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Neil Blumberg

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Everything posted by Neil Blumberg

  1. I've summarized the data in this letter: https://www.bmj.com/content/366/bmj.l4968 In randomized trials, the fresher blood arm is associated with a higher incidence of nosocomial infection (immunomodulation, presumably). There has never been any data examining clinical outcomes that actually favors using very fresh blood. Mostly just "expert opinion" and "it seemed like a good idea." That's not good enough now, in my view. Two key references (one only published in abstract form) are: Alexander PE, Barty R, Fei Y, et al . Transfusion of fresher vs older red blood cells in hospitalized patients: a systematic review and meta-analysis. Blood2016;127:400-10. doi:10.1182/blood-2015-09-670950 pmid:26626995 Abstract/FREE Full TextGoogle Scholar ↵ Schmidt A, Gore E, Cholette JM, et al . Oxidation reduction potential (ORP) is predictive of complications following cardiac surgery in pediatric patients[abstract]. Transfusion2016;56(Supplement S4):20A-1A. Google Scholar
  2. Our neonatal intensive care transfusions are all irradiated because many severe immunodeficiency states are not evident until weeks to months after birth. These are rare, and leukoreduced transfusions probably mitigate the risk of GVHD somewhat, but we are erring on the side of caution. We irradiate just before transfusion so the storage based problems with irradiated red cells are less of a concern. We define fresh as <21 days of storage, because the data suggest very fresh blood is actually more dangerous to patients than blood stored 7-21 days or so. Seat of the pants, to be sure, but somewhat data driven. No one knows for sure, but very fresh blood (<7 days storage) is totally unnecessary in terms of proven benefit and may actually be more dangerous, for reasons that are largely unknown.
  3. All you need to do is document platelet recovery (should be at least 80%) and pH. Nothing else is required. No platelet function tests, etc. since these are not used with unwashed platelets. Would recommend washing in platelet additive solution rather than saline.Washed platelet buffy coat platelet additive manual.pdf
  4. Should mention that Terumo has a similar process that is licensed in Europe using riboflavin. Both Cerus and Terumo have licenses for whole blood platelets but for some reason these have not been introduced in the USA, so only apheresis platelets are pathogen reduced at present. Which makes little sense from a resource or cost standpoint. There are no clinical advantages to pathogen reduced apheresis platelets over whole blood platelets and apheresis platelets carry a greater risk of acute lung injury due to the five fold increase in plasma from a single "dangerous" donor.
  5. Pathogen reduced platelets are treated with a Cerus Corp. method of using light to activate a photo-activated psoralen compound that cross links DNA and RNA, thus making it impossible for cells to replicate, and, more importantly, viruses, bacteria and fungi to replicate. Thus the risks of bacterial infection after platelet transfusion become near zero. Increases the cost by about $150 from your blood supplier. Saves the occasional life threatening post-transfusion bacterial septic infection, and may reduce line infections too I'd guess.
  6. There is absolutely no scientific or clinical reason that a vaccine could not be stored with frozen blood components. That doesn't mean you won't get some overly officious inspector who will decide it's a bad idea. But currently there are no regulatory or accreditation issues that I am aware of.
  7. We used to do universal irradiation but then became aware of two things. One, irradiation of red cells causes increased hemolysis during storage. That's been known for some time. But in recent years, the toxic effects of infusing free hemoglobin or increasing hemolysis in vivo have become evident (e.g., sickle cell anemia; levels of hemolysis correlating with morbidity in surgical patients). So we stopped irradiating everything at that point. Just per protocol. Leukoreduction reduces GVH in the British data.
  8. No one knows what to do for sure. We keep such patients on irradiated for life, since these recipients are not immunologically normal in many cases. But there are no data to support or refute this practice. Seems low risk and prudent to us.
  9. I would not be performing one hour post-transfusion vital signs unless the patient has signs or symptoms that require assessment. I would not be reacting to one hour post-transfusion data unless they were consonant with a transfusion reaction. If fever was the only sign or symptom, it's probably not transfusion related in the vast majority of cases. Routine vital signs in the absence of a clinical rationale are a problem, not a solution.
  10. Agree with Malcolm. We would tend to give Rh negative blood transfusions so we can tell when the recipient's cells are largely gone. We might do this in particular if the recipient is a female of child bearing age or younger. But we would not be giving Rh immune globulin in the vast majority of settings for the reason that Malcom mentioned.
  11. IM injections hurt. IV hurt much less. Both acutely and over the next day or two. That's the likely motivation. Most physicians don't administer IV meds in their office as it requires more time and skill.
  12. Obviously worth repeating. Sample mixup, technical error are other possibilities.
  13. Should add that individuals with sickle trait have % S that is usually less than 50%. At those levels, even patients with SS disease usually are asymptomatic. Sickle trait individuals do not have symptoms under anything less than extreme physiologic stress, although some believe that occasional individuals have had complications when severely hypoxic or stressed. These case reports tend to neglect the fact that individuals who do not have S hemoglobin can have similar symptoms under extreme physiologic or hypoxic stress, so it's not clear these individuals with sickle trait are truly at greater risk. Larger cohort studies have sometimes suggested a higher rate of symptoms among AS (sickle trait) individuals, but there remains some doubt, at least in my mind :).
  14. Sounds like a good plan. Reducing needless work is a great idea. I find it absurd to require busy practitioners to attest to the urgency of a clinical request by installing bureaucratic obstacles. It may be required by regulators and accreditation agencies, but it is bureaucratic nincompoopery (sic) to my mind, serving no real purpose. A discussion of the pros and cons of giving out red cells without an antibody screen should occur with every such request when time allows. Almost no one does a physical crossmatch these days anyway, to my knowledge, except if alloantibodies are present. This requirement is obsolete. Documenting in the medical record what you did and why should be the priority, not filling out forms taking responsibility for that which one is obviously entirely responsible. The transfusion service doesn't decide when to transfuse patients, so obviously a decision to urgently transfuse partially tested or untested blood is the responsibility of the ordering practitioner. Duh.
  15. Patients with sickle trait do not have sickle crises at all, except in very rare cases when they become seriously hypoxic. There are rare cases reported in military personnel and athletes. It's not clear whether they are sickle crises in some cases or just similar symptoms seen in non-sickle cell patients. These are truly rare cases, and usually at higher stress than an altitude of 8,000 feet, which really isn't terribly high. No personal experience. In extreme circumstances, patients heterozygous for S may be slightly more susceptible to symptoms like mountain sickness, just like everyone else. Don't know for sure. They have lower hematocrits and this may be one factor. Distinguishing between sickle cell symptoms and mountain sickness may be difficult for some clinicians. Lots of people get sick at altitude, especially if they exert themselves or make the ascent rapidly, or are dehydrated. I would guess that is what happened to this group. There is no need for hemoglobin S negative units for routine transfusions to non-sickle cell, hemoglobin homozygous patients.
  16. People heterozygous for hemoglobin S have no clinical level problems with transporting oxygen, so there is no need (except for being overly cautious) to provide hemoglobin S tested blood for newborns, or, as I mentioned above, anyone who is not being monitored for % S. Another one of those "it seemed like a good idea at the time" but not evidence based approaches.
  17. The answer is a bit more complicated. If there is no target for %S, there is no need to test for hemoglobin S in donor blood. In other words, if the transfusion is purely for anemia, not treatment of acute chest syndrome or prevention of stroke, there is usually no target %S being used by the treating physician. The reason for testing for S in the donor is not the risk to the patient, but because transfusing S containing blood can confuse the calculation of % S overall. It's probably unnecessary because the %S contribution of a single unit of S heterozygous red cells in an exchange transfusion or red cell apheresis is very small. S hemoglobin in a red cell that is from a heterozygous donor does not contribute to sickling complications. This is well known because individuals who are heterozygous for S do not have complications of sickle cell disease. Thus while it is traditional to test for hemoglobin S in donor blood for sickle cell recipients, this is probably unnecessary unless the treating physician is trying to achieve a specific %S, as in stroke prevention.
  18. I disagree. First of all, most patients with IgA deficiency and anti-IgA do not experience anaphylaxis. Secondly patients with anaphylaxis (a rare event indeed) do not have usually have IgA deficiency, much less anti-IgA antibody (see work by G. Sandler and colleagues refuting the ancient report of a handful of patients). Thus, to me, this is a waste of time and money and unnecessary. The key to safe plasma transfusion from this standpoint is to take about 30 minutes to run in the first 15 milliliters or so, and have a crash cart with epinephrine available should anaphylaxis occur (which, 99,999 out of 100,000 times it won't). And take a history of previous anaphylactic reactions to insect stings, dietary constituents, etc. Those patients you might want to be very careful with.
  19. We have about 30 patients in our ICU and about 60 outside the ICU. Almost no transfusions to these patients, and our intensivists and hospitalists are not enthusiastic about transfusions of any sort in these patients. Skeptical about the net benefits of convalescent plasma as well, particularly in the most severely ill patients, for a variety of reasons. We will only be transfusing convalescent plasma as part of randomized trials as a general rule. Most importantly, transfusions should not be based primarily on laboratory abnormalities such as the hematocrit/hemoglobin, PT, PTT, etc. in the absence of life threatening anemia or bleeding.
  20. No, I meant ABO identical. Giving A plasma to O patients is not a good idea, despite 100 years of practice, give or take. A plasma contains soluble A antigen glycolipids and glycoproteins, and these interact with the anti-A in the group O recipient, forming huge immune complexes. We and others have observed that patients receiving "compatible plasma" have increased bleeding, increased lung injury and increased risks of infection. The studies that suggest this isn't true are fatally flawed by characterizing the patients receiving platelets or plasma by their first transfusion (ABO identical or not), regardless of what subsequent transfusions they received. Stick with ABO identical if at all possible.
  21. Would suggest using only ABO identical plasma. ABO mismatched plasma creates soluble immune complexes that, at least in vitro, damage endothelial cells, impair platelet function and cause dysfunction in the coagulation cascade (thrombin generation). Probably not a good thing in patients who already have these problems ongoing.
  22. These patients have a number of potential mechanisms for false positives. Drug is one, and the others are excessive fibrin formation due to DIC and complement activation, which are both seen in seriously ill patients. I assume you are not using anti-complement reagents in your antibody screening, so that is less likely.
  23. Transfusing platelets (and plasma)prophylactically to patients without serious bleeding, based solely upon laboratory abnormalities of hemostasis/platelet count, is a serious clinical error in my opinion. Platelets and plasma impair host defenses against viral and bacterial infection, promote inflammation and thrombosis, and likely increase the risk of multi-organ failure. Thus I would reserve these products for situations where these serious toxicities are outweighed by the potential for treating life-threatening bleeding. This opinion is shared by one of the world's experts on hemostasis and thrombosis, the London based hematologist Beverly Hunt, who has tweeted her recommendations for these patients. See this link for her four pager on the subject. https://twitter.com/bhwords?ref_src=twsrc^google|twcamp^serp|twgr^author
  24. In a statewide web conference, the blood suppliers in New York State and the NY metro area (parts of New Jersey) provided the reassuring news that by setting up alternate fixed sites for (mostly) whole blood collection, the blood supply has been about normal. Platelets are collected at fixed sites and the donors have been wonderful. Transfusion in our area (Rochester NY) is slightly down as we are not transplanting patients without urgent indications (myeloma can sometimes wait, for example) and elective surgery is not happening. So right now, things in New York State, the worst hit part of the country, are remarkably and thankfully reasonable for blood supply. We can thank the dedicated staff of the Red Cross and NY Blood Center, and, of course, our courageous and committed donors for this good news. Hang in there, not that there's any other place to hang.
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