections 7.1e & 7.4a-c: the haemoglobinopathies. So I revisited the four PowerPoint presentations I had already posted on the website of advice for the specialist portfolio. All of which have now been tweaked in one way or another.
The most significant change was the addition of a slide on non-HbS sickling haemoglobins. Personally I'm not entirely convinced that this term isn't a misnomer. All the non-HbS sickling haemoglobins I could find are effectively variants of Hb S:

  • Hb S-Providence  beta 6(A3) Glu>Val A & beta 82(EF6) Lys>Asn
  • Hb S-South End  beta 6(A3) Glu>Val & beta 132(H10) Lys>Asn
  • Hb Jamaica Plain beta 6(A3) Glu>Val & beta 68(E12) Leu>Phe
  • Hb S-Cameroon  beta 6(A3) Glu>Val & beta 90(F6) Glu>Lys
Mind you some have higher or lower solubity that Hb S. For example HbS Antilles sickles in the heterozygous form, so is probably worth a mention.
I wonder if I'm going into too much detail....

May 7, 2011 (Saturday) - Female Smoker Syndrome

An e-HEMATimage case – last time I did one I said “Overall I’m satisfied with my result, but do feel I could have done better. However I shall put that down to unfamiliarity with the software. Now I’ve found the zoom function I’m intrigued to see how much better I’ll do next time…

Today I got to do my second on-line exercise. I was presented with a screen of various blood cells and had to determine the nature of all of the cells, identify all abnormalities present, suggest further testing which should be carried out, and a possible diagnosis.
Having made my judgements I got immediate feedback on how well I’d done.

Last time I wasn’t impressed with my diff counting ability, but put that down to not having found the zoom function. Now I can zoom I’m quite happy with the diff I got compared to the reference answer..
I spotted all of the significant abnormalities and correctly identified all the further testing that needed to be done. I got the diagnosis wrong though. Given the clinical symptoms and the blood picture, my first thought was Hodgkin’s disease. This wasn’t actually the case. The patient had my second choice of diagnosis: polyclonal B lymphocytosis with binucleated lymphocytes (or female smoker syndrome).
Seeing how I’m (relatively) familiar with Hodgkin’s disease, and I’ve barely heard of female smoker syndrome, I’m quite pleased with how I did.

On reflection I’m warming to the whole idea of e-HEMATimage. I do similar morphology exercises at work, and only ever get feedback when I’ve made a serious error, and that comes a month after the error and once the blood film has been safely lost. e-HEMATimage gave me feedback within a day of my submitting my answer. I really would like to continue with it. I hope I can afford to…

May 4, 2011 (Wednesday) - Audit

Today’s lunchtime seminar was a presentation of a couple of audits done in the blood bank. Following the presentation was a discussion on the concept of audit. I must admit I am still not sold on the idea of audits. I would be *if* they were done properly, and for the proper reasons, such as the audits mentioned in today’s presentation.

In theory audit is a useful tool which can find unexpected shortcomings in any system, and help to rectify these failures, and monitor their resolution. Too often this is overlooked. Or worse, not even considered – it is often enough that an audit is done. And that is terrible. Given that an individual or a department churns out one audit a month, the quality process is seen to have been done – even though (in reality) it hasn’t.
Having done the audit (how much time does fatso waste on his tea break?) nothing is done with the findings because nobody cares. All that matters is that “quality” is seen to have been done because an audit has been done.

So often it seems that it is far better to have a box folder bulging with meaningless audits than to have one or two audits that actually proved something. If only we as a profession could move to a culture where audit is part of an ongoing process of betterment rather than simply a box-ticking exercise….

May 3, 2011 (Tuesday) - Budd-Chiari Syndrome

Budd–Chiari syndrome is the clinical picture caused by occlusion of the hepatic veins. It presents with the classical triad of abdominal pain, ascites and hepatomegaly. Examples of occlusion include thrombosis of hepatic veins. The syndrome can be fulminant, acute, chronic, or asymptomatic. It occurs in 1 out of a million individuals and is more common in females. Some 10-20% also have obstruction of the portal vein.

The acute syndrome presents with rapidly progressive: severe upper abdominal pain, jaundice, hepatomegaly (enlarged liver), ascites, elevated liver enzymes, and eventually encephalopathy. The fulminant syndrome presents early with encephalopathy and ascites. Severe hepatic necrosis and lactic acidosis may be present as well. Caudate lobe hypertrophy is often present.
However the majority of patients have a slower-onset form of Budd–Chiari syndrome. This can be painless. A system of venous collaterals may form around the occlusion which may be seen on imaging as a "spider's web". Patients may progress to cirrhosis and show the signs of liver failure.


The cause cannot be found in about half of the patients. However for those cases with a discernable cause:

  • 75% have thrombosis of the hepatic vein
  • 25% have compression of the hepatic vein by an outside structure (e.g. a tumor)

Hepatic vein thrombosis is associated with the following in decreasing order of frequency.

  • Polycythemia vera
  • Pregnancy
  • post partum state
  • use of oral contraceptive
  • paroxysmal nocturnal hemoglobinuria
  • Hepatocellular carcinoma.
Often, the patient is known to have a tendency towards thrombosis, although Budd–Chiari syndrome can also be the first symptom of such a tendency. Examples of genetic tendencies include Protein C deficiency, Protein S deficiency, the Factor V Leiden mutation, and Prothrombin Mutation G20210A.
An important non-genetic risk factor is the use of estrogen-containing forms of hormonal contraception. Other risk factors include

  • antiphospholipid syndrome
  • aspergillosis
  • Beh├žet's disease
  • Dacarbazine
  • Pregnancy
  • trauma.
Many patients have Budd–Chiari syndrome as a complication of haematological disease:

  • Polycythemia vera
  • Paroxysmal nocturnal hemoglobinuria
  • thrombophilia
A related condition is veno-occlusive disease, which occurs in recipients of bone marrow transplants as a complication of their medication. Although its mechanism is similar, it is not considered a form of Budd–Chiari syndrome.

Interestingly toxicologic causes of veno-occlusive disease include traditional herbal remedies such as plant & herbal sources of pyrrolizidine alkaloids:

  • Borage
  • Boneset
  • Coltsfoot
  • T'u-san-chi
  • Comfrey
  • Heliotrope (sunflower seeds)
  • Gordolobo
  • Germander
  • Chaparral.