Low volume TRALI?

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Apollyon

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Had a pt in the ED on Tuesday night with an INR of 14.9. Hospitalist declined to admit her (?? - I said, "I thought INR of 5-9 with serious bleeding or INR >9, irrespecitive of bleeding, gets admitted"), and suggested 4U FFP.

After 3 units of FFP, sudden onset SOB with RA SaO2 of 88%. Better with bolt upright and supp O2, and CXR with fluffy infiltrates. Afebrile, no back pain.

I suspected TRALI, and called the (same) hospitalist back, and admitted the pt. On his admission, he called it "CHF". As such, I would imply that he was going to diurese her, but, I thought, Lasix is actually possibly detrimental in these patients.

My question - ever seen TRALI in a pt with blood products, but minimal volume infusion? This pt's Ab screen was negative, and she had had a transfusion 6 years ago, without reaction.
 
Sounds too acute for TRALI to me. You didn't say why she was on Warfarin. Most likely AF, ?diastolic dysfunction as well? 3U FFP in such a pt could easily result in acute diastolic failure, and pulmonary oedema.

I've never seen TRALI with products, but I suppose there is no reason why it shouldn't occur since even FFP still has other cells in it despite blood bank's best efforts.
 
TRALI can occur with any product - it results from antibodies, not from cells. In fact, I believe FFP and platelets are far more likely to induce TRALI than other products, because they have more plasma. And while I don't know what you guys actually see clinically, our teaching in pathology (and our experience) is that it can occur quite acutely. Antibody screen will be negative (at least, the T&S RBC antibody screen will, in general). 3 units FFP is not really minimal volume infusion for TRALI - TRALI would likely occur from only one of these units (the one that came from the patient with the appropriate antibodies), and not from the other two. It doesn't really have anything to do with prior transfusion - TRALI is a donor problem, not a recipient problem. Donors linked to TRALI incidents are deferred indefinitely.

Did this patient have a WBC that fell after infusion of the blood products? That's often a good indicator that it really is TRALI. WBC sequester in the lungs. In our workup of these cases, the fact that she got better after sitting up, got 3 units of FFP ( and did not require more aggressive therapy) suggests CHF. Blood bank can also often do BNPs on both the pretransfusion T&S sample as well as a post transfusion sample. In TRALI it should not rise.

All that being said, TRALI is underdiagnosed.

Now back to my hole in the wall of the lab.
 
As far as Coumadin, she was on it for AFib, but HR stayed between 70 and 90 for the whole stay. The blood bank only looked for clerical errors.

The WBC stayed at 16.8, even though the H&H dropped 2/6 points (which implies that it rose, if she was hemoconcentrated).

It was unclear why her INR went up, as her dose had been lowered, and she's very reliable. I even asked about black licorice, ouzo, and Sambuca (but she only 'fessed to vodka).

TV infused was, what, 150mL?
 
Doesn't sound like TRALI - she probably would have had a more severe decompensation. Like I said, I am no clinician, but sometimes it doesn't take much to push people over the edge.

If this was a recent case, you could probably still ask the BB if they could do the BNPs, they save the T&S samples for a few days. But it might not change that much given that she didn't get a ton of volume. So maybe wouldn't help.

A unit of FFP is over 200 ml, so with 3 units she probably got 600-700 mL of fluid, in addition to any other fluids that had been running.

And yes, to my knowledge TRALI can occur very acutely. 2 hours is not too acutely.
 
Why not just give her vitamin K instead of ffp. If she's not actively bleeding and she's not going to the or I don't see any need to give her ffp. Your going to have to give her a **** load of ffp to bring her INR down to therapeutic range. This lady is probably very elderly and malnourished hence the high inr. Anyway, that wbc seems pretty high does this lady have something else going on. fluid overload doesn't give you a high wbc. Did her CXR/clinical exam improve with diuresis. If not I would be concerned about trali?
 
Don't forget ffp comes from pooled donors so your throwing everybody's **** together and transfusing it so you're much more likely to have trali reactions. I think they're trying to make changes with this though.
 
It took about 3 hours for the infusion, as the blood bank was thawing each one separately, one at a time. From my research, TRALI can occur within 2 hours.

Fair 'nuff!
 
Bernard GR, Artigas A, Brigham KL, et al. The American-European Consensus Conference on ARDS. Definitions, mechanisms, relevant outcomes, and clinical trial coordination. Am J Respir Crit Care Med. 1994;149(3 Pt 1):818-824.

basically said:

Conference on ALI/ARDS provided us with a clinically applicable definition of these syndromes:

Acute onset in the proper clinical setting
Arterial hypoxemia: PaO2/FiO2 ratio
Bilateral radiographic infiltrates
Not explained by increased hydrostatic pressure (eg, heart failure)


also, if you put someone in failure with 700ml of fluid, they must have significant CV pathology.


this could absolutely BE TRALI. type and screen is also not 100%. i have seen TRALI with transfusion of 1 unit of PRBCS. a safe transfusion is NOT predictive of future safe transfusions.
 
Common things happen commonly.
A patient with heart disease that develops S.O.B and bilateral infiltrates after 3 units of FFP should be treated for cardiogenic pulmonary edema.
So, give diuretics and vasodilators and see what happens.
By the way was she on antibiotics for some reason?
Antibiotic effect on intestinal flora is a very common reason for Vit K deficiency and exaggerated response to Coumadin.
 
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this could absolutely BE TRALI. type and screen is also not 100%. i have seen TRALI with transfusion of 1 unit of PRBCS. a safe transfusion is NOT predictive of future safe transfusions.

Remember about TRALI though - TRALI is not due to anything in the recipient that is preventable. TRALI comes from antibodies that are in the DONOR. Thus, when TRALI happens, it is because of a single unit. If you get multiple units, you increase your chances of getting TRALI, but only because you are increasing the chances that the next unit you get is the one with the offending antibodies. Type and screen is not at all an indicator of which patients will get it. It is a donor problem.
 
Common things happen commonly.
A patient with heart disease that develops S.O.B and bilateral infiltrates after 3 units of FFP should be treated for cardiogenic pulmonary edema.
So, give diuretics and vasodilators and see what happens.
By the way was she on antibiotics for some reason?
Antibiotic effect on intestinal flora is a very common reason for Vit K deficiency and exaggerated response to Coumadin.

No Abx.

This Coumadin check was Tuesday - last INR was last Thursday, and was 4.

SaO2 dropped, but BP and HR were unchanged. No peripheral edema or stigmata of CHF in the past. She's well-managed (her cardiologist is spot-on, and her PMD is in the same group as mine).
 
I agree treat as if CHF with trali on the differential. Vitamin K should be sq not oral. How old is this lady anyway? An 88 y/o with htn and a.fib is much different than a 50-60yr old. I would have chased the ffp units with some lasix irregardless.
 
The current recommendation by the ACCP in Chest June 2008 is for vitamin K PO. They do not recommend SQ dosing. If there is serious bleeding then IV dosing is recommended. The risk of anaphylaxis is higher in IV dosing but still miniscule (3 per 10,000 doses) according to one retrospective review (PubID: 12392385).

Doesn't sound like this patient needed FFP, no matter what the hospitalist thought.
 
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The current recommendation by the ACCP in Chest June 2008 is for vitamin K PO. They do not recommend SQ dosing. If there is serious bleeding then IV dosing is recommended. The risk of anaphylaxis is higher in IV dosing but still miniscule (3 per 10,000 doses) according to on retrospective review (PubID: 12392385).

Doesn't sound like this patient needed FFP, no matter what the hospitalist thought.
So why don't you tell us what happened?
 
Another vote for CHF.

Horses, not zebras.
 
Any role for Profilnine in this pt. We use it for acute head bleeds in coumadin pts. No indication I suppose if you're just looking at a number in space. (ie no trauma, no hypotension).


-B
 
Gotta agree with the Plank here. If it looks like a duck..... And what do you have to lose by initiating treatment for acute pulm oedema? If it doesn't work, then consider TRALI. Acute pulm oedema will kill the patient faster than TRALI.

Of course, you could always give some Paracetamoxyfrusebendroneomycin, and kill two birds with one stone......😀
 
Don't forget ffp comes from pooled donors so your throwing everybody's **** together and transfusing it so you're much more likely to have trali reactions. I think they're trying to make changes with this though.

Cryo and platelets are frequently pooled, but I think FFP comes from a single donor.
 
Had a pt in the ED on Tuesday night with an INR of 14.9. Hospitalist declined to admit her (?? - I said, "I thought INR of 5-9 with serious bleeding or INR >9, irrespecitive of bleeding, gets admitted"), and suggested 4U FFP.

After 3 units of FFP, sudden onset SOB with RA SaO2 of 88%. Better with bolt upright and supp O2, and CXR with fluffy infiltrates. Afebrile, no back pain.

I suspected TRALI, and called the (same) hospitalist back, and admitted the pt. On his admission, he called it "CHF". As such, I would imply that he was going to diurese her, but, I thought, Lasix is actually possibly detrimental in these patients.

My question - ever seen TRALI in a pt with blood products, but minimal volume infusion? This pt's Ab screen was negative, and she had had a transfusion 6 years ago, without reaction.


Do you know what the status of her pump was?
 
No signs of CHF? Echo's and BNP and other diagnostic labs were invented because as clinicians our PE diagnostic skills are not 100% lucky if they approach 50%.

I only use PE as part of evidence for diagnosis. I agree with need for ECHO, Whats the CVP? Give me objective data to rule out the common etiology of CHF. If CVP is high and echo shows TR with dilated atria then i would consider a congestive hepatopathy reason for elevated INR. But once again common things being common i would investigate whether the patient had a change in there dosing ( was written to take 1/2 a 5mg tab instead of 2.5 tabs of 1 mg and the patient ended up taking 12.5 mg), a change in their diet (stopped eating green leafy veggies or drinking their BOOST) and as someone mentioned was started on ABX or another med.

Trali not ignored but rule out CHF, PNA (wbc 16.8), alveolar hemorrhage ( elevated INR) MI first and then use TRALI as an exclusionary dx
 
No signs of CHF? Echo's and BNP and other diagnostic labs were invented because as clinicians our PE diagnostic skills are not 100% lucky if they approach 50%.

I only use PE as part of evidence for diagnosis. I agree with need for ECHO, Whats the CVP? Give me objective data to rule out the common etiology of CHF. If CVP is high and echo shows TR with dilated atria then i would consider a congestive hepatopathy reason for elevated INR. But once again common things being common i would investigate whether the patient had a change in there dosing ( was written to take 1/2 a 5mg tab instead of 2.5 tabs of 1 mg and the patient ended up taking 12.5 mg), a change in their diet (stopped eating green leafy veggies or drinking their BOOST) and as someone mentioned was started on ABX or another med.

Trali not ignored but rule out CHF, PNA (wbc 16.8), alveolar hemorrhage ( elevated INR) MI first and then use TRALI as an exclusionary dx


I agree with the above.
 
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