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No reactions were seen with panel cell 1 and 2. This rules out M,N,and s.Notice that C, E, Fya, and P1 are not present on these cells so as not to interfere with ruling-in or ruling-out of the remaining antibodies.ConclusionThrough the processes of ruling-in and ruling-out and matching of reaction patterns, the antibodies that are identified are C,E, Fya, and P1.If the patient has not been transfused in the past 3 months, antigen typing for Fya may be done to further confirm the presence of Fya.Elution and autoadsorptions may also be necessary to confirm the presence of C,E, Fya and P1.

Is there any process in health care that can run at or above Six Sigma level? Transfusion medicine has actually achieved above and beyond Six Sigma, confirming that a Six Sigma level of quality can actually be achieved not only in aviation or manufacturing, but in health care as well. Transfusion medicine is one of the most regulated and earliest adapters of a quality system approach to quality management. Let us look at how transfusion medicine measures up when we translate this statistic into Six Sigma.Based on the FDA Center for Biologics Evaluation and Research (CBER) "Fatalities Reported to FDA Following Blood Collection and Transfusion" annual summary, there were 52 transfusion-related fatalities in the fiscal year of 2007 (October 1, 2006, through September 30, 2007). According to the National Blood Collection and Utilization Survey conducted by AABB, a total of 30,044,000 units of blood components were transfused during 2006. Three opportunities for defect (pre-analytical, analytical and post-analytical) will be used to determine transfusion safety in the United States. By using the formula from the previous page, we can determine both the DPMO and process sigma.DPO = 52/(30,044,000 x 3) = 0.0000005769DPMO = 0.0000005769 x 106 = 0.58Process Sigma = 6.36Transfusion medicine did not achieve Six Sigma level of quality overnight, and other industries who are operating at Six Sigma level, such as the aviation industry, have taken decades to achieve this level of quality.

This is a higher power view of this same smear demonstrating a neutrophil that is filled with Toxopasma gondii tachyzoites (blue arrow).There are a few free organisms in this image well, indicated by the red arrows. Again, the typical morphology for toxoplasmsa organisms is lavender cytoplasm with a red granular cluster in the center of each parasite.This patient was negative for Toxoplasma gondii prior to a transplant but had received 15 units of blood products due to cytopenias.It is believed that a donor for one of the transfused units had been exposed to Toxoplasma gondii either through cats or contaminated food and had transient circulating Toxoplasma gondii in his or her blood when the donation was made. In this case, the recipient was profoundly immunocompromised, which lead to rapidly developing systemic disease.

False-positive results using the solubility test may be obtained in persons with increased red blood cell counts as occur in polycythemias; extremely high white counts, as in some leukemias; and extremely high platelet counts. Increased levels of lipids or globulins may also cause a false-positive. Hemoglobins that show a positive solubility test include HbC-Harlem, HbC-Georgetown, and HbC-Ziquinchor.False-negatives in the solubility test may be obtained on persons with severely decreased hemoglobins/hematocrits and those recently transfused. Infants less than six months old may also demonstrate false-negative results due to higher levels of HbF.False results in the solubility test can occur due to problems with technique: too much or too little blood added will result in false-positive and false-negative respectively; use of incorrect size test tube, holding the test tube too close to the background, and using deteriorated reagents can all lead to false-negative results.

Besides exchange transfusion, postnatal treatment of HDFN may include the following:RBC TransfusionMany infants who have received IUTs also require simple RBC transfusions in the first few weeks of life to treat ongoing hemolysis caused by persistent maternal antibody in the newborn's circulation.Phototherapy Phototherapy is used to treat jaundice in preterm infants without HDFN and in infants with mild HDFN. Intensive phototherapy has also been used to treat moderate and severe HDFN and decrease the need for exchange transfusion. The newborn is placed under a "blue light" which chemically alters the bilirubin in the surface capillaries to a harmless substance. Human Serum AlbuminHuman serum albumin can also be transfused, either separately or as part of an exchange transfusion in place of FFP. Albumin binds unconjugated bilirubin, thus preventing its deposition in the fat-rich brain cells. Albumin must be used judiciously, because it can aggravate congestive heart failure.

The Red Blood Cells (RBC) that are chosen for exchange transfusion must meet these criteria: ABO-compatible with mother and infant (usually group O) and lack antigens to any maternal IgG antibodies; If mother has anti-D, RBCs are group O Rh negative; No greater than 7 days old; Reconstituted with AB Fresh Frozen Plasma (FFP) to obtain a prescribed hematocrit, e.g., 45–60% (0.45–0.60); CMV negative (or equivalent, e.g., leukoreduced by filtration); Negative for hemoglobin S to prevent blood from hypoxia-induced sickling; Irradiated with a minimum dose of 25 Gray (Gy) to prevent graft-versus-host disease.RBC are normally crossmatched with maternal plasma, although the infant's plasma can be used if a maternal blood specimen is unavailable.

Homozygous "hh" individuals do not form H substance and thus have no way for late sugars to attach. The blood group resulting from the homozygous "hh" condition is called the Bombay blood group (Bombay phenotype). Due to the presence of anti-H in the serum of a person with the Bombay phenotype, only blood from another person with the Bombay phenotype may be transfused.

As noted, policies for administering RhIg to mothers with a variant of D vary among countries and within some countries. An Rh(D) red blood cell phenotype with a weak or variant expression of the D antigen occurs in 0.2% to 1% of whites and is slightly more common in African Americans. The phenotype is routinely called weak D, although several variants exist. A simple model includes these D variants: 1. Weak DMultiple weak D variants exist. Red cells have fewer D antigens/red cell (quantitative difference) and only minor variations in D antigen proteins. Some, but not all, weak D phenotypes are detected by today's Rh typing sera and may be classified as Rh positive or Rh negative by routine testing but will be positive when a weak D test (IAT with anti-D) is done. An extreme form of weak D is the Del phenotype, in which the D antigen is so weakly expressed that it may be demonstrated only by adsorption and elution of anti-D. Weak D individuals do NOT produce anti-D and can be considered to be Rh positive for transfusion and RhIg purposes.2. Partial DPartial D variants have altered Rh(D) proteins that differ sufficiently from normal D antigens (qualitative difference) to allow anti-D production. Partial D red cells may react with some but not all anti-D typing reagents. There are many categories of partial D antigens (e.g., DIIIa, DVI, DAR), each with a unique genetic basis.Some persons with partial D have weakly expressed D epitopes and are designated "partial weak D."In practice, partial D and weak partial D can be considered similarly, i.e., ideally they should be transfused with Rh negative RBC and are candidates to receive perinatal Rh immune globulin depending on the policy in their location.

The following signs and symptoms are associated with acute HTR due to ABO incompatibility but can be associated with other blood group incompatibilities. ABO incompatibility typically results from patient misidentification.The more serious symptoms result from intravascular hemolysis (IVH) caused by antibodies such as anti-A and anti-B that can bind complement to C9.Signs and symptoms typically appear within minutes of the transfusion but can occur anytime during the transfusion. They may include: 1. Burning sensation along the vein being transfused (IVH due to complement activation to C9)*2. Lower back pain in the area of the kidneys (renal failure with subsequent oliguria/anuria) *3. Unexplained bleeding/oozing from a surgical site (fibrinolysis following DIC)*4. Hypotension leading to hypovolemic shock (release of vasoactive substances caused by C3a and C5a)5. Tightness in substernal area of the chest (bronchial constriction due to release of vasoactive substances caused by C3a and C5a fragments)6. Other symptoms: fever, chills, skin flushing, dyspnea, wheezing, anxiety, malaise, nausea, headache. * If untreated, these complications may lead to patient death.

In this case the patient's antibody has disappeared from the plasma by adsorbing to transfused donor red cells. It is detectable but unidentifiable in the post-transfusion red cell eluate. Several trial and error procedures exist to enhance weak antibodies. Which methods will enhance the reactivity of a given antibody depend on its characteristics. Methods to investigate weak antibodies include: Use a higher plasma to red cell ratio (add more antibody-containing plasma or eluate) Increase incubation time (if consistent with manufacturer instructions, if applicable) Use enzyme-treated panel red cells (enzymes enhance IgG antibodies in Rh and Kidd blood systems but denature some antigens, e.g., Fya, Fyb, S) Try alternative antibody detection methods, e.g., if using LISS routinely, try polyethylene glycol (PEG) or column agglutination methods such as gel, providing they have been validated for use in the TS laboratory.

A standard follow-up to antibody identification is to antigen phenotype: Patient's red cells (expecting them to lack the corresponding antigen) Donor red cells (in this case, those transfused before an antibody was identified, or, more typically, to find suitable antigen-negative donors to crossmatch prior to transfusion).If you had wanted to type the patient for any antigens at this point in the investigation (2-weeks post-transfusion), which specimen would you have used? Think about any antigen typing problems and how to overcome them before proceeding to the next page.

Adverse complications of transfusions can be classified into several categories: Immune-mediated transfusion reactions are those that trigger a response from the patient's immune system. Many transfusion reactions are mediated by the recipient's immune system. These reactions occur as a result of antigen-antibody interactions. Antibodies involved include those with specificity towards antigens on red cells, white cells, or platelets. In general, the immune responses occur in three stages: the immune system detects foreign material (antigen) the immune system processes the antigen the immune system mounts a response to remove the antigen from the body Non-immune mediated hemolytic transfusion reactions are caused by the physical or chemical destruction of transfused RBCs, bacterial contamination, circulatory overload, or citrate toxicity. Acute reactions are those that occur during or within 24 hours after the transfusion. There is usually a rapid onset of symptoms and these reactions may be fatal. Delayed reactions occur weeks or months after the transfusion of blood or blood components.

Acute hemolytic transfusion reactions (AHTR) are caused when red cells are transfused to a patient with a pre-existing antibody that destroys the transfused incompatible red cells through intravascular or extravascular hemolysis. Life threatening acute hemolytic reactions most commonly occur from the transfusion of ABO incompatible blood. Naturally occurring ABO antibodies bind complement on the red cell surface and have efficient lytic properties which cause intravascular hemolysis. Extravascular hemolysis is characterized by antigen-antibody complexes which do not activate complement. AHTRs feature rapid destruction immediately after transfusion. Rapid hemolysis of as little as 10 mL of incompatible red cells can produce symptoms of an AHTR. Signs and symptoms can occur within minutes after starting the transfusion. Fever is the most initial symptom followed by the chills. These reactions are mostly associated with the transfusion of ABO-incompatible red cells. Causes include clerical errors, such as mislabeled patient samples and mislabeled blood products. Although acute hemolytic reactions are rare with an incidence of 1 to 9 in 100,000 transfusions, they are the most dangerous and are severely life threatening.

Mild allergic reactions result from a patient's hypersensitivity to soluble allergens in the plasma of the donor unit. The blood recipient forms antibodies to these allergens which are bound to IgE on mast cells and causes the release of histamines. Histamines increase vascular dilation and permeability which allows vascular fluids to escape into the tissues. Swelling occurs and itchy, raised, red welts appear. Allergen substances may be drugs or food consumed by the blood donor. Anaphylactoid and anaphylactic reactions (collectively referred to as anaphylaxis) result from the recipient's forming anti-IgA, which targets IgA proteins in the donor plasma. Recipients have a genetic IgA deficiency. It is also believed that these types of reactions may be caused by other substances in the donor blood such as a peanut allergen transfused to a patient with a peanut allergy.

The AABB published an interim standard in 2005 that states, "Donors implicated in TRALI or associated with multiple events of TRALI shall be evaluated regarding their continued eligibility to donate." A donor is associated with TRALI when one of his/her donor units is transfused 6 hours before the clinical presentation of TRALI in a patient. A donor is implicated in TRALI if he/she is found to have an antibody to an HLA class I or II antigen and the antibody is specific for an antigen on the recipient's leukocytes or a positive crossmatch is obtained.*It is suggested that donors at greatest risk of developing HLA antibodies be tested, such as multiparous women. It has also been suggested that donors that present with demonstrable antibodies and have been implicated in TRALI be permanently deferred from donating. Studies have shown that donors implicated in TRALI reactions may present a future danger to transfusion recipients. Although, there are some instances where donors with HLA antibodies have not caused TRALI reactions. Another option would be to wash all red cell products from these donors in special circumstances such as rare donors. Reference: Association bulletin #05-09. AABB; August 2005. Available at: http://www.aabb.org/resources/publications/bulletins/Pages/ab05-09.aspx. Accessed November 12, 2010.

The symptom most commonly associated with a delayed hemolytic transfusion reaction (DHTR) is unexplained decrease in hemoglobin and hematocrit. Patients may also present with fever and jaundice. Hemolysis occurs slowly and is primarily extravascular. Unlike an acute hemolytic transfusion reaction (AHTR), hemoglobinuria, acute renal failure, and disseminated intravascular coagulation (DIC) are not generally seen. On some occasions, patient's may not present with any symptoms. Serologic findings include a positive direct antiglobulin test (DAT) and/or a positive antibody screen in post-transfusion testing. In many cases, the physician will send a request for an additional transfusion because of the decreased hemoglobin levels, and not suspect a DHTR. The positive antibody screen will trigger an investigation including antibody identification. The DAT may have a mixed field appearance because of the antibody-sensitized transfused red cells and the non-sensitized patient red cells. Segments from the donor unit can be tested for the offending antigen once the antibody has been identified.Antibodies that are most often reported as the cause of DHTR are anti-Jka and anti- Jkb. Other antibodies that are also commonly implicated in a DHTR include Kell, Rh, and Duffy system antibodies.The patient's physician should be notified so that additional clinical and laboratory evidence can be evaluated.