I spent a few minutes this morning working on my website of advice for students tackling the IBMS pre-registration portfolio.
I’ve now revisited all of the set questions for section 1a, and have been through the various other evidences and added a page of evidences specifically aimed at providing evidence for section 1b. The obvious next steps are to do the same for sections two and three.
Perhaps I’m now wasting my time in that yesterday I applied for another of my students to have his portfolio assessed. This with be the third of my current batch of six students. Perhaps I’ve left it a bit late to be revising the website. The trouble is it takes this long to build up the experience to be able to make the suggestions.
Mind you I will always have more students in the future. And I suspect that word is getting around about this website….
Yesterday I was lecturing on the subject of anaemia, and mentioned that when considering anaemia, one shouldn’t overlook other problems causing a reduced oxygen supply to the tissues – a low haemoglobin level isn’t the only cause of such a problem.
Today I learned about Eisenmenger's syndrome. A congenital heart deformity in which there is a hole between the left and right ventricles of the heart (ventricular septal defect). The hole allows blood that has already picked up oxygen from the lungs to flow back into the lungs, instead of going out to the rest of the body. The increased blood flow and high pressure generated by the (effectively) single ventricular chamber damages the small blood vessels in the lungs.
And because of the ventricular blood mixing, the blood getting to the tissues isn’t as oxygenated as it might be, which leads to the breathlessness and fatigue which one may associate with an anaemia.
What with one thing and another we were short of a speaker for the CPD seminar today, so I stepped into the breach. Over the years I’ve prepared a few talks that I can give at short notice. The talk I gave today was on anaemia – a subject with which I have a passing acquaintance.
With an audience of double the average attendance of last year’s sessions, I was quite pleased with the turn out.
Mind you, I have noticed that no matter how much I prepare and practice and rehearse, when it comes to actually give the talk, I over-run. What should have lasted fifteen minutes went on for nearly twenty five minutes. I need to stick to my pre-prepared spiel, and stop ad-libbing things that come to mind as I’m wittering on.
In my considered opinion, the most difficult part of the IBMS pre-registration portfolio is finding evidence for Sections 1a.1 – 1a.8. They are all very “admin & management” and are rather difficult for the new starter to get to grips with. To that end I’ve put together some set questions to provide evidence specifically for those sections.
Whilst they are based on something I shamelessly blagged from other people many years ago, now they bear very little (if any) relation to their original form. I’ve been working on (yet another) revision of these questions, and am about two thirds of the way through. Over the last week or so I’ve touched on such topics as professionalism, the working day, accountability and incident reporting. Over the next week I intend to beef up the secions on Health & Safety, the European Working Time Directive, CPD, and dealing with adversity.
If any of my loyal readers have any other ideas or suggestions for Portfolio section 1a.1 – 1a.8 evidences, I’d be very pleased to hear from you…
Whilst browsing the web (on my day off!!!) I found something worrying. Malaria was eradicated from
fifty years ago. Now it’s back. One can’t help but wonder if this is an isolated occurrence, or whether this is a shift in the global distribution of mosquitoes that the global warming pundits have been threatening. Spain
After all, the marshes just down the road from me were malarious ot that long ago…
The fact that I now have to update my pre-prepared lectures on malaria is now the least of my malaria-related worries….
Today's lunchtime session was on a new development - the massive blood transfusion protocol.
I can remember the bad old days when a serious trauma case in A&E was synonymous with panic in the blood bank. Nowadays there's a policy which gives guidance, saves money and has a higher survival rate.
Wish we’d had it years ago….
I was asked today "What exactly can you see in a blood film?"
I'm not going to answer that here - it would take a series of essays or lectures to do justice to that question. But I thought I might make a start answering that question by having a look to see what the oracle of all wisdom had to say on the matter.
As it happened (as you would probably expect), Wikipedia’s opening paragraph on the subject was frankly gibberish - "Aq blood film or peripheral blood smear is a microscope slide made from a drop written by zamir blood". The rest of the article wasn't *too* bad, but it wasn't *too* good either, so I made a start on putting the page right by correcting the first sentence. I might go back later and do some more
I suppose I could benefit humanity at large and (at the same time) satisfy the fourth CPD standard by doing more editing on Wikipedia’s haematological articles...?
Look what I saw today. Whilst reported enough in the literature, it’s actually rather obscure. And then I had a worry…
Platelet clumping is common, and is widely recognised as a cause of thrombocytopenia. Could platelet satellitism be a similar cause of thrombocytopenia, albeit a more obscure one.
But then, if the (apparent) thrombocytopenia is relevant, we would look at a blood film anyway, and if the satellitism is especially marked, then this would stuff the optical properties of the neutrophil and again prompt scrutiny of a blood film. Either way the problem would be spotted.
On reflection I don’t think there’s grounds for concern….
To the right hand side of this page is a section which reads “THE AUTHOR'S OTHER CPD PROJECTS”…
I’ve doubled the size of the CPD presentation archive. There’s still not a lot there, but it will grow with time.
Following on from what I shall take as a glowing endorsement of my website of advice for students tacking the pre-registration portfolio on Tuesday, I’ve carried on updating the set questions which can be used as evidence for Section 1.
I have also utterly revamped my website of advice for students tacking the specialist portfolio in haematology and blood transfusion and relocated it to its new home.
I shall leave the original where it was, and all future efforts will go on this new-improved Mark II version. It still needs a lot of work; especially in the areas of blood transfusion. I expect I shall get round to those bits eventually. Blood transfusion isn’t exactly my forte….
Today's lunchtime seminar was on Crohn's disease. This is something I read as a diagnosis almost on a daily basis, and I always attribute the (almost standard) hypochromic microcytic blood picture to the concurrent iron deficiency. Other than that, I've always been somewhat vague on the specifics of the disease.
Today's session brought together a lot of things I've accumulated over the years. A very useful talk.
Some time in the mid 1990s I can remember going to the graduation ceremony of the first trainee whose training I oversaw. Since then I’ve formally overseen the training of undergraduate and newly appointed people at work. So far I’ve successfully seen the qualification of seventeen trainees. Today made eighteen.
One of the parts of my job that I like the most is when I get to go to the University or to other hospitals to asses and inspect other student’s pre registration portfolios. One of the parts of my job that I like the least is when someone else comes to inspect my student’s pre registration portfolios. We had such an inspection today.
We had a rather nerve-racking time waiting for the inspector to arrive. And an even more nerve wracking time waiting for him to inspect the portfolio. In the event she passed with flying colours. We knew she would anyway, but it’s still worrying.
For myself I was very interested to see what the inspector thought of her portfolio. I’ve put a lot of effort into producing a website of advice for students compiling pre registration portfolios over the last year. It would seem my efforts were vindicated. He was very impressed, especially praising the grid of evidences, a concept I have tried to drum into the heads of the students. He also asked if he could use one or two of my ideas at his own lab.
I suppose that my ideas for compiling pre-registration portfolios are along the right lines. I shall continue working on my website…
A patient reported for ante-natal clinic at which a blood count was performed. She proved to be a tad anaemic, and the analyser suspected nucleated red cells (which isn’t an uncommon thing for it to suspect in pregnancy). For these reasons a blood film was made, and spherocytes were seen.
DOB 29/09/1977 Sex F Pat No 666999 Source ANC Received 12:58
Address SOMEWHERE IN
Specimen No : AW203214B (Haematology)
07/10/2010 11:15 EDTA
Haemoglobin 10.7 g/dl ( 11.0 to 15.0 ) Auth
White Blood Cells 10.5 10^9/l ( 4 to 11 ) Auth
Platelets 414 10^9/l ( 150 to 400 ) Auth
Red Blood Cells 3.55 10^12/l ( 3.8 to 4.8 ) Auth
Haematocrit 0.320 ratio ( 0.36 to 0.46 ) Auth
Mean Cell Volume 91.3 fl ( 80 to 100 ) Auth
Mean Cell Haemoglobin 30.1 pg ( 27 to 32 ) Auth
Mean Cell Haemoglobin Con 33.0 g/dl ( 32 to 36 ) Auth
Neutrophils 7.7 10^9/l ( 2 to 7.5 ) Auth
Lymphocytes 2.0 10^9/l ( 1.5 to 4 ) Auth
Monocytes 0.6 10^9/l ( 0.2 to 1 ) Auth
Eosinophils 0.2 10^9/l ( 0.02 to 0.5 ) Auth
Basophils 0.0 10^9/l ( 0 to 0.1 ) Auth
XE FLAG1 Spherocytosis ++ Auth
XE FLAG2 ^A blood film has been reviewed Auth
Cursor Down for more
The patient’s (real) name rang a bell – I knew this patient had hereditary spherocytosis. This is a condition in which the patient’s red cell survival is decreased because of a problem with red cell membrane structure. Rather than being biconcave discs, the patient’s cells are spherical. Therefore not so flexible, and don’t live as long. Normally this condition is well compensated, but when the patient is unwell for other reasons, the HS can be aggravated and cause an anaemia.
Usually spherocytes are detected microscopically. In the case above a blood film was made because blood count parameters fell outside the reference range, and the automated analyser suspected nucleated red cells (which isn’t uncommon in pregnancy).
However I’m left wondering. Someone with HS having a blood count for any other reason may well have normal numerical results (it happens!), and with no blood film being made, the condition would go unnoticed. In fact the patient under consideration has had six previous blood counts over the last three years, none of which triggered the making of a blood film by the automation.
So we have a potential failing in the system. We are (potentially) not finding cases of hereditary spherocytosis. At first thought I was rather concerned, but then again, does this actually matter? Many cases of HS (and the related HE) are often not clinically significant. Some patients with these conditions can (and do) go their entire lives with absolutely no problems being generated by the well-compensated haemolytic process.
It was suggested that cases of HS have raised reticulocytes and so we could use that as a pointer, but performing reticulocyte counts on every blood count would get rather expensive and would slow the process down. In conversation with colleagues it was suggested that the spherocytic cells may well scatter light differently to biconcave discs, and that maybe one of the XE channels might find spherocytes. I relayed this suggestion to the analyser’s manufacturer who said not, but they were rather flummoxed by this problem. After some discussion we came to the conclusion that a case of HS which actually needs to be diagnosed will present either clinically with jaundice and/or anaemia, or will have an obvious problem with the blood count. And in 99.9% of the time will be suspected from a family history.
So there’s no need to change practice (at the moment…)
Labels: Service Improvement
A diagnosis I’d not heard of before….
Tetralogy of Fallot is a congenital heart defect which is classically understood to involve four anatomical abnormalities (although only three of them are always present). It is the most common cyanotic heart defect, representing 55-70%, and the most common cause of blue baby syndrome.
It was described in 1672 by Niels Stensen, in 1673 by Edward Sandifort, and in 1888 by the French physician Étienne-Louis Arthur Fallot, for whom it is named
Tetralogy of Fallot involves four heart malformations which present together:
A ventricular septal defect (VSD): a hole between the two bottom chambers (ventricles) of the heart. The defect is centered around the most superior aspect of the ventricular septum (the outlet septum), and in the majority of cases is single and large. In some cases thickening of the septum (septal hypertrophy) can narrow the margins of the defect.
Pulmonary stenosis: a narrowing of the right ventricular outflow tract and can occur at the pulmonary valve (valvular stenosis) or just below the pulmonary valve (infundibular stenosis). Infundibular pulmonic stenosis is mostly caused by overgrowth of the heart muscle wall (hypertrophy of the septoparietal trabeculae), however the events leading to the formation of the overriding aorta are also believed to be a cause. The pulmonic stenosis is the major cause of the malformations, with the other associated malformations acting as compensatory mechanisms to the pulmonic stenosis. The degree of stenosis varies between individuals with TOF, and is the primary determinant of symptoms and severity. This malformation is infrequently described as sub-pulmonary stenosis or subpulmonary obstruction
Overriding aorta: An aortic valve with biventricular connection, that is, it is situated above the ventricular septal defect and connected to both the right and the left ventricle. The degree to which the aorta is attached to the right ventricle is referred to as its degree of "override." The aortic root can be displaced toward the front (anteriorly) or directly above the septal defect, but it is always abnormally located to the right of the root of the pulmonary artery. The degree of override is quite variable, with 5-95% of the valve being connected to the right ventricle
Right ventricular hypertrophy: The right ventricle is more muscular than normal, causing a characteristic boot-shaped (coeur-en-sabot) appearance as seen by chest X-ray. Due to the misarrangement of the external ventricular septum, the right ventricular wall increases in size to deal with the increased obstruction to the right outflow tract. This feature is now generally agreed to be a secondary anomaly, as the level of hypertrophy generally increases with age
(shamelessly blagged from Wikipedia)
I spent some time with the students today. One chap was doing reflective work for his pre reg portfolio, and I felt quite at home guiding his reflections into positive comments and experiences, and away from the bollox that reflection can so easily become.
One of the girls was doing proper science, and I didn’t have the faintest idea what the Henderson–Hasselbalch equation was all about. I’m slightly more familiar with it now.
It worries me that I am far more comfortable with woolly reflective practice than I am with proper science….
On September 23rd I mentioned that I’d done some work on my website of advice for students tackling the pre-registration portfolio. I’d revised my set of questions about the role of the Health Professions Council. One of my new questions for the students was: “Describe (briefly) the role that the HPC plays in the daily life of the average biomedical scientist”. My reasoning in asking this question was that the students’ immediate answer would be “bugger all!”, but further research on their part would prove to be enlightening.
Today I received an email from the HPC. They had sent their latest newsletter. I opened this missive, expecting to find all manner of goodies relevant to my question. So what has the HPC been doing in the life of the average biomedical scientist?
Let’s just say that “In Focus Issue 31” has left me feeling somewhat let down by those in authority above me…
Labels: HPC Newsletter