Grand Rounds!

[Annadele]

Poll: Does your Transfusion Service have a program resembling rounds? How does it work and do you have a mechanism in place for helping all shifts benefit from it?

We have a solid continuing education program thanks to a great coordinator but don't have something like grand rounds. I'm thinking about suggesting it as a way to help everyone in the lab learn from unusual, extraordinary, less common cases or even deviations (especially new technologists). We have about 35 technologists in our Transfusion Service over three shifts and since we're located near a couple of universities with CLS programs, technologist turnover seems relatively high. There are four new techs starting this summer.

I trained in a micro lab that had daily grand rounds - in that case it was set up to benefit medical residents - and I think that it helped a great deal to contribute to a team-oriented, educational work atmosphere in which everyone was an equal participant. In that case, an MD led the grand rounds through each "station" with each technologist in micro who would present any interesting cases from that day (if they had any). Afterwards, the same MD would quiz the group rotating through with questions about that bug (or similar bugs) usually present - both medically and in the lab. They also had weekly rounds just for pediatric cases in which the residents reviewed all of the cases from that week as a group with their attendings. They invited any micro technologists who wanted to attend who brought up the physical plates as well. (Credit here should be granted to the attendings who clearly felt it was important for the residents to have at least a general understanding of culture.)

As you can imagine, both forms of rounds really opened up an excellent line of communication between the residents, attendings, and technologists. All participants seemed to have a good understanding of the other side's role in patient care. And I have no doubt that their patients benefit from that kind of open communication. The laboratory itself rarely has openings but when they do, graduating technologists who have trained there are quick to snap them up and I'm sure that that is thanks at least in part to rounding.

I'm not sure that something similar involving direct patient caretakers is really possible in Transfusion where many areas of the hospital are "frequent flyers" but perhaps a lab-centered format that just involved our senior technologists and/or medical directors would still have a great impact as far as expanding communication is concerned.

I'd love to hear from those of you who currently use similar programs in your place of work - how it's structured and what kind of impact you think that it's had.

[Malcolm Needs ☆]

The hospitals served by NHSBT-Tooting Centre in London (where I work), have a meeting called the South Thames Technical Advisory Group every three months, to which their lead Biomedical Scientists in Blood Transfusion are all invited.

At this, I discuss all of the rare antigens and antibodies we have dealt with over the previous three months.

Of course, staffing being what it is, not all of the hospitals can send representatives, but what I have said and written about these cases is embedded into the minutes and these are sent around to all of the hospitals.

This allows the cases to be discussed at a local level.

Whether they are or not is a different matter, but the material is there for them!!!!!!!!!!!!

[Malcolm Needs ☆]

This is a rather extended version of one of these (actually, this one is about three meetings long!).

Tooting “Rares” 16.06.11.

1 x R₁R_z partner of a pregnant lady with anti-c+E.

1 x Anti-E+Ch.

1 x Anti-S+U (pregnant).

1 x Anti-M, U- sickler, with a possible alloanti-e (despite looking like an R1r or Ror’).

This is a possible e variant at both chromosome 1 RHe loci.

1 x anti-c (504 IUmL^-1) and anti-E (Titre 256) in pregnancy.

1 x anti-Lu^b in a group A, rr MDS patient.

Requires regular transfusion.

4 x DAR/Weak D Type 4.2.

The genetic background to this/these D phenotypes are mutations at positions 602 (C>G), 667 (T>G) and 1025 (T>C), resulting in amino acid changes at codons 201 (Threonine to Argenine), 223 (Phenylalanine to Valine) and 342 (Isoleucine to Threonine).

Anti-Cr^a (pregnant).

This antibody does not cause HDN. This antigen lies on the decay-accelerating factor molecule (DAF), and it is thought that the abundance of DAF on apical the surface of trophoblasts in placenta may adsorb maternal antibodies to antigens in the Cromer system.

It has only ever been implicated in very moderate haemolytic transfusion reactions and, of course, weakens throughout pregnancy, and so is no danger to the mother having a transfusion.

1 x Partial DIVa-2 with alloanti-D in pregnancy.

The genetic background to this D phenotype is mutations at positions 186 (G>T), 410 (C>T), 455 (A>C) and 1048 (G>C), resulting in amino acid changes at codons 62 (Leucine to Phenylalanine), 137 (Alanine to Valine), 152 (Aspargenine to Threonine) and 350 (Aspartic acid to Histidine).

1 x anti-Ge2.

Rarely clinically significant, unless really strong (this one was very weak).

1 x pregnant DHK/DAU-4.

DHK has a mutation at position 697 (G>A), resulting in an amino acid change at codon 233 (Glutamic acid to Lysine).

DAU-4 has mutations at positions 697 (G>A) and 1136 (C>T), resulting in amino acid changes at codons 233 (Glutamic acid to Lysine) and 379 (Threonine to Methionine).

1 x pregnant anti-U (titre 4 at 28/40).

Not a problem (yet!).

1 x Adult ii donor with novel mutations.

The donor was found to be heterozygous for two novel exons of IgnTC.

1054 (G>A), encoding a Glycine to Argenine change in the glucosaminyl (N-acetyl) transferase 2 I branching enzyme.

1184 (C>T) encoding an Alanine to Valine change in the glucosaminyl (N-acetyl) transferase 2 I branching enzyme.

1 x DIII Type 5, with anti-D in pregnancy.

DIII Type 5 has mutations at positions 186 (G>T), 410 (C>T), 455 (A>C), 602 (C>G), 667 (T>G) and 819 (G>A), resulting in amino acid changes at codons 62 (Leucine to Phenylalanine), 137 (Alanine to Valine), 152 (Asparagine to Threonine), 201 (Threonine to Argenine) and 223 (Phenylalanine to Valine).

1 x Weak D Type 1, reacting much weaker than normal, because the D^wCe haplotype is in the trans position with an dCe haplotype (Ceppellini effect).

Weak D Type 1 has a mutation at position 809 (T>G), resulting in an amino acid change at codon 270 (Valine to Glycine).

1 x normal RHD gene, with anti-D in pregnancy!

1 x Dad dcE/dce, Mum D^*Ce/---, Baby dcE/---!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

*Weak D Type 1.

Mum typed as R₁R₁, with a weak D during the pregnancy, and we originally thought that she was probably another example of D^wCe/dCe showing the “Ceppellini” effect. When the baby was born, however, it typed as r”r” (thus excluding the Mum). No in vitro fertilisation history, no egg donation and a baby swap ruled out.

At this point, we thought about an amorphic --- RH haplotype in the Mum and baby, sent samples down to the IBGRL for genotyping, and, Bob’s your uncle, we were correct.

The regulator type Rh_null type is rare enough, but the amorphic Rh_null type is even rarer, and so to find a mother, with a Weak D Type 1 in one RH haplotype, and an amorphic RH_null haplotype in trans was amazing!

Dad’s Rh type is none too shabby in terms of frequency, and, of course, baby’s Rh type is amazingly rare!

Tooting “Rares” 15.09.11.

1 x anti-P1, reacting at 37^oC (still only requires cross-match compatible blood, rather than P1- blood).

1 x anti-E+Co^a (only requires cross-match compatible blood, but we wre able to provide E-, Co(a-) units).

3 x DHK/DAU-4.

DHK has a mutation at position 697 (G>A), resulting in an amino acid change at codon 233 (Glutamic acid to Lysine).

DAU-4 has mutations at positions 697 (G>A) and 1136 (C>T), resulting in amino acid changes at codons 233 (Glutamic acid to Lysine) and 379 (Threonine to Methionine).

Pregnant sickle cell patient found to be Lu(a+b-) (no anti-Lu^b – yet!).

1 x anti-U in pregnancy.

1 x alloanti-JMH in pregnancy (will not cause any problems).

1 x Partial D DCS-2.

DCS-2 has a mutation at position 676 (G>C), resulting in an amino acid change at codon 226 (Alanine to Proline). This is usually found in the DcE haplotype.

How rare is it? Joyce Poole has seen one other example!

1 x sickle cell patient S-, s-, U-.

1 x O_h in pregnancy.

1 x A_x in pregnancy.

1 x probable A₃.

Tooting “Rares” 09.12.11.

? anti-Yt^a post-natal.

r’r sickle cell patient.

1 x DIII type 5 with anti-D.

DIII Type 5 has mutations at positions 186 (G>T), 410 (C>T), 455 (A>C), 602 (C>G), 667 (T>G) and 819 (G>A), resulting in amino acid changes at codons 62 (Leucine to Phenylalanine), 137 (Alanine to Valine), 152 (Asparagine to Threonine), 201 (Threonine to Argenine) and 223 (Phenylalanine to Valine).

1 x anti-S+U in pregnancy.

1 x anti-Fy3 in pregnancy (too weak for titration).

1 x anti-Lu^b in pregnancy (too weak for titration).

2 x anti-U in pregnancy (titres 8 and 128).

Anti-DOLG in pregnancy (titre 8 at 24 weeks gestation).

St. Helier ? e mutation.

Anti-In^b in pregnancy.

Anti-D in a Partial DIVa-2 in pregnancy (1.1 IUmL-1 at 20 weeks gestation).

Anti-U in pregnancy (titre 16 at 33 weeks gestation).

? Anti-U in pregnancy (small sample).

Strange GYPA.

Weak D testing on a 98-year-old. A new, if unwanted, record!!!!!!!!!!!!!!

Anti-hrS in a pregnant lady (too weak for titration).

RHCE sequencing at the IBGRL revealed the following mutations.

This lady was found to have a homozygous mutation at position 712A>G in Exon 5, resulting in a Methionine to Valine change at position 238 of the RhCcEe protein.

She was found to have a heterozygous mutation at position 787A>G in Exon 5, resulting in an Argenine to Glycine change at position 263 of the RhCcEe protein.

She was found to have a heterozygous mutation at position 800T>A in Exon 5, resulting in a Methionine to Lysine change at position 267 of the RhCcEe protein.

She was found to have a heterozygous mutation at position 818C>T in Exon 6, resulting in an Alanine to Valine change at position 273 of the RhCcEe protein.

She was also found to have a heterozygous mutation at position 1132C>G in Exon 8, resulting in a Leucine to Valine change at position 378 of the RhCcEe protein.

The likely allele combinations are, therefore, ceBI and ceEK.

Other than that, her RHCE gene appeared to be quite normal!

1 x anti-k in a cancer patient who may require regular transfusions.

1 x Partial D DHK or Weak D DAU-4.

DHK has a mutation at position 697 (G>A), resulting in an amino acid change at codon 233 (Glutamic acid to Lysine).

DAU-4 has mutations at positions 697 (G>A) and 1136 (C>T), resulting in amino acid changes at codons 233 (Glutamic acid to Lysine) and 379 (Threonine to Methionine).

1 x DDOL.

The genetic background to this phenotype is mutations at positions 509T>C (exon 4) and 667T>G (exon 5), resulting in amino acid changes at positions 170 (Methionine to Threonine) and 223 (Phenylalanine to Valine) of the mature RhD protein.

A donor who is R₂R₂, Kp(a+b-).

1 x anti-hr^B in a sickle cell patient.

She was found to have homozygous mutations in exon 5 at position 733C>G, resulting in a Leucine to Valine (L245V) change at position 245 of the mature RhCcEe protein, and in exon 7 at position 1006G>T, resulting in a Glycine to Cysteine (G336C) change at position 336 of the mature RhCcEe protein.

In addition, she had a heterozygous mutation in exon 1 at position 48>C>G, resulting in a Cysteine to Tryptophan (C16W) change at position 16 of the mature RhCcEe protein.

These results combined are indicative of the d©ce^S variant (also known as r’^S). This variant has the phenotype D-, C+^wk, c+, E-, e+^var, V-, VS+, hr^B-.

1 x DAU-2.

The genetic background to this phenotype is mutations at positions 209G>A (exon 2), 998G>A (exon 7) and 1136C>T (exon 8), resulting in amino acid changes at positions 70 (Argenine to Glutamine), 333 (Serine to Aspargenine) and 379 (Threonine to Methionine) of the mature RhD protein.

1 x DNB, with anti-D,

The genetic background to this phenotype is a mutation at position 1063G>A in exon 7,resulting in a Glycine to Serine change at position 355 of the mature RhD protein.

BUT in a DcE haplotype, and not a DCe haplotype; THIS IS A FIRST!

1 x anti-Vel.

1 x auto-anti-A in an apparent ii adult.

2 x Vel-, both with anti-Vel.

2 x anti-k.

[galvania]

DEar Malcolm

I guess you're near enough to London Zoo to have access to enclosures for all those zebras!!

[Malcolm Needs ☆]

Those zebras make my life sooooooooooooooooo interesting. I get paid for doing a hobby!!!!!!!!!!!!!!!!!!!!!!

[esa]

Hello Malcom

[Malcolm Needs ☆]

Hello esa. Glad you have joined!

[Smarty pants]

We do brown bag sessions once a week where MTs and Residents discuss an interesting case for the week. Usually presented by the resident who cared for the patient (donor). The MTs really enjoy going to these... they are under an hour, and everyone eats lunch at the same time. We've done it this way for years! (An email is sent early in the week with the topic so interested parties know to plan on it - may be Donor Center related, Transfusion Services, or Lab related)