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Neil Blumberg

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Neil Blumberg last won the day on May 25

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    Hematologist/Transfusion Medicine Physician

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  1. 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.
  2. 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.
  3. 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.
  4. 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.
  5. 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.
  6. 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.
  7. 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
  8. 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.
  9. IVIgG can contain detectable rbc alloantibodies, although it would be unusual to be anything other than anti-A and anti-B.
  10. N Engl J Med. 2010 Feb 18;362(7):600-13. doi: 10.1056/NEJMoa0904084. Dose of prophylactic platelet transfusions and prevention of hemorrhage. Slichter SJ1, Kaufman RM, Assmann SF, McCullough J, Triulzi DJ, Strauss RG, Gernsheimer TB, Ness PM, Brecher ME, Josephson CD, Konkle BA, Woodson RD, Ortel TL, Hillyer CD, Skerrett DL, McCrae KR, Sloan SR, Uhl L, George JN, Aquino VM, Manno CS, McFarland JG, Hess JR, Leissinger C, Granger S. Author information Abstract BACKGROUND: We conducted a trial of prophylactic platelet transfusions to evaluate the effect of platelet dose on bleeding in patients with hypoproliferative thrombocytopenia. METHODS: We randomly assigned hospitalized patients undergoing hematopoietic stem-cell transplantation or chemotherapy for hematologic cancers or solid tumors to receive prophylactic platelet transfusions at a low dose, a medium dose, or a high dose (1.1x10(11), 2.2x10(11), or 4.4x10(11) platelets per square meter of body-surface area, respectively), when morning platelet counts were 10,000 per cubic millimeter or lower. Clinical signs of bleeding were assessed daily. The primary end point was bleeding of grade 2 or higher (as defined on the basis of World Health Organization criteria). RESULTS: In the 1272 patients who received at least one platelet transfusion, the primary end point was observed in 71%, 69%, and 70% of the patients in the low-dose group, the medium-dose group, and the high-dose group, respectively (differences were not significant). The incidences of higher grades of bleeding, and other adverse events, were similar among the three groups. The median number of platelets transfused was significantly lower in the low-dose group (9.25x10(11)) than in the medium-dose group (11.25x10(11)) or the high-dose group (19.63x10(11)) (P=0.002 for low vs. medium, P<0.001 for high vs. low and high vs. medium), but the median number of platelet transfusions given was significantly higher in the low-dose group (five, vs. three in the medium-dose and three in the high-dose group; P<0.001 for low vs. medium and low vs. high). Bleeding occurred on 25% of the study days on which morning platelet counts were 5000 per cubic millimeter or lower, as compared with 17% of study days on which platelet counts were 6000 to 80,000 per cubic millimeter (P<0.001). CONCLUSIONS: Low doses of platelets administered as a prophylactic transfusion led to a decreased number of platelets transfused per patient but an increased number of transfusions given. At doses between 1.1x10(11) and 4.4x10(11) platelets per square meter, the number of platelets in the prophylactic transfusion had no effect on the incidence of bleeding. (ClinicalTrials.gov number, NCT00128713.)
  11. For platelets you can cut the dose in half with no worsening of clinical outcomes. Randomized trial in NEJM called the PLADO (platelet dose) study some years ago (Sherrill Slichter was the senior author). Most platelets do little or no good, so this is actually a good idea for patients and helps with inventory in times of shortage. Try to give ABO identical as the increment is higher, the duration of increment is longer and the patients bleed less.
  12. Probably the primary stimulation was not the fetus, but previous pregnancy, transfusion, tattooing, needle sharing, non-sterile tattooing, etc. Pregnancy is a situation in which B cells are upregulated (type 2 immunity) and T cells down regulated (roughly speaking) and pregnancy may have increased B cell activity to the point where previously undetectable antibodies are now detectable. Just a theory ;).
  13. Best guess is that the antigenic stimulation (at least primary) was not the fetus. Sharing needles, tattooing, blood sharing ceremonies and transfusions the patient was not aware of may have been the sources of stimulation of the primary immune response. Pregnancy stimulates Type 2 immunity (B cells mostly) which may increase the detectability of previously existing antibodies, at least in theory.
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