Neil Blumberg

Here's one paper that involves extended cold storage of room temperature platelets.  They actually seemed more functional.
Xu F, Gelderman MP, Farrell J, Vostal JG. Temperature cycling improves in vivo recovery of cold-stored human platelets in a mouse model of transfusion. Transfusion. 2013 Jun;53(6):1178-86. doi: 10.1111/j.1537-2995.2012.03896.x. Epub 2012 Sep 24. PMID: 22998069.
 
 
Background: Platelet (PLT) storage at room temperature (RT) is limited to 5 days to prevent growth of bacteria, if present, to high levels. Storage in cold temperatures would reduce bacterial proliferation, but cold-exposed PLTs are rapidly cleared from circulation by the hepatic Ashwell-Morell (AM) receptor, which recognizes PLT surface carbohydrates terminated by β-galactose. We cycled storage temperature between 4 and 37°C to preserve PLT function and reduce bacterial growth.
Study design and methods: Temperature-cycled (TC) human PLTs were stored at 4°C for 12 hours and then incubated at 37°C for 30 minutes before returning back to cold storage. PLTs stored at RT or at 4°C (COLD) or TC for 2, 5, and 7 days were infused into SCID mice and the in vivo recovery was determined at 5, 20, and 60 minutes after transfusion.
Results: PLTs stored for 2 days in COLD had significantly lower in vivo recoveries than RT PLTs. TC PLTs had improved recoveries over COLD and comparable to RT PLTs. After 5- and 7-day storage, TC PLTs had better recoveries than RT and COLD PLTs. PLT surface β-galactose was increased significantly for both COLD and TC PLTs compared to RT. Blocking of the AM receptor by asialofetuin increased COLD but not TC PLT recovery.
Conclusion: TC cold storage may be an effective method to store PLTs without loss of in vivo recovery. The increased β-galactose exposure in TC PLTs suggests that mechanisms in addition to AM receptors may mediate clearance of cold-stored PLTs.

My condolences to her family, colleagues and friends.

Here's one paper that involves extended cold storage of room temperature platelets.  They actually seemed more functional.
Xu F, Gelderman MP, Farrell J, Vostal JG. Temperature cycling improves in vivo recovery of cold-stored human platelets in a mouse model of transfusion. Transfusion. 2013 Jun;53(6):1178-86. doi: 10.1111/j.1537-2995.2012.03896.x. Epub 2012 Sep 24. PMID: 22998069.
 
 
Background: Platelet (PLT) storage at room temperature (RT) is limited to 5 days to prevent growth of bacteria, if present, to high levels. Storage in cold temperatures would reduce bacterial proliferation, but cold-exposed PLTs are rapidly cleared from circulation by the hepatic Ashwell-Morell (AM) receptor, which recognizes PLT surface carbohydrates terminated by β-galactose. We cycled storage temperature between 4 and 37°C to preserve PLT function and reduce bacterial growth.
Study design and methods: Temperature-cycled (TC) human PLTs were stored at 4°C for 12 hours and then incubated at 37°C for 30 minutes before returning back to cold storage. PLTs stored at RT or at 4°C (COLD) or TC for 2, 5, and 7 days were infused into SCID mice and the in vivo recovery was determined at 5, 20, and 60 minutes after transfusion.
Results: PLTs stored for 2 days in COLD had significantly lower in vivo recoveries than RT PLTs. TC PLTs had improved recoveries over COLD and comparable to RT PLTs. After 5- and 7-day storage, TC PLTs had better recoveries than RT and COLD PLTs. PLT surface β-galactose was increased significantly for both COLD and TC PLTs compared to RT. Blocking of the AM receptor by asialofetuin increased COLD but not TC PLT recovery.
Conclusion: TC cold storage may be an effective method to store PLTs without loss of in vivo recovery. The increased β-galactose exposure in TC PLTs suggests that mechanisms in addition to AM receptors may mediate clearance of cold-stored PLTs.

I don't think the AABB comments are evidence based.  Washing with 37 degree saline is extremely unlikely to cause false negatives with clinically significant antibodies,  and I'm unaware of any evidence that this is so.  Any such antibody would be very low affinity to be washed away by saline at any temperature, and unlikely to have in vivo/clinical significance. 
As argued persuasively above by Malcolm Needs, anything that doesn't react at 30 degrees or above in typical serologic testing isn't going to cause clinical problems.  Patients are neither at 30 degrees nor centrifuged :).  Our serologic techniques are overly sensitive,  in general,  for clinically insignificant agglutinins. 
No need for cold panels ever, with rare exception, and more for intellectual curiosity than clinical decision making.  Perhaps a mini-cold screen someetimes just to confirm you are indeed detecting a weak cold agglutinin in 37 degree testing, which disappears with prewarm technique. 
Like Malcolm, I've never seen a patient with an hemolytic reaction due to an antibody that disappears with prewarming, in close to 50 years of clinical practice.  I know there are in vitro examples of clinically significant antibodies that weaken or disappear with prewarm, but I've never seen any clinical consequences.

I don't think the AABB comments are evidence based.  Washing with 37 degree saline is extremely unlikely to cause false negatives with clinically significant antibodies,  and I'm unaware of any evidence that this is so.  Any such antibody would be very low affinity to be washed away by saline at any temperature, and unlikely to have in vivo/clinical significance. 
As argued persuasively above by Malcolm Needs, anything that doesn't react at 30 degrees or above in typical serologic testing isn't going to cause clinical problems.  Patients are neither at 30 degrees nor centrifuged :).  Our serologic techniques are overly sensitive,  in general,  for clinically insignificant agglutinins. 
No need for cold panels ever, with rare exception, and more for intellectual curiosity than clinical decision making.  Perhaps a mini-cold screen someetimes just to confirm you are indeed detecting a weak cold agglutinin in 37 degree testing, which disappears with prewarm technique. 
Like Malcolm, I've never seen a patient with an hemolytic reaction due to an antibody that disappears with prewarming, in close to 50 years of clinical practice.  I know there are in vitro examples of clinically significant antibodies that weaken or disappear with prewarm, but I've never seen any clinical consequences.

I don't think the AABB comments are evidence based.  Washing with 37 degree saline is extremely unlikely to cause false negatives with clinically significant antibodies,  and I'm unaware of any evidence that this is so.  Any such antibody would be very low affinity to be washed away by saline at any temperature, and unlikely to have in vivo/clinical significance. 
As argued persuasively above by Malcolm Needs, anything that doesn't react at 30 degrees or above in typical serologic testing isn't going to cause clinical problems.  Patients are neither at 30 degrees nor centrifuged :).  Our serologic techniques are overly sensitive,  in general,  for clinically insignificant agglutinins. 
No need for cold panels ever, with rare exception, and more for intellectual curiosity than clinical decision making.  Perhaps a mini-cold screen someetimes just to confirm you are indeed detecting a weak cold agglutinin in 37 degree testing, which disappears with prewarm technique. 
Like Malcolm, I've never seen a patient with an hemolytic reaction due to an antibody that disappears with prewarming, in close to 50 years of clinical practice.  I know there are in vitro examples of clinically significant antibodies that weaken or disappear with prewarm, but I've never seen any clinical consequences.

I don't think the AABB comments are evidence based.  Washing with 37 degree saline is extremely unlikely to cause false negatives with clinically significant antibodies,  and I'm unaware of any evidence that this is so.  Any such antibody would be very low affinity to be washed away by saline at any temperature, and unlikely to have in vivo/clinical significance. 
As argued persuasively above by Malcolm Needs, anything that doesn't react at 30 degrees or above in typical serologic testing isn't going to cause clinical problems.  Patients are neither at 30 degrees nor centrifuged :).  Our serologic techniques are overly sensitive,  in general,  for clinically insignificant agglutinins. 
No need for cold panels ever, with rare exception, and more for intellectual curiosity than clinical decision making.  Perhaps a mini-cold screen someetimes just to confirm you are indeed detecting a weak cold agglutinin in 37 degree testing, which disappears with prewarm technique. 
Like Malcolm, I've never seen a patient with an hemolytic reaction due to an antibody that disappears with prewarming, in close to 50 years of clinical practice.  I know there are in vitro examples of clinically significant antibodies that weaken or disappear with prewarm, but I've never seen any clinical consequences.

RhIg after giving 12 Rh pos units is futile. The patient will either make anti-D or not, too late to prevent at this point without exchange transfusion, which seems like overkill. We always say the female of childbearing age has to live in order to worry about anti-D in a future pregnancy, so we worry about that first.
Our policy is to revert to the patient's actual type after a massive situation. We would give A neg. Now, if the patient starts massively bleeding again, we would revert to A pos. Until the patient makes that anti-D of course. 
Even though you've already given Rh pos to this patient, you did it during a mass transfusion, which is physiologically different than tranfusing an Rh pos unit low and slow. 

In emergencies, we always accept verbal orders for transfusion.  These should be followed up by a request documented in our electronic medical record, but that's after the fact.  If you have a paper system, then the followup order is documented that way.  There is a regulatory/accreditation requirement, which I consider bureaucratic, obstructive and useless,  that these emergency requests require a signed release from the ordering practitioner, if the transfusion is not fully tested for the recipient.  

In emergencies, we always accept verbal orders for transfusion.  These should be followed up by a request documented in our electronic medical record, but that's after the fact.  If you have a paper system, then the followup order is documented that way.  There is a regulatory/accreditation requirement, which I consider bureaucratic, obstructive and useless,  that these emergency requests require a signed release from the ordering practitioner, if the transfusion is not fully tested for the recipient.  

In emergencies, we always accept verbal orders for transfusion.  These should be followed up by a request documented in our electronic medical record, but that's after the fact.  If you have a paper system, then the followup order is documented that way.  There is a regulatory/accreditation requirement, which I consider bureaucratic, obstructive and useless,  that these emergency requests require a signed release from the ordering practitioner, if the transfusion is not fully tested for the recipient.  

In emergencies, we always accept verbal orders for transfusion.  These should be followed up by a request documented in our electronic medical record, but that's after the fact.  If you have a paper system, then the followup order is documented that way.  There is a regulatory/accreditation requirement, which I consider bureaucratic, obstructive and useless,  that these emergency requests require a signed release from the ordering practitioner, if the transfusion is not fully tested for the recipient.  

In emergencies, we always accept verbal orders for transfusion.  These should be followed up by a request documented in our electronic medical record, but that's after the fact.  If you have a paper system, then the followup order is documented that way.  There is a regulatory/accreditation requirement, which I consider bureaucratic, obstructive and useless,  that these emergency requests require a signed release from the ordering practitioner, if the transfusion is not fully tested for the recipient.  

In emergencies, we always accept verbal orders for transfusion.  These should be followed up by a request documented in our electronic medical record, but that's after the fact.  If you have a paper system, then the followup order is documented that way.  There is a regulatory/accreditation requirement, which I consider bureaucratic, obstructive and useless,  that these emergency requests require a signed release from the ordering practitioner, if the transfusion is not fully tested for the recipient.  

Agree that a urine specimen isn't indicated for an allergic reaction, so no worries.

Sounds like total rubbish from both a clinical and scientific viewpoint. Another instance how the administrative/legal model of reality is undermining civilization :).

The fact is that we have little to no evidence that platelet transfusion of any sort will mitigate post-pump bleeding.  This is expert opinion only that has driven this practice. What we have learned in the last few years is that platelet transfusion as currently practiced (ignoring ABO for one thing) actually increases bleeding and mortality in some clinical settings.  I'd rather have some oozing than be transfused with platelets empirically, both as a patient and a hematologist.  With life threatening bleeding and abnormal platelet function as measured by a closure time or TEG/ROTEM, platelet transfusion makes sense and has some data driven support.  Oozing, no data whatever.

Sounds like total rubbish from both a clinical and scientific viewpoint. Another instance how the administrative/legal model of reality is undermining civilization :).

The fact is that we have little to no evidence that platelet transfusion of any sort will mitigate post-pump bleeding.  This is expert opinion only that has driven this practice. What we have learned in the last few years is that platelet transfusion as currently practiced (ignoring ABO for one thing) actually increases bleeding and mortality in some clinical settings.  I'd rather have some oozing than be transfused with platelets empirically, both as a patient and a hematologist.  With life threatening bleeding and abnormal platelet function as measured by a closure time or TEG/ROTEM, platelet transfusion makes sense and has some data driven support.  Oozing, no data whatever.

Short periods of time (<12 to 24 hours say) at refrigerator temperatures have no known deleterious effect on platelet transfusion efficacy, so I would use them as I would use any platelet component stored at room temperature.  I routinely approve this at my own institution when this happens.

I should have added that I recognize that some cardiac surgeons transfuse platelets routinely post-bypass in the hope of reducing bleeding.  I suggest this is a traditional practice without the slightest shred of evidence for benefit.  Purely guesswork and expert opinion, for which there is now evidence of harm.   So whether you give cold or room temp platelets probably doesn't matter as (1) there is likely no benefit to either approach,  and (2) there is likely equivalent harm either way. 
So my short answer is it doesn't matter,  but that platelet transfusion to non-bleeding surgical patients likely doesn't help,  and may increase the risk of thrombosis, inflammation and reduced host defenses against post-operative infection. 

Sounds like total rubbish from both a clinical and scientific viewpoint. Another instance how the administrative/legal model of reality is undermining civilization :).

I should have added that I recognize that some cardiac surgeons transfuse platelets routinely post-bypass in the hope of reducing bleeding.  I suggest this is a traditional practice without the slightest shred of evidence for benefit.  Purely guesswork and expert opinion, for which there is now evidence of harm.   So whether you give cold or room temp platelets probably doesn't matter as (1) there is likely no benefit to either approach,  and (2) there is likely equivalent harm either way. 
So my short answer is it doesn't matter,  but that platelet transfusion to non-bleeding surgical patients likely doesn't help,  and may increase the risk of thrombosis, inflammation and reduced host defenses against post-operative infection. 

I'd also add that none of the cell washers are FDA approved for washing platelets. We've been washing platelets on the 2991 for about 40 years :).  I believe there may be a paper on using the ACP-215 to wash platelets but as yet we do not have any hands on experience.  We have developed a manual method of platelet washing using a Sorvall centrifuge.  If your volume isn't too high, you might consider a manual wash method.  It takes a bit longer, but actually has higher recoveries (>90% vs. about 80-85% with the 2991). 
 
Folks will tell you that washed platelets don't work clinically and the count increment is Washed Tx Leukemia.pdfWashed Tx Leukemia.pdflower.  The increment is indeed lower, but if you employ platelets that aren't ABO incompatible with the recipient and remove the supernatant, the clinical results are actually better than the clueless advice to give ABO major incompatible platelets routinely (e.g., group A to group O recipients).  The PLADO study had a bleeding rate using this abominable practice of about 70%.  Our bleeding rate avoiding infusion of ABO incompatible antigen or antibody is 5%, with or without washing.  A fourteen fold difference. So by all means give washed platelets to patients with severe or recurrent reactions, or avoid infusion of ABO incompatible plasma, and, if you believe our randomized trial data, to improve the survival of younger patients with acute myeloid leukemia. References attached if anyone is interestedWashing AML Greener_et_al-2017-American_Journal_of_Hematology.pdf.
Washing Review IJCTM-101401-the-clinical-benefit-of-washing-red-blood-cells-before-transfusion.pdf Washing AML Greener Am J Hemat AML Washing Supplementary Figures and Tables.pdf Jill's washing paper.pdf Plt Washing Vo.pdf

I agree with the procedures above. But these are basic urgent communications required of any clinical service,  and I wouldn't characterize them as critical values, which are emergencies.  Perhaps it's just semantics :).