Transfusion Reaction Differentiation : TACO vs TRALI

[Panda]

I'm currently working on a case study and need some help. Here's some basic info first~

A 38 year old Caucasian male patient was diagnosed with IgA nephropathy & renal arteriosclerosis and ending up developing hypertension and end stage renal disease in 2007.

In 2008 he was elected for a living related kidney transplant. During the transplant he had hemorrhaging which resulted in 2 liters of lost blood. He had 8 liters of crystalloid fluid, 4 liters of colloid fluid, and 4 units of PRBC's transfused within 60 minutes.

I'm thinking circulatory overload for sure but the case study mentions to look up TRALI as a possible cause of death. They also had talked about the patient being typed A+ and in his post mortem autopsy they never did a DAT.

So what are the similarities and differences of TRALI and TACO?

I've been searching in the internet and haven't found much information on the two that can help me present this to a group clearly.

If you want the full case study for a better insight than my brief, ask and I will post it.

Any help would be greatly appreciated!

[AMcCord]

A BNP could help differentiate between TACO and TRALI. The BNP would be elevated for TACO and not for TRALI. Of course, it would be best if you have a pre-transfusion sample BNP result to compare with, to see if your patient was already in heart failure or not.

An excellent reference for the topic would be Transfusion Reactions, edited by Mark A Popovsky. It's an AABB publication.

[Panda]

In the case study there's no mention of a BNP being done pre-transfusion or post transfusion. The only things that they did were run EKG's his BP and his chemistries, along with typing him as A+. His creatinine, BUN and potassium are elevated which is related to his renal disease. Other than that they didn't say anything else.

I've got the DAT and hemolysis to differentiate the two but I need to be able to separate the two very clearly. I also know the HLA antibodies are prevalent with TRALI along with FFP and apheresis platelets.

[Yanxia]

Panda,you are right, HLA antibodies are prevalent with TRALI, but some TRALI the HLA antibodies is neg, as to DAT , I don't think it can different the two.

I remember 2009's Transfusion has a paper about the two's differ, it mentioned BNP as AMcCord mentioned.

It is a pity I can't provide this paper to you, if someone can help to provid it, it will be welcom.

[AMcCord]

Transfusion Reactions states that TRALI is diagnosed by excluding everything else, so that makes it a tough call for the physician. The same reference also notes that respiratory distress, cyanosis and tachypnea are prominent features in circulatory overload and that tachycardia and hypertension are usually present. Another possibility to look into...did they do chest Xrays? If heart enlargement was noted post-transfusion but not pre, that could be an indicator of volume overload. Evidence of pumonary edema on the X-ray could be another indicator. TRALI might show itself as severe bilateral pulmonary edema with severe hypoxemia, fever and mild to moderate hypotension may be present. (The hypotension associated with TRALI may not respond to IV fluids.) There is a 'classic white-out' pattern on the chest films of some TRALI patients. BUT There are no definitive tests according to anything I've read - lab or X-ray.

Another reference you can check out for free, I think, is the CDC Hemovigilance project. Google The National Healthcare Safety Network (NHSN) Manual Biovigilance Component. Appendix B of the manual portion is a nice listing/definition of reactions with signs, symptoms and diagnostic test recommendations. You can also get the same information at www.aabb.org.biovigilance - though I don't know if you have to be an AABB member or not to access it there.

[Panda]

Another possibility to look into...did they do chest Xrays? If heart enlargement was noted post-transfusion but not pre, that could be an indicator of volume overload. Evidence of pumonary edema on the X-ray could be another indicator. TRALI might show itself as severe bilateral pulmonary edema with severe hypoxemia, fever and mild to moderate hypotension may be present. (The hypotension associated with TRALI may not respond to IV fluids.) There is a 'classic white-out' pattern on the chest films of some TRALI patients. BUT There are no definitive tests according to anything I've read - lab or X-ray.

The patient's preoperative workup included a chest imaging, KG, and lab studies, all normal with the exception of creatinine, BUN, and K+ levels which were all elevated. Hhis BPwas 107mmHg/60mmHg and had a heart rate of 77bpm.

Then the last recorded stable blood pressure and heart rate was 155/91 and 98bpm

His Post-Mortem & Transfusion Medicine Lab Findings --

The patient had bilateral pulmonary congestion [combined lung weight of 2010 grams], intra-alveolar hemorrhages, and frothy and bloody secretions present in the bronchi and trachea. He also had bilateral small end stage kidneys with sever renal arteriosclerosis. Additionally, he had cardiomegaly [550 grams] and a significant pericardial serosanguineous effusion [200 mL]

Since the patient expired in the PACU, no blood samples were able to be sent to the Transfusion MEdicine Lab. Therefor, the DAT and visual assessment of gross hemolysis were not done. A clerical check revealed that the appropriate units of RBC's were released to the appropriate patient. Upon searching the Transfusion Medicine LAb database, the donors of the 4 RBC units were found to be young, healthy males.

[Panda]

Panda,you are right, HLA antibodies are prevalent with TRALI, but some TRALI the HLA antibodies is neg, as to DAT , I don't think it can different the two.

I remember 2009's Transfusion has a paper about the two's differ, it mentioned BNP as AMcCord mentioned.

I totally agree with you. I've read so many articles and sites on the web and at least half present that the HLA and DAT can be negative. So this makes it a lot harder. I would mention BNP naturally to separate the two but that would be bringing in a new element to my case study in which I'm not sure I want to do since there's many other factors I have to present and explain.

[Panda]

Here's the entire case:

CLINICAL HISTORY

A 38-year-old Caucasian male was diagnosed with biopsy-proven essential proliferative IgA nephropathy and renal arteriosclerosis in 2007. He developed hypertension, end-stage renal disease, and was on hemodialysis three days a week. His blood pressure had been recorded between 101-149 mmHg systolic and 60-88 mmHg diastolic.

In 2008, the patient was admitted to the hospital for an elective living-related kidney transplant. On his admission, his physical exam was normal. Of note, his blood pressure was 107 mmHg/60 mmHg and heart rate was 77 beats/minute. He had a preoperative workup including chest imaging, EKG, and laboratory studies; all were normal with the exception of a creatinine of 15 mg/dL, BUN of 63, and elevated potassium of 5.9 mEq/L. The patient was typed as ABO blood group A and Rh positive. The patient received Campath and steroids along with hemodialysis the evening prior to his transplant.

The next morning the renal transplant procedure was started; the initial portion of the operation was performed without difficulty. However, on reperfusion of the transplanted kidney there was a significant amount of hemorrhaging from deep in the hilum that resulted in approximately 2 liters of blood loss. The patient required large-volume intravenous fluid resuscitation, including 8 liters of crystalloid fluid, 4 liters of colloid fluid, and 4 units of packed red blood cells; all of this was given over a 60 minute period in the latter half of the operation. The blood loss was ultimately controlled with surgical repair. Following the repair, the kidney appeared to be well-perfused and began to make urine immediately. The remainder of the transplant procedure was performed without incident. The last recorded stable blood pressure and heart rate was 155 mmHg/91 mmHg and 98 beats/minute, respectively.

The patient exhibited what the Anesthesia team felt were all the appropriate signs for a safe endotracheal extubation, including being awake with spontaneous purposeful movement and good carbon dioxide and oxygen levels (PCO2 34mmHg, PaO2 166 mmHg). No central venous pressures are available. He was extubated in the operating room. However, shortly after the extubation he was unable to breathe adequately and oxygen saturations dropped precipitously (last recorded SaO2 70%). A nasal trumpet was placed and copious, bloody fluid emanated from it. The Anesthesia team attempted rigid laryngoscopy for reinsertion of an endotracheal tube, but were unable to visualize the vocal cords. A needle cricothyroidotomy attempted by the Anesthesia attending was unsuccessful. At this time, an airway code was announced. No additional blood gases were drawn.

The surgical fellow was notified, and ACLS protocol was initiated. A surgical cricothyroidotomy was performed and an endotracheal tube was placed directly into the airway under direct vision. A copious amount of watery frothy bloody fluid emanated from the endotracheal tube that required extensive suctioning before end-tidal carbon dioxide could be obtained. After end-tidal carbon dioxide was obtained, the patient was bag ventilated and ACLS protocol continued. He remained pulseless and asystolic. During this time, he became increasingly difficult to bag ventilate. Breath sounds were again confirmed, but they were decreased and eventually became inaudible. Additional fluid was suctioned out and bilateral chest tubes were placed successfully to rule out pneumothorax. However, there was no air rush on either side. A copious amount of frothy fluid continued to emanate from the mouth and endotracheal tube during this time consistent with nasopulmonary edema.

The patient was warm and the temperature greater 36 degrees Centigrade and ACLS had been performed for at least 20 minutes without oxygen saturation measured. At that time the Surgery and Anesthesia attendings agreed to cease ACLS efforts and the patient was pronounced dead. The Surgery and Anesthesia teams requested that TRALI (transfusion-related acute lung injury) be investigated as a potential cause of death. An autopsy was authorized.

POST-MORTEM and TRANSFUSION MEDICINE LABORATORY FINDINGS

On post-mortem examination, the patient had bilateral pulmonary congestion (combined lung weight of 2010 grams), intra-alveolar hemorrhages, and frothy and bloody secretions present in the bronchi and trachea. The patient also had bilateral small end-stage kidneys with severe renal arteriosclerosis. Additionally, he had cardiomegaly (550 grams) and a significant pericardial serosanguineous effusion (200 mL).

Since the patient expired in the PACU, no blood samples were able to be sent to the Transfusion Medicine Laboratory. Therefore, the DAT (direct antibody testing) and visual assessment of gross hemolysis was not done. However, a clerical check revealed that the appropriate units of red blood cells were released to the appropriate patient. Upon searching the Transfusion Medicine Laboratory database, the donors of the four red blood cell units were found to be young, healthy males.

[Yanxia]

I am suspicious he is TACO.

[David Saikin]

Since the pt did not receive any plasma products, I would think that TRALI is ruled out . . . I don't really think this is TACO either, more like fluid overload. A lot depends on how fast the bleed was. I've seen exciting bleeds with 4 units going in over 10-15 minutes, so 4 in an hour does not seem like a lot (but it depends on the bleed).

[heathervaught]

Wow...2 liters out plus 13 liters in sure sounds like enough for circulatory overload to me! To David's point - it's probably not the RBCs that did him in, but the other 12L of fluids that did.

According to the Technical Manual, "...hypertension is a constant feature in TACO, whereas it is only a transient manifestation in TRALI." (16th ed, page 735). You only have 2 BPs listed, but there should be more information in the patient's chart that would tell you if that BP of 155/91 is persistent or transient.

[Yanxia]

Yes, David is right. And this patient had kidney disease, to expel fluid's function is not good, so this maybe one reason .

[Panda]

Wow...2 liters out plus 13 liters in sure sounds like enough for circulatory overload to me! To David's point - it's probably not the RBCs that did him in, but the other 12L of fluids that did.

Would it be from the fluids containing electrolytes that caused this?

[Liz]

Panda,

Have a look that this thread, it’s helpful.

• TRALI investigation
  

[David Saikin]

I don't think the composition of the fluids makes any difference . . . seems like an awful lot of volume that did the trick.

[Panda]

Panda,

Have a look that this thread, it’s helpful.

• TRALI investigation
  

Thank you for recommending that thread to me, it was a great help.