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5 Cards in this Set

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Alloimmunization to blood antigens occurs after the following:
Alloimmunization to blood antigens occurs after the following:
Transfusion
Pregnancy
Transplantation
Sharing intravenous needles (rare)
Delayed hemolytic transfusion reactions lab test
Delayed hemolytic transfusion reactions
The most reliable laboratory sign is a failure to observe the expected posttransfusion increase in blood hemoglobin levels (approximately 1 g/dL/U) in the absence of bleeding.
In some cases, the loss of circulating cells can be higher than expected if only antigen-positive cells were cleared. This phenomenon results from bystander hemolysis, which is caused by the deposition of activated complement on both donor and recipient RBCs.


Laboratory signs of hemolysis include elevated lactate dehydrogenase, indirect bilirubin, and reticulocyte levels and decreased hematocrit and haptoglobin levels.
Intravascular hemolysis is characterized by the presence of free plasma hemoglobin and possibly hemosiderinuria.
The results of direct and indirect antiglobulin tests (ie, Coombs test) are often positive.
Alloantibodies can be eluted from RBCs, and their specificity can be determined. In case of hemolysis, sensitive elution techniques should be done to identify alloantibodies, even if serum antibodies are undetectable and the direct antiglobulin test is negative. Often (about 15-20%), patients with DHTR have multiple antibodies and some may be detectable only by elution.
Type the donor RBCs for affected antigens and re-crossmatch them with the patient's serum if segments from the transfused units are available.
Refractoriness to platelet transfusions
Refractoriness to platelet transfusions
Refractoriness to platelet transfusions is defined as repeated failure to achieve the expected increment in platelet count after 2 or more platelet transfusions. The expected increment can be calculated based on the number of platelets transfused and the patient's blood volume using the formula as follows:
% Maximum increment = ([pretransfusion count – posttransfusion count in platelets/µL] X blood volume in mL) ÷ (number of platelets transfused, ie, number of U X 6 X 105)
The expected increment is 45-75% of the maximum increment, resulting from normal sequestration by the spleen.
Blood volume can be calculated roughly as body weight (kg) multiplied by 69 (males) or by 65 (females); the number of platelets transfused assumes an average content of 6 X 1010 platelets/U; an average apheresis unit contains the equivalent to 6 units of platelets (4 X 1011 platelets).
Observed increments of less than 30% at 10-60 minutes or less than 20% at 18-24 hours indicate platelet refractoriness.
A simple screen for platelet refractoriness is failure to achieve an increment of >5 X 109/L (5,000/µL) at 20-24 hours after transfusion of a standard platelet dose (1 unit/10 kg of pooled platelets or one single donor apheresis unit).
Note that many cases of refractoriness result from causes other than alloimmunization (see Differentials).
Medical Care
Delayed hemolytic transfusion reactions
Medical Care
Delayed hemolytic transfusion reactions
Most patients tolerate DHTR well and only require observation and supportive care.
Good communication with a blood bank is essential to attempt to provide transfusion support with antigen-negative RBCs. If these RBCs are not available, weigh the risk of further hemolysis against the indications for transfusion.
If the load of antigen-positive packed RBCs is large (>5 U), consider exchange transfusion. Administer intravenous human immunoglobulin (IVIG) to block further hemolysis in cases in which antigen-positive blood is transfused. The IVIG dose is 400 mg/kg, infused slowly within 24 hours posttransfusion.
Refractoriness to platelet transfusions
Refractoriness to platelet transfusions
Avoiding the use of platelet transfusions as much as possible is important in alloimmunized patients. Preventive transfusions are not recommended. Measures to minimize the likelihood and extent of bleeding (eg, rapid treatment of infection; avoidance of invasive procedures; correction of coagulation deficiencies, anemia, and renal insufficiency; use of antifibrinolytic agents) should be used extensively.
After diagnosing alloimmune platelet refractoriness, use the sequence of measures that follows, initiating each subsequent intervention if the previous one fails.
Rule out nonimmune, autoimmune, and drug-related causes of platelet refractoriness, or treat accordingly. Providing immune-compatible platelets is unlikely to be effective in the presence of nonimmune causes of refractoriness.
Consider alternatives to platelet transfusion to control bleeding, including the use of antifibrinolytic agents such as alpha-aminocaproic acid, or activated recombinant factor VIIa.[9]
Transfuse ABO-compatible fresh (aged < 48 h) platelet concentrates. ABO-matched and fresher platelets result in more recoveries than mismatched and older (aged >3 d) platelets.
Transfuse with platelets from blood relatives. Obtaining platelets from blood relatives is worthwhile because the chance of matching 2 or more HLA and platelet antigens is high (resulting in good recovery) and relatives are often willing to donate frequently. Irradiation of blood products from relatives is mandatory to prevent graft versus host disease.
Select HLA-matched platelets. Perform HLA typing of patients who receive multiple transfusions before they become pancytopenic. Matching for both private (ie, HLA-A, HLA-B) and public (ie, cross-reacting groups) antigens is best achieved by computerized selection of donors, based on the results of the PRA assay.
Select crossmatched platelets. Crossmatch-compatible platelets can significantly improve platelet recovery in approximately 50% of patients who are refractory to random-donor platelets. Selecting crossmatched platelets is indicated especially for patients with high PRA levels or those who do not respond to HLA-matched platelets.
The use of HPA1a/5b-negative platelets has been successful in cases of posttransfusion purpura and neonatal platelet alloimmunization. These antigens are involved in most (95%) cases of neonatal or posttransfusion purpura, but they represent no more than 10-20% of immune refractoriness to platelet transfusions.
Pretreat with IVIG before transfusion. IVIG pretreatment can result in successful recovery after platelet transfusion in patients who are alloimmunized. Success rates vary (as much as 70%) and depend on the degree of alloimmunization. IVIG does not reduce the number of alloantibodies but does decrease platelet-associated immunoglobulins and possibly interferes with platelet destruction mechanisms. IVIG is more effective in improving short-term (1-6 h) recovery of platelets than platelet survival (>24 h).
Use high-dose platelet transfusion. Empirical use of high doses of random platelet units (eg, 1 unit/10 kg tid or 2-3 units/10 kg before invasive procedure) may result in titration of the antibody, overwhelming of the mononuclear-phagocyte system, and increased survival of transfused platelets.
Attempt large-volume plasmapheresis. Plasmapheresis (eg, 2 plasma volumes for 1-3 d) before bone marrow transplantation results in beneficial responses in most patients who are alloimmunized to platelets. Perfusion of the plasma through a staphylococcal protein A column is an experimental treatment undergoing evaluation.
Consider administering immunosuppressive drugs. While steroids are not effective, isolated reports suggest that immunosuppressive therapy is effective for reverting platelet refractoriness. The use of vincristine and cyclosporin A has been successful but requires 2-3 weeks to take effect.