Hi! Just wanted some input on this situation.....

58 yr old female presented to the ER on Friday, 3/11 with :

hemoglobin of 4.4 g/dL, 12.9%

BUN 45 mg/dL

Creat 2.30 mg/dL

Trpn 0.2 ng/mL

Total Bili - 0.5 mg/dL

The patient is admitted for chest pain, acute renal failure and anemia. She is typed and screened for 2 units of PRBC's.

Screen result is negative, crossmatch is compatible (using gel).

Plasma appears to be a light gray color as it is slightly lipemic.

First unit is issued around 0700, 3/11.

Cardiac collected at 1020, 3/11 shows troponin of 0.8, 1620 - 2.1, 2235 - 3.8.

Plasma now appears to be a dark brown/green color. Tech questions serum appearance and calls the nurse to check on the status of the patient and is told she is exhibiting no signs of a transfusion reaction (other than chest pain). Over 2 days, the lab observes the patients labwork and notices her:

Total bili increases to 2.1

Indirect bili increases from 0.3 to 1.6

BUN increases to 53

LDH is 1909

(haptoglobin levels are being tested now, will update when I get a result)

plasma appears to be getting darker/more brown/red color

urine shows 4+ hemoglobin with only 2-5 RBC's per high power field

Techs start getting worried that the patient is in fact having a transfusion reaction so they repeat the screen (still negative) and perform a Polyspecific DAT (which is negative). The pathologist is contacted just in case. So...what is your thoughts? Is it possible for something along the lines of compliment and we just can't detect it because of the gel being IgG plus the fact that we use EDTA plasma for testing? I have been reading up where a DAT can be negative during a HTR. Is all this just her renal failure/meds?

:confused::confused:

We had a patient with very similiar results not too long ago. Ours came in to ED with blackish green plasma two days post outpatient transfusion, PANIC ensued. After all was said and done, our patient was having a hemolytic episode due to a combination of immune response to antibotics and his chronic myelodysplastic syndrome. He also had an Anti-K ( historical) had received K neg units and his DAT was not positive for several days. It was only microscopically pos at that. So, after checking his peripheral smear ( major schistocytes and spherocytes) we noticed that his was reacting non specifically to the gel, which has antibiotics added to it, we washed his cells X4 and used tube method only and found all the non specific stuff gone. The patient was taken off the antibiotics and we have had no other issues.

And I have read an essay in TRANSFUSION said there is a case of transfusion induced Malaria reactive. The symptom is hemolysis but no immune cause have been found.

Edited March 15, 201114 yr by shily

I did forget to mention that if your patient is experiencing a reaction that is extravascular in nature, the DAT may never be positive. For instance, RH antibodies do not fix complement, and those cells involved are removed by the RES quite quickly and destroyed extra vascularly.

This would result in the DAT not becoming positive because: 1. Those cells are removed, and 2. The hemolysis is occuring outside of the circulation.

Did the patient's hgb rise or keep falling after transfusion? Most of the antibiotic induced hemolytic anemia (at least the cephalosporins) would show a pos DAT as long at the patient's cells were coated with antibiotic.

This sounds more like hemolysis, but remember that iron dextran therapy can give the plasma a color that looks a lot like hemolysis. There was a nice photo in Transfusion a few years back.

Color of plasma and the bilirubin numbers certainly indicate there is a hemolytic process going on. Since this patient is a renal patient, have you tried to get a transfusion history on her? She must be periodically transfused somewhere. Next thing is to get a list of meds. Perhaps she is getting something that can cause a hemolytic anemia or perhaps should not be administered with blood, 3rd, you can try doing an eluate if you suspect a delayed reaction. Sometimes it can be positive for a weak antibody when the DAT is negative. Let us know what happens.

Her haptoglobin pre and post transfusion was 2. Her H/H did continue to fall, but it is unknown as to wether it is her active bleed or hemolysis. She did reach 9.5 prior to discharge. We could not find a transfusion history on her, locally. I will look more into her meds just for my own curiosity. She was shipped out to a larger hospital and they repeated her workup as well. Nothing new discovered so that is good.

Hi! Just wanted some input on this situation.....

58 yr old female presented to the ER on Friday, 3/11 with :

hemoglobin of 4.4 g/dL, 12.9%

BUN 45 mg/dL

Creat 2.30 mg/dL

Trpn 0.2 ng/mL

Total Bili - 0.5 mg/dL

The patient is admitted for chest pain, acute renal failure and anemia. She is typed and screened for 2 units of PRBC's.

Screen result is negative, crossmatch is compatible (using gel).

Plasma appears to be a light gray color as it is slightly lipemic.

First unit is issued around 0700, 3/11.

Cardiac collected at 1020, 3/11 shows troponin of 0.8, 1620 - 2.1, 2235 - 3.8.

Plasma now appears to be a dark brown/green color. Tech questions serum appearance and calls the nurse to check on the status of the patient and is told she is exhibiting no signs of a transfusion reaction (other than chest pain). Over 2 days, the lab observes the patients labwork and notices her:

Total bili increases to 2.1

Indirect bili increases from 0.3 to 1.6

BUN increases to 53

LDH is 1909

(haptoglobin levels are being tested now, will update when I get a result)

plasma appears to be getting darker/more brown/red color

urine shows 4+ hemoglobin with only 2-5 RBC's per high power field

Techs start getting worried that the patient is in fact having a transfusion reaction so they repeat the screen (still negative) and perform a Polyspecific DAT (which is negative). The pathologist is contacted just in case. So...what is your thoughts? Is it possible for something along the lines of compliment and we just can't detect it because of the gel being IgG plus the fact that we use EDTA plasma for testing? I have been reading up where a DAT can be negative during a HTR. Is all this just her renal failure/meds?

:confused::confused:

Vic, I have a method: If you know the Rh type of the donor's and patient's, then chose an antigen that is differ, to type the after transfusion specimen, to see if the destroyed cells is donor's or donor's and recipient's. If only donor's cells is destroyed then there is immune hemolysis, if not, there maybe other underlying reason, such as renal disease or others.

If you're really concerned it may be a HTR, then I suggest crossmatching the patients pre and post samples against the suspected units completely through AHG phase. This will indicate whether or not you need to do an antibody screen for rarer, lower frequency antigens that may not be present on your screening cells. If the coombs crossmatch is compatible then you most likely have nothing to worry about.

Just a thought or two from out in left field.

Could the hemolysis and related lab values be the result of mechanical destruction of the RBCs such as a new heart valve? Did some one put the first unit(s) through a warmer or an IV pump that is not acceptable for blood transfusion, the kind with real serious roller pumps?

Don't get too hung up on requiring this to be serological. Lots of other things can cause hemolysis.

I would also make sure that the only fluid used with infusion was 0.9% saline. If somebody piggybacked on an antibiotic, Ringer's or something else (I know, they aren't supposed to, but...), you could see hemolysis due to an incompatible fluid running with the blood. We caught an anesthetist putting the saline in a blanket warmer before running blood - not a good plan, either. Was a cell warmer used?...has it been checked for proper temp lately? With such a low Hgb, did someone get excited and squeeze the units in with a pressure cuff (or a blood pressure cuff, Yikes!), perhaps too fast for the size of the IV catheter?

The last two posts have very interesting ideas for non seroligic reasons for hemolysis. Do you have a QA RN to do the investigations for you? Sometimes nurses get a little terretorial when lab folks look into this stuff. Do you have a transfusion committee?

There are also some infections that can cause serious hemolysis. Clostridium is one I have seen personally. I am sure there are others.

I have seen two cases of Clostridium hemolysis. Both patients died within the day. They were pretty dramatic.

The last two posts have very interesting ideas for non seroligic reasons for hemolysis. Do you have a QA RN to do the investigations for you? Sometimes nurses get a little terretorial when lab folks look into this stuff. Do you have a transfusion committee?

I investigate it myself with an assist from a pathologist if I need bigger teeth, if we need info from the patient's physician and to review patient medical history. It is touchy territory sometimes, but I've worked at developing relationships with nurses and other staff members in various areas of the facility over the years. That helps tremendously (our facility is about 170 beds). Some staff members just aren't going to help - period! - but fortunately they are in the minority. Nurses I don't know well (or at all), I approach with the phrase "I really need your help" and explain why, in a carefully non-accusing way. This works amazingly well a lot of the time. If that doesn't work, I talk with a supervisor or someone on another shift who is caring for the patient...someone I may know better...and ask them to do some digging for me. I also have full access to the patient's electronic medical record - a BIG help. I'm on a first name basis with the BioMed guys, so checking up on equipment issues is a piece of cake. One way or another, we can usually get what we need.

The 'saline in the blanket warmer' incident was uncovered because a staff member from pre-op was concerned about it. She questioned the person doing it, but wasn't satisfied with the response she got. I think because I have been open and encouraging about questions on blood related issues, it seemed natural to her to approach me with what she saw as a problem. I took it straight to the medical director. He went to the head of anesthesia...problem solved.

Our transfusion committee is not very active. They will rule on something or write a letter if we bring them the incident, analysis and corrective action, but rarely initiate anything. We do have nursing QA and QI staff. We do bring problems to their attention, but prefer to have the investigation complete, specific patient cases and a copy of regs in hand when we talk to them. If we can get them to agree that there is a problem in terms of patient care and regulatory compliance, they'll take over.

I have seen markedly increased myoglobin levels in patients with an MI. That would explain the funny plasma color and the hemoglobinuria (myoglobin also gives a positive blood reaction). Doesn't explain the bili or the dropping hgb, but it is something to think about....

Hi! Just wanted some input on this situation.....

58 yr old female presented to the ER on Friday, 3/11 with :

hemoglobin of 4.4 g/dL, 12.9%

BUN 45 mg/dL

Creat 2.30 mg/dL

Trpn 0.2 ng/mL

Total Bili - 0.5 mg/dL

The patient is admitted for chest pain, acute renal failure and anemia. She is typed and screened for 2 units of PRBC's.

Screen result is negative, crossmatch is compatible (using gel).

Plasma appears to be a light gray color as it is slightly lipemic.

First unit is issued around 0700, 3/11.

Cardiac collected at 1020, 3/11 shows troponin of 0.8, 1620 - 2.1, 2235 - 3.8.

Plasma now appears to be a dark brown/green color. Tech questions serum appearance and calls the nurse to check on the status of the patient and is told she is exhibiting no signs of a transfusion reaction (other than chest pain). Over 2 days, the lab observes the patients labwork and notices her:

Total bili increases to 2.1

Indirect bili increases from 0.3 to 1.6

BUN increases to 53

LDH is 1909

(haptoglobin levels are being tested now, will update when I get a result)

plasma appears to be getting darker/more brown/red color

urine shows 4+ hemoglobin with only 2-5 RBC's per high power field

Techs start getting worried that the patient is in fact having a transfusion reaction so they repeat the screen (still negative) and perform a Polyspecific DAT (which is negative). The pathologist is contacted just in case. So...what is your thoughts? Is it possible for something along the lines of compliment and we just can't detect it because of the gel being IgG plus the fact that we use EDTA plasma for testing? I have been reading up where a DAT can be negative during a HTR. Is all this just her renal failure/meds?

:confused::confused:

I agree with John. It may not be immune in nature but someting occuring during transfusion or dialysis. Aside from mechanical, what is being transfused with the blood, or could it be due to the temperature of the room and/or units, a cold autoimune process? Also, the other person that related it to meds the patient may be taking at or away from the hospital. Interesting case, hope you have some luck with figuring it out and the patient does ok.

I would probably check something like this with poly AHG reagents as I have seen Anti-Jka that does not react in anything except poly. That could definitely hide and also cause a hemolytic reaction.

Couple of thoughts...

1. I recall at 1 Institution I worked at that we had a patient that kept hemolyzing when transfused. We could NEVER isolate an antibody in the serum (and DAT was Negative). We finally just gave them Jka Negative blood (cannot recall now if we have a non-transfused specimen and performed Kidd typings, or just "took a shot at it?" We certainly see anti-Jka much more frequently than Jkb. The patient stopped hemolyzing when transfused with Jka- RBCs.

2. At another Institution I worked at, we had a patient come into the ER with the clinical picture you described. In that case, the patient had not been recently transfused; but of course there was always the possibility of warm autoimmune hemolytic anemia. But a Warm Auto was not demonstrable. Never did figure that patient out. They were out at sea fishing one day; and in the ER hemolyzing the next.

Don't know your patient's history, but you may need to "think outside of the box" on this one.

If you have a pre-transfusion specimen, one thought is to perform Jka and Jkb antigen typing.

Brenda Hutson, CLS(ASCP)SBB

Hi! Just wanted some input on this situation.....

58 yr old female presented to the ER on Friday, 3/11 with :

hemoglobin of 4.4 g/dL, 12.9%

BUN 45 mg/dL

Creat 2.30 mg/dL

Trpn 0.2 ng/mL

Total Bili - 0.5 mg/dL

The patient is admitted for chest pain, acute renal failure and anemia. She is typed and screened for 2 units of PRBC's.

Screen result is negative, crossmatch is compatible (using gel).

Plasma appears to be a light gray color as it is slightly lipemic.

First unit is issued around 0700, 3/11.

Cardiac collected at 1020, 3/11 shows troponin of 0.8, 1620 - 2.1, 2235 - 3.8.

Plasma now appears to be a dark brown/green color. Tech questions serum appearance and calls the nurse to check on the status of the patient and is told she is exhibiting no signs of a transfusion reaction (other than chest pain). Over 2 days, the lab observes the patients labwork and notices her:

Total bili increases to 2.1

Indirect bili increases from 0.3 to 1.6

BUN increases to 53

LDH is 1909

(haptoglobin levels are being tested now, will update when I get a result)

plasma appears to be getting darker/more brown/red color

urine shows 4+ hemoglobin with only 2-5 RBC's per high power field

Techs start getting worried that the patient is in fact having a transfusion reaction so they repeat the screen (still negative) and perform a Polyspecific DAT (which is negative). The pathologist is contacted just in case. So...what is your thoughts? Is it possible for something along the lines of compliment and we just can't detect it because of the gel being IgG plus the fact that we use EDTA plasma for testing? I have been reading up where a DAT can be negative during a HTR. Is all this just her renal failure/meds?

:confused::confused:

This patient has since left and now has returned along with an Anti - Kell! Her DAT is still negative, tube and gel.

I assume you do not have any segments left from those units transfused in March? It would be interesting to type them for Kell. How does her serum look now?