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Neil Blumberg

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Neil Blumberg last won the day on October 13

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    Hematologist/Transfusion Medicine Physician

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  1. 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.
  2. 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.
  3. 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.
  4. Obviously worth repeating. Sample mixup, technical error are other possibilities.
  5. 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 gre
  6. 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
  7. 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 everyon
  8. 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.
  9. 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 transfus
  10. 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,
  11. 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 t
  12. 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
  13. 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.
  14. 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.
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