GilTphoto

How are these temps being taken? A temp of 91 to 94 are very low. While the guideline is 1C or 2F increase, this usually means from normal (98.6). Fever starts at a temp of 100F. Anything less is not a fever and a reaction should not be called. a temp change from 91 to 94 is an improvement!

I don't like the antigen typing procedures that require 2 readings (I.S., then incubate negatives for 15 minutes.) Why can't we just incubate all tubes for 15 minutes, then take only 1 reading? Are we really in that much of a rush? We only document the final result and have never been questioned by CAP or AABB. We don't document the incubation time either., That is in the procedure.

I wish I could get the doctors to order 4 FFP. In my hospital 90% of FFP orders are only for 2 units. And they wonder why the PT, PTT didn't get better. That is if they bother to check them again. About 30% never reorder the PT, PTT. We want to make it a policy that post transfusion testing of the trigger indicator is done for all products. Has anyone done that? and cares to share the policy? oopps. I moved off subject! sorry!

I would also like to know. My hospital is having a big problem with overtransfusion. About 15 patients per month are transfused to greater than 12 Hgb. We are considering a policy that H+H's must be done between units, unless rapidly bleeding, to avoid overtransfusion. Many were having more than a 2 gram increase per unit. We reviewed the patient's weight to see if they were small, but most occurred after Lasix was given, but a few were due to a diluted sample drawn by ER staff for the pre-transfusion H+H. If an H+H had been done between units, most of the overtransfusion would be eliminated. We are using 2 hours, but no hard reference. Most doctors are ordering: Transfuse 2 units and CBC in AM, which is causing the problem. A very high percentage are also receiving Lasix. WE must have a high number of CHF patients!

Most of the time it will be a cold auto or alloantibody. But a small number of patients may have a newly forming IgM antibody that only reacts at cold temps I have seen 3 in past 2 years in my hospital, two had an IgM anti-E and one anti-K. Neither reacted at IAT. The logic to not work it up, is that since the antibody is not yet IgG, only a mild reaction, or deceased RBC survival will occur, and spending time working up the other 95% will be wasted. Our antibody screens already don't identify all significant antibodies, so we take a risk on the low incidence ones (Cw, V, Di(a), Kp(a), Js(a), etc) We take the same risk again by only doing I.S. crossmatches. If an anti-Cw was not detected in the screen, a coombs XM of a Cw+ unit would detect it. What is the incidence of this happening? Both a patient with a low incidence antibody and a unit that is antigen positive, so it's considered low risk. My personal feelings is that antibody ID is the fun part of Blood Bank. Negatives all day long is boring! While you can attempt to not detect them by only doing a screen at 37 and IAT, they still rear their heads and are detected in the I.S. crossmatch, or the ABO reverse. The only way to eliminate seeing them in the crossmatch, is to go electronic XM, which is essentially not doing a crossmatch at all. Another way to avoid detecting cold antobodies, is to not delay I.S. readings and to not use a microscope. The purpose of an Immediate spin phase is to check for ABO compatibility, and those reactions are usually very strong. Don't look so close! If still detected, we work them up by first doing a short cold panel. Screening cells I, II, Auto Control, (an O cord is optional), and ABO compatible cells if not type O A1, A2 cells if type A B cells if type B A1, A2, B cells if type AB Immediate spin and 15 min room temp, (4C phase usually not necessary to ID as almost everyone reacts at this temp) If the Auto is positive, we can stop right there. Cold autoantibody reported If the patient is an A or AB, and only A1 cells reacting, then we check for subgroup of A with anti-A1 (A1 Lectin) Otherwise we do a full panel to identify the antibody, significant or not Being only a medium sized hospital, the workload usually allows time for identification. Having the techs gain more experience with identification, so as to not panic when they get an antibody. Small places have more General techs working multiple departments may not have a lot of antibody ID experience, so any chance to teach them more skills is taken, even if ID is for an insignifcant antibody only, it builds confidence when working up a significant one.

We use the 10 mL pink top. We were getting tired of having patients redrawn when a panel was needed. The 6-7 mL tubes just came up short sample too many times.

Serological workup on this patient was negative. Basically, the reason I asked this question, was that the pathologist called it Febrile only. To me it looked like both Febrile and allergic (rash). The SOB, increased pulse and pO2, initially made me consider TACO, especially since the patient has CHF (Chronic Heart Failure) and the platelets were infused rather fast (293mL in 45 minutes), but since nothing on Chest Xray, made me eliminate it from consideration. I just didn't agree with the pathologist. Febrile reactions don't cause rashes do they?

I had a tech who constantly reported rouleaux when in fact it was a weak cold agglutinin. You must NEVER do Saline Replacement after Immediate spin phase. First incubate the antibody screen or crossmatch at 37C, if it goes away, it was a cold. If still there, then do Saline Replacement.

I can't believe the antitrust investigation case was closed. Someone must have been paid off! Meanwhile, the prices of reagents keep doubling every year. I work for a TENET hospital that uses the company Broadlane to negoiate price contracts for the whole corporation, plus other hospital chains. It doesn't appear that these negoiations do any good, since the prices doubled again. Anti-A, Anti-B and Anti-D are now $68-69/bottle 5mL Anti-S is now $1029.53. That's $10 per drop! This is just outright ridiculous. I don't see how they get away with it, and why the government doesn't do anything about it. Obama, I thought you wanted to lower health care costs? My health insurance also just doubled!! (with half the benefits).

A 79 y/o female with CHF was transfused a 5 unit pool of Platelets. The transfusion was completed in 45 minutes (293 mL). About 2 hours after transfusion, the patient developed a rash on the back, temp spiked from 97.9 to 102.5, pulse went from 62 to 107, and patient had SOB. The patient had an ABG and chest x-ray ordered. pH = 7.306 (previously 7.419) pCO2 = 50.9 (previously 35.1) The chest x-ray showed no pulmonary infiltrates, but a suggestion of mild COPD. How would you classify this reaction?

The charge is turned off, so we have to bill manually in the hospital computer system

We require a copy of the signed consent and a copy of the doctor's order. It's to make sure we are giving out the right product, and that it's indicated. We had a couple of cases that caused us to review orders. 1. Doctor ordered: crossmatch 3 units RBC's and transfuse 2. (Nurse transfused 3) 2. Doctor ordered: transfuse 10u of Cryo if Fibrinogen < 150. (Fibinogen was 650 and nurse transfused)

The reason specimens are rejected for hemolysis, is because antibodies can either agglutinate or cause hemolysis, and if the specimen is already hemolyzed, you may miss the reaction. Antibodies that hemolyze are not common. Another way to tell that hemolysis occured, is that the cell button would disappear, so as long as you can see a cell button, it's OK to test hemolyzed samples.

Anti-E is an antibody that requires special consideration. If the patient is also c negative, we always give E=c= (R1R1) blood. This is mentioned in the AABB Technical Manual Rh chapter, Concomitant antibodies. "An R1R1 patient with anti-E, has almost certainly been exposed to c as well. The anti-c may be weaker or undetectable"

I'm wondering if I have a similar situation with a patient now. A pregnant woman came to our ER with Abd pain and vaginal bleeding. She was A1 neg with an anti-D and cold auto in plasma. Since she had received antepartum RhIG, our tech assumed the anti-D was passive, and gave her another dose of RhIG. Upon reviewing the case, the reactivity was too strong at IAT (3+) to be passive, so I performed a titer using R1R1 cells and got a titer of 64, score=74. Her DAT was 2+ IgG, neg C3d. An eluate was positive with all cells tested (including cells negative for high incidence antigens - k, Kp(, Js(, Lu( ) I am concerned about the autoantibody in eluate, since she is pregnant. Does this sound like an LW? After reading that Rh null patients are LW(a-b-) I did a phenotype, but she was c+e+.

DO NOT CHANGE WEB SITE NAME! No one will ever find the other other names. They are not search engine friendly. Take it from someone who has done website development. I did not vote, as there was no choice for none of the above.

We charge manually

In the past 6 months, we have had 2 patients with saline reactive (IS + RT) newly developing anti-K. Both were negative at IAT. I believe in identifying all antibodies before prewarm.

I need to replace the tubing on 2 Ortho/Sorvall Cell Washers CW2. Anyone know who supplies the tubing in the US? Supplier? part number? Thanks, Gil

If the patient is black, has a high incidence antibody, and types S-s- you can assume anti-U. I gave my techs an educational excersize with this. The 16 cell panel had 2 U negative cells, but they were listed on the back. I purposely made up phenotyping results that would help rule out most other antibodies. No one got it right. 3 months later I gave them a panel with all 16 cells positive and made all phenotyping positive except S and s. Similar history, patient is black. Almost everyone got it correct, even though there were no cells to rule out!

We only do a forward ABO/Rh and DAT with IgG only on all cords. The report also includes the mother's ABO/Rh. If the mother is type O and the baby is not, and the baby's DAT is positive, ABO incompatibility is assumed and the doctor will monitor the bilirubin. There is no reason to prove the presence of anti-AB. The only thing that matters is the bilirubin. Most bilirubin increases takes a few days, but rarely require anything other than more time under the bili light. If the mother has an antibody that causes HDN, we will phenotype the baby if Rh antibody, or do Gamma Elu-KIt if other antibodies (since you can't do phenotyping if DAT is positive). If ABO is also a possibility, we will also do Lui Freeze/Thaw with A1 and B cells. Someone above mentioned doing A1 and B cells with Gamma Elu-KIt. This is not a good method for ABO. We had a type B baby with Fy(a), Jk(a) and anti-B in eluate a few days ago. The mother also had an anti-M. The baby was discharged with a 7 total bili on day 3.

We also recheck type on add ons and record the results in computer.

I just realized there is no mention of whether this patient has been transfused before, or if female and been pregnant. If never transfused or pregnant, could be interference from cold antibodies.

another thing to consider: If the patient is Black and S=s=, it's most likely anti-U.

If the titer is > 64, it's most likely a HTLA antibody. At that point we given phenotype specific (same as with warm autos) Doing a plasma neutralization for Chido or Rogers is a waste of time. It is not necessary to distinguish one HTLA antibody from another, as they are all cllinically insignificant.. If not a HTLA antibody, you should run cells negative for high incidence antibodies, or send to a Reference Lab.