A blood and plasma transfusion; mixing both work and play

When I first started documenting my thoughts 21^st century style (i.e. online) I thought this particular subject matter would be an easy post. There have been many mental notes made, but now, as I take a break from designing New Zealand’s new flag, I am surprised and disappointed that I never committed these thoughts to paper. Or to file; whatever you call typing. Past Liv has let present Liv down as, five months or so later, shrouded in fatigue, I am attempting to recall these little gems. And gems they were, I can assure you, even if the content from here forth resembles quite the opposite.

Ok, I confess, the gem part was not exactly true. Initially I thought this entry would be rather interesting; a woman who works processing and issuing blood receives a blood transfusion – the next bestselling novel! But no. Each time I prepared myself mentally to write about it, I was struck down with vicious boredom.  Baring in mind that I am an awkward uber nerd – you should have heard my shriek of excitement when I discovered a monocyte participating in some hearty thrombophagocytosis on a blood film just the other day – yet still, writing this post was difficult and tedious. Even now I am procrastinating, two paragraphs and nothing interesting has been said. Except thrombophagocytosis. I am somewhat concerned that this will end up reading much like a reflective learning piece rather than a documentation of my thought processes, if this happens I do apologise, but be rest assured it will help me should I ever be audited by HCPC. The next paragraph, particularly, contains a bit of science. You have been warned.

We are flashing back to December 2014. My New Zealand readers are probably imagining glorious sunshine, the spring green grass beginning to turn yellow and their first sunburn of the season. Humph. I am yearning for a New Zealand summer, so I am dismissing your mental visualisations with contempt. No, this was Britain, so it was grey, bleak, cold, wind blowing from three directions, wet and the green grass was really brown sludge. Gumboots are fashion items over here. I had begun my sojourn in hospital. Upon admission my liver function enzymes were deranged, so my liver was not operating at its best. The liver produces some factors that enable coagulation. These factors allow platelets to form a plug and stop one bleeding to death. The liver dependent clotting pathway is measured by an INR test; most commonly used for monitoring patients taking Warfarin. Warfarin is a vitamin K antagonist, vitamin K is needed for hepatic cells to synthesise some clotting factors. I am trying really hard here not to launch into a full scale animated coagulation pathway lecture including an analogy where tissue factor is a fire alarm, platelets are firemen, contact activation is the water from the firemen’s hoses, and vitamin K is the dalmatian running around offering moral support. I could go on. And on. 

Warfarin patients tend to clot too readily, hence their need for warfarin. Fun fact, warfarin is also rat poison; the poor bastards bleed to death internally. It is the one flaw in Wild Tales. The therapeutic INR range for warfarin patients is 2.0 – 3.0, for non-warfarinsed patients it is 1.0. My INR was raised, 1.4 for those interested (which at this point I believe is probably no one) so I was at no risk of spontaneously haemorrhaging but if I was to undergo a procedure, say a lymph node biopsy, I had a high risk of bleeding.

Could this be New Zealand's new flag?

As I was to undergo a couple of procedures, the decision was made to give me three days of Vitamin K. This did not involve increasing my kale intake Brooklyn style, but intravenous administration. Some interesting notes, kale tastes better than intravenous vitamin K so eat your greens kids, and the vitamin K made me feel moderately unwell. Another amusing side note, I still received my tinziparin injections. After three days of vitamin K and no change to my INR, I was informed that a plasma transfusion was the only solution. 

I had recently undergone intense training in the occupation of issuing blood products for transfusions, and we all know that a little knowledge is a dangerous thing. What could go wrong with a plasma transfusion? Well, what couldn’t go wrong?!! TRALI, circulatory overload, anaphylactic reactions… not to mention CJD. I was not born in the UK now I run the risk of contracting mad cow disease? I do not even eat meat! I mumble a demand of methylene blue plasma. An attempt by the consultant to reassure does not mollify me ‘we only use Octaplas plasma so all viruses are deactivated’ ‘It’s the prions I am worried about, not viral transfer’. A scolding look from the consultant ensued. I assume my fellow transfusionists are shaking their heads at me; Octaplas treatment also damages prion ligands, so I was safe and sound and should have been well aware of that fact. But I was dying at the time (cue background violins), so please allow a little leeway. Another irrational concern of mine was they had not tested my INR since my morning dose of vitamin K. What if I became over coagulated? Skip the DVT, my brain is being exceedingly illogical here, it would be straight to pulmonary embolism and instant death. Have I mentioned it was an out-of-hours transfusion? Yip, 2am as my procedure was scheduled first thing in the morning. More first thing than 2am. I ask the night nurse to inform the lab of the midnight request. I have worked nights, I would appreciate the warning.

The plasma (FFP) transfusion itself is mildly painful. It is quite a viscous solution and, as it stored in frozen form, it is transfused at a rather coolish temperature. My already petite veins contract in protest. Being the middle of the night, I begin my obligatory uncontrollable lymphoma rigors, not perfect timing given I am thirty minutes into a product transfusion. I desperately try to reassure the nurse that this, for me, is a normal circadian response and not induced by the FFP. A sympathetic smile; this is my third evening under her care, she is quite aware of my nightly antics. Three bags of FFP transfused, no adverse side effects and a corrected INR. Oh and the procedure is cancelled. Too risky, the surgeon refuses. The large purple bruise on my right hand, a prominent feature for the week prior, heals in about twelve hours. Quite phenomenal.

By now it is Christmas Eve 2014, I have been in hospital for 10 days. The frequently promised lymph node biopsy is again scheduled. Once that is complete I will be discharged! The nodes are a little problematic, the abdominal nodes are massive but inaccessible. Small things like kidneys, bowels, aortas, they’re getting in the way. My neck nodes are more accessible but barley enlarged, and are nicely nested in a pod of blood vessels and nerves.  The biopsy has been planned and postponed three times already. Christmas Eve, however, it is a success and I profusely thank the radiologist. That biopsy was probably the best Christmas present I could have wished for. I wait eagerly in my bunker bed with Mike in anticipation of my discharge. Not since I was ten have I been this excited on Christmas Eve. The haematology team are rockin’ around the helium Christmas tree at the foot of my bed, it is 5pm. They announce they are going to ‘top me up’ as my Hb is 82. I am to receive a blood transfusion.

My helium Christmas tree

I, once again, respond irrationally to this. My heart starts racing, stomach flipping, abdominal muscles tense, if there had been any colour left it would have drained from my face. Why the prospect of a red blood cell blood transfusion provoked more anxiety than a gigantor needle protruding from my neck I cannot explain. But it did. I was unprepared for this announcement. Firstly, it was nearly closing time on Christmas Eve and I thought I was going home. And again a little knowledge…. 

At best a blood unit takes two hours to transfuse, and nobody has only one unit. I had at least four more hours of occupying my bunker. I have to admit I nearly turned the transfusion down. A haemoglobin of 82 is not that low you know, I can survive on that. I believe the only reason I did not decline it was because I was afraid they would refuse to treat me if I did not accept it. This, of course, would not have been the case, but at the time I was convinced it would be. 

When I am at work issuing blood I had never thought much about it; this was my job, you take the blood unit out of the fridge, you cross-match it with the patient’s plasma, make sure nothing nasty will happen, place it in another fridge then mentally give yourself a pat on the back for helping someone in need. But as a patient accepting their first blood transfusion, it was quite a big deal. I do not know why the red cells bothered me more than the plasma. If anything, it should have been the other way around. With the plasma I was paranoid about clinical manifestations, with the red cells it was almost entirely psychological. It is because whole blood is red, it made it more real, even though scientifically red cells are just another blood component. Scientifically, colour is irrelevant.

I did also have clinical concerns. I had intended, but never had the opportunity, to play around with my blood in the transfusion lab, for educational purposes of course. Blood typing is far more complicated than ABO D Pos/Neg. For example, there is more than one type of ‘A’ and so many variations of D that I do not wish to give a precise number as I will probably be wrong. Do not fear, I am not going to delve into the science behind transfusion medicine. If you are at all interested I encourage you to check one of my two internet crushes, blood bank guy. Sigh, blood bank guy. The other crush is Bo Burnham if you must know; yes I am well aware that he is far too young for me. Mike does know of both these crushes and funnily enough does not feel threatened.

I'm R1R1!

Anyway, although I knew I was A Pos from previous blood donations in New Zealand, I did not know my Rh phenotype nor if I had any other cool antigens. Nerdy excitement rose inside me when my first unit arrived and it showed that I was R1R1; how many times have I anxiously searched through our blood bank stock hoping to find R1R1 units! I was comforted that my blood may have possibly made some NZ medical scientist’s day back in 2010 or whenever my last successful donation was. I even WhatsApp’d a friend, who has been known to occasionally share my geeky enthusiasm, mid transfusion on Christmas Eve, an image of my unit. It is fair to say I got the desired response back. 

But suddenly, a feeling of unease overcame me. Not an impending feeling of doom, but a complete doubt of my phenotype. I have never been known for my convenience, it is highly unlikely that my genetics would offer such a thing. I cannot possibly be R1R1. It would make perfect laboratory protocol sense not to phenotype me and, as a woman of childbearing age, just issue R1R1 K neg blood. However I am currently a haematology patient and potentially facing further transfusions, although only the development of a little c antibody is clinically significant, if I do develop an antibody it will make any further blood transfusions a pain in the ass for both me and the transfusion scientist. 

Looking back, my logic was entirely flawed. Statistically, I was most likely to be R1r, so R1R1 blood would not stimulate any sort of cde antibody production. Also, I was that inconvenient patient that made some poor scientist, on Christmas Eve, search through the fridge for appropriate units! In fact, I was meant to have been that scientist, as I was listed to work Christmas Eve at the hospital ten miles down the coast. For the record I have subsequently found out that I am R1R1, and to be fair my immune system at that point was fairly incapable of amounting any sort of response, let alone developing a falsely concerning blood antibody.

The final note I make regarding my entwinement of work and leisure, is that I did not receive irradiated units. Hodgkin’s patients need irradiated units as they are at risk of GVHD (donated passenger white cells bury themselves into your marrow and start replicating as if they were your own, but they are not, so your body tries to destroy them and ends up destroying itself in the process).  At this point my official diagnosis was a mere formality, we all knew I had Hodgkin’s lymphoma, I was in the cancer ward and under the haematology team. I was obviously not at risk of GVHD, because they would not have chanced that particular side effect, so if anyone out there can tell me why I was not at risk then but am now I would be eternally grateful. I assume it has something to do with the chemo. Also, if anyone could tell me why Hodgkin’s lymphoma patients are more susceptible in the first place that would be appreciated, because I have not yet found it in scientific literature. Thanks!