Dr. Pepper

Malcolm, Judd and Case were excellent guesses, and I have had the pleasure of hearing Mr. Case speak, but that's incorrect. My daughter, son-in-law, infant grandson and two dogs moved in with us a few months ago while relocating. Perhaps getting a UPS delivery of mother's milk on dry ice from North Carolina jogged the memory of this story. (Yes, my freezer was full of milk "samples" but we didn't use them in our coffee. I learn from the wisdom of my elders! Besides, we take it black.) This was a somewhat unfair question, kind of like "What did Sandy talk about at lunch break today?" How would you know if you weren't there? So let's make it a multiple choice question. Pick the winner: a. Alexander Wiener b. Robert Race c. Peter Issitt d. W. Laurence Marsh e. Ruth Sanger f. Karl Landsteiner g. Robert Orr

I'd like to say I knew that off the top of my head, but I found it in Immunobiology of Transfusion Medicine, 1994, edited by George Garratty. OK, here's my question: What pioneering blood banker told the following little story (as near as I can remember it) at a lecture I attended? " We were investigating the I system and looking at the distribution of the antigens in other tissues and fluids. I wanted to see if it was found in breast milk. As luck would have it, there was a home for unwed mothers next door to the lab, and obtained a sample of milk. When I got to work the next day, though, I couldn't find the milk in the fridge. I asked my coworkers if they had seen the sample. They all looked down, a bit squeemishly, at their coffe cups...."

Oops - I exaggerated - it was 12 days in the last 3 weeks, not 2 (they do make me work from time to time).

1. Anton (Wj)? 2. What I had 12 days of in the last 2 weeks (sorry to rub it in)

Malcolm, speaking of things that were not entirely unexpectedly absent, years ago I took my daughter to our pediatrician. She was having stomach cramps. The doctor asked for a urine sample, then proceded to put a drop of the raw urine on a slide, cover it with a cover slip, and look at it through a monocular microscope that might have dated from the late 1800s. "There's nothing there", he announced. I told him "I'm not surprised, in my lab we centrifuge the urine and remove the supernatant which concentrates it 10,000 times and gives you a fighting chance of seeing something in there." He gave me the stink-eye. I found a new pediatrician.

We have found that 2 adsorptions are usually sufficient to get rid of all the autantibody, as compared to 3 or 4 using WARM. So there is less dilutional effect from residual saline in the red cells. As for the procedural dilution of the test serum by adding an equal volume of PEG, that's pretty much what happens if you were using PEG on unadsorbed serum. The Tech Manual notes that some have reported a weakening of antibody reactivity compared to other methods, and that some use 6 drops of adsorbed serum/PEG mixture instead of 4. We tested several spiked samples using PEG vs. WARM - adsorbed sera. We found equal or higher titers with the PEG sera (6 drops) and feel quite comfortable with the technique. If you know where you're headed, you can do a serum panel, DATs, eluate and panel, autoadsorptions and crossmatches and get the blood out the door in less than 2 hours.

Whenever I review panels I look for patients with at least a 1+ antibody and grab all the old lab specs from other depts I can lay my hands on. I pool the serum/plasma and aliquot in 1-2 ml samples and freeze. They seem to keep their reactivity well at -28o. If they're weak you can always do a little demo on differences in sensitivity between LISS, PEG, enzyme, gel etc. I agree about the monoclonal reagents; if I use them I warn the students to just cross out and look for the specificities and that the human-source ones don't react like that. Quotient offers free or cheap deals on expired antisera for student use.

Liz, if I can put in yet another plug for the PEG autoadsorption technique from the AABB Technical Manual: we switched to this technique after using WARM for several years. It is easier, quicker, more efficient, uses less cells, produces more adsorbed serum and is substantially cheaper.

We are in the process of updating our surgical consent form (the informed consent for transfusion needed fleshing out). We have a change of document form that needs to be signed off by several of the powers that be. I faxed over to the chief of staff MD the change form, a cover letter explaining the revision, and a sample of the new surgical consent form. He signed, dated and faxed back the surgical consent form.

We've had a Serofuge 2001 that we've never liked. The control pad sticks out of the front and bounces around when you shut the lid; we've had to put rubber pads under it to stabilize it. The cell buttons seem a little fuzzy, even with a longer spin time. I think it may brake a little too hard but without the brake on it doesn't stop until next Tuesday. I've heard good things about the Helmer product.

Malcolm, I had heard the story of the Lutheran misnaming but not Colton. What should Colton have been?

The mutation evolved independently of and is different from other Duffy null mutations. A mutation of the FYA gene instead of the FYB gene? I'm on thin ice here.

Hi Stacey - Welcome to BBT. It's fun, you learn a lot, and it beats the heck out of working on next year's budget.

jcdayaz, we do the same thing for emergency release and downtime. We document on a downtime form that the unit appearence and check of patient/donor data and special requirements is OK and catch up in the computer later.

Takes me back! We had 4 primary forms: 1. Incoming blood log (RBC): our inventory #, drawing facility and #, component, weight, retype reactions and interpretation, tech, date received, ourdate, and disposition (if transfused this was the page in the crossmatch logbook). 2. Crossmatch logbook: Date, donor #, donor type, patient name, patient MR#, room #, XM results, ab screen results, billing record, issue data. 3. Typing logsheet. 4. Incoming FFP/cryo log Our crossmatch forms had a big face sheet that ended up in the chart as the permanenet record of the transfusion, a smaller copy to be the bag tag, another bag tag that we kept in the BB, and a billing copy with checkoff boxes for the appropriate charges. If you leave me a private message with a fax #, I'd be happy to fax samples of 1, 2 and 4.

We are starting the process of picking a small volume BB analyzer (Tango, Echo, Provue). This has been a most helpful thread. Has anyone had experience with multiple platforms to able to say, "If I were you I'd pick....", and has anyone successfully interfaced with Meditech?

We do this for the rare patients who don't like something in the potentiating medium. To approach the sensitivity of using enhancement media, I would suggest extending the incubation period to 60 min. and mixing the tubes a couple of times during the incubation so the settled-out cells get back in contact with the serum. Otherwise, I like the idea of getting the blood out the door quicker with a 10-30 min. incubation with LISS or PEG.

I would hope that she received good care, although after one knee redo she fell and messed it up and it had to be redone again She was convinced that we had screwed it up and went to a different hospital. I'm not sure that we were sorry to see her go there. All of her surgeries seemed to be balancing acts and it was sometimes difficult to explain to the doctors that if we deglyced her units to have them ready and they didn't need them we would be wasting priceless, irreplacable blood. Once her surgeon told me they'd be extra special careful and wouldn't need blood. This disturbed me as one would hope that they would always be careful; did this mean they might do a crappy job on my knee because I'm a run-of-the-mill O Pos? Anyhow, we know the moral of this story: Never get sick, because then you might get treated!

Oops, I forgot to pass on the question baton. Deny or Malcolm?

Malcolm and Deny, you are correct that Bhende et al first described the phenotype. They investigated three individuals: one was hurt in a railroad accident, the second admitted for a stab wound, and the third a first time donor found in a deliberate search of 160 donors. (Since the incidence of Oh in India is 1:7600, I want that tech in my lab screening units for my next problem patient with multiple antibodies. He/she had the golden touch!). They postulated a new homozygous and recessive allele at the ABO locus, and called the patients' antibodies "the most potent examples of human anti-H so far reported". Malcolm, you are correct that Levine et al's seminal paper in Blood in 1955 described the relationship between the H, h, A and B genes. They studied a "remarkable family", three members of which were of this unusual phenotype apparently identical to those investigated earlier. Of particular interest was how an apparent group O mother and a group A father could produce a group AB daughter. They correctly concluded that the mother carried a B gene but could not express it herself. They suggested that a homozygous dose of a "x" gene could supress ABO phenotype and secretion of ABH substances. Xx were replaced by Hh, and a hugely important cornerstone in our understanding of blood group serology was laid. And now it's time for my part of the story. In 1973 I was a fledgling blood banker just weeks out of school. In those days we typed every patient admitted to the hospital. We used A1, A2, B and O cells for the backtype. One of our routine admission patients front typed an unremarkable O but agglutinated the O cells on the backtype. An antibody screen was positive as well, and she agglutinated all panel cells 4+ in all phases but not her own cells. I actually did consider Bombay, and I believe typed her with anti-H which was outdated and didn't have a package insert! I seem to remeber getting a reaction and dismissing Bombay. (I didn't say we were good blood bankers in those days!) We called the floor and found that she was not going to need blood and sent her off to the reference lab at Pfizer. We were thrilled when the report came back saying she was indeed a Bombay. I shared the news with a worker at another hospital, who said they had found one back in the 50s. It soon became obvious that we had been beaten to the serological punch: our patient was the propositus in the Levine study. And Malcolm, you did remember that she was an American of Italian ancestry, but didn't remember that she was from Providence, Rhode Island. We saw her many times over the years. She had kidney issues and arthritis and had several total knee replacements and redos. She was not a great candidate for autologous donation, having poor viens, a chronic 10 gram hemoglobin and a rather crusty attitude (Levine told her that her blood was so rare that people should pay her every time her blood was drawn.) Eventually she figured out that Bombay blood does not grow on trees and we got a few units frozen away at our local blood center. The routine became only transfuse if the post-op hgb got too low, otherwise give her erythropoetin. The last time we went to tranfuse her, we got the deglyced unit from the blood center and cut off the segment to do the retype (ha!) on the bag and a crossmatch. When the tech returned to the unit she discovered, to her horror, that the last seal on the tubing was faulty and the bag had filled with air! We clamped it off with a hemostat. After some discussion with her surgeon and our medical director, it was decided not to give her the unit. I am fascinated by the history of science, and in particular our own field of immunohematology. Pretty much all of the trailblazing articles and publications are readily available through your hospital's library and their connected sources, and make for fascinating reading. I have presented several times in seminars on Bombay and other serological oddities, and promise to convert my powerpoint and write out the whole Bombay story, historical and personal, when I have that mythical free moment. There are still some serological irregularities in the Levine study that have yet to be explained (and probably never will). It was stated earlier in the thread that classic Bombays are Le(a-b-). They are hh and sese. Unless I am very mistaken, I was under the impression that the Lewis transferase can still function and add its L-fucose to the subterminal sugar of type 1 chains and create Lea antigen. Classic Bombays cannot be Le(b+), though, as that requires a Se gene. Both Levine and I found our Bombay patient to be Le(a+b-). Our profession, sadly but inevitably, has become increasingly depersonalized. Techs don't go up on the floors any more to draw blood. Faces and names are being replaced by bar codes and cup numbers on an analyzer. Once in a while, however, we should pause and reflect that most advances in our science have a human story behind them, often not a happy one. To have met, talked with, tested, and helped our Bombay patient has been a great honor and priviledge. She passed away of sepsis at our hospital a few days ago at the age of 81.

I sincerely hope that Malcolm is home sipping wine, not still at work! I'll wait until tomorrow morning to respond to him or whoever else might have the answers, and I'll tell you why I asked the questions.

OK, back to Bombays......I'll offer up a 3 part question: 1. Who wrote the original paper describing the phenotype? 2. Who worked out the relationship between the Hh (they called them Xx) and A and B genes? 3. Where was the patient from who, along with her family, supplied the clues for #2 above?

Would that be Sc2?

The AABB has a nice little booklet on validation of pneumatic tube systems for transport and outlines the variables that should be considered. Regarding coolers that keep blood <10o for x # of hours, I have always felt that if a cooler is sitting around in an OR or on the ward awaiting possible use, then it is storage, not shipping, and should be kept <6o. We had a recent AABB assessment and were told that the AABB considers blood in coolers going to the OR for possible use to be "transport" (it was explained that the blood "takes a little trip to the OR, stops and enjoys the scenery for a while, then continues the trip back to the lab...") and the <10o rule applies. The FDA, however, (and this is also from the AABB home office), says to consider the intent of the cooler use: if it's going from point A to point B to be moved into another storage medium like an OR fridge, it's transport (<10o rule). If it's going to sit around for possible use, then return from whence it came, it's storage (<6o rule). So there's a dichotomy here.

I agree that CAP would like you to sign off on new and revised P&P but does not require annual review and signing. (Our signoff sheets parrot back the CAP item # TRM.31190I verbiage). Brenda, you are right that annual review is not a bad thing if, as you say, they actually do it. That's the hard part, and it's a lot of info, often tedious, to go over. I have one wonderful core blood banker who knows it all, and 15 other generalists of varying degrees of wonder and BB experience. What I find useful for annual competency review is to include, among other things,the following: 1. Pet peeves of mine (such as "writing over" incorrect log entries instead of drawing a line through it and dating and initialing. After the competency no one can say, "I didn't know...") 2. Issues not generally encountered on a daily basis (such as P&P on maintaining blood services if the lab has to be evacuated, disaster plans, etc.). 3. Issues and "what if" scenarios where you suspect everyone might not be on the same page. 3. Opportunities for education, such as interpreting both a standard panel and an enzyme panel to remind techs which antigens are enzyme-labile, or having questions like "How many units should you have to screen to find 4 that are negative for E, K, Fya and S, and in what order would you use the antisera?" Educational info from the Principle sections of the P&P can be included as well. 4. "Scavanger hunts" through the procedure manuals. If they can't find what they need to find, then I haven't done a good enough job making it easy to do so. It's also a great way to find and correct ambiguous, misleading or outdated material in the manuals. 5. A few joke questions and silly pictures (the internet is a very rich source of zany pictures). I also ask my core BBer and the top 2nd and 3rd shifters if they have any issues they would like addressed. As a manager you can't see everything that happens, and if you're not routinely on the bench you don't have the point of view of a front-liner. Award a few modest raffle items (vendor pens and other swag, hospital coffee mugs, Doncan Donut cards, etc.). Along with the written exercise, we also do direct observation and occassional wet exercises. We are licensed in our state and require continuing ed; I award an hour CEU for the competency (the carrot on the end of the stick).