Which listed transfusion reaction is most often associated with transfused patients lacking iga?
|
The most common complications of transfusion are Show
The most serious complications, which have very high mortality rates, are Other complications include Early recognition of symptoms suggestive of a transfusion reaction and prompt reporting to the blood bank are essential. The most common symptoms are chills, rigor, fever, dyspnea, light-headedness, urticaria, itching, and flank pain. If any of these symptoms (other than localized urticaria and itching) occur, the transfusion should be stopped immediately and the IV line kept open with normal saline. The remainder of the blood product and clotted and anticoagulated samples of the patient’s blood should be sent to the blood bank for investigation. NOTE: The unit in question should not be restarted, and transfusion of any previously issued unit should not be initiated. Further transfusion should be delayed until the cause of the reaction is known, unless the need is urgent, in which case type O Rh-negative red blood cells (RBCs) should be used. Febrile reactions may occur without hemolysis. Antibodies directed against white blood cell (WBC) human leukocyte antigen (HLA) in otherwise compatible donor blood are one possible cause. This cause is most common in multitransfused or multiparous patients. Cytokines released from WBCs during storage, particularly in platelet concentrates, are another possible cause. Most febrile reactions are treated successfully with acetaminophen and, if necessary, diphenhydramine. Patients should also be treated (eg, with acetaminophen) before future transfusions. If a recipient has experienced more than one febrile reaction, special leukoreduction filters are used during future transfusions; most hospitals use previously stored, leukoreduced (WBC-depleted RBCs) blood components. About 20 people die yearly in the US as a result of acute hemolytic transfusion reaction. AHTR usually results from recipient plasma antibodies to donor RBC antigens. ABO incompatibility is the most common cause of acute hemolytic transfusion reaction. Antibodies against blood group antigens other than ABO can also cause AHTR. Mislabeling the recipient’s pretransfusion sample at collection and failing to match the intended recipient with the blood product immediately before transfusion are the usual causes.
An acute phase usually develops within 1 hour of initiation of transfusion, but it may occur late during the transfusion or immediately afterward. Onset is usually abrupt. The patient may complain of discomfort and anxiety. Dyspnea, fever, chills, facial flushing, and severe pain may occur, especially in the lumbar area. Shock may develop, causing a rapid, feeble pulse; cold, clammy skin; low blood pressure; and nausea and vomiting. Jaundice may follow acute hemolysis. If AHTR occurs while the patient is under general anesthesia, the only symptom may be hypotension, uncontrollable bleeding from incision sites and mucous membranes caused by an associated DIC, or dark urine that reflects hemoglobinuria. If AHTR is suspected, one of the first steps is to recheck the identification labels on the sample and patient. Diagnosis is confirmed by a positive
direct antiglobulin test
Direct antiglobulin (direct Coombs) test If AHTR is suspected, the transfusion should be stopped and supportive treatment begun. The goal of initial therapy is to achieve and maintain adequate blood pressure and renal blood flow with IV 0.9% saline and furosemide. IV saline is given to maintain urine output of 100 mL/hour for 24 hours. The initial furosemide dose is 40 to 80 mg (1 to 2 mg/kg in children), with later doses adjusted to maintain a urinary flow of > 100 mL/hour during the first day. Drug treatment of hypotension must be done cautiously. Pressor drugs that decrease renal blood flow (eg, epinephrine, norepinephrine, high-dose dopamine) are contraindicated. If a pressor drug is necessary, dopamine 2 to 5 mcg/kg/minute is usually used. Symptoms and signs include fever, rash (centrifugally spreading rash becoming erythroderma with bullae), vomiting, watery and bloody diarrhea, lymphadenopathy, and pancytopenia due to bone marrow aplasia. Jaundice and elevated liver enzyme levels are also common. Graft-vs-host disease occurs 4 to 30 days after transfusion and is diagnosed based on clinical suspicion and skin and bone marrow biopsies. GVHD has > 90% mortality because no specific treatment is available. Prevention of graft-vs-host disease is with irradiation (to damage DNA of the donor lymphocytes) of all transfused blood products. It is done
Treatment with corticosteroids and other immunosuppressants, including those used for solid organ transplantation, is not an indication for blood irradiation. Although
transfusion-associated circulatory overload is underrecognized and underreported, it has been recognized as the most common cause of transfusion-related deaths reported to the FDA
(1
General references The most common complications of transfusion are Febrile nonhemolytic reactions Chill-rigor reactions The most serious complications, which have very high mortality rates, are Acute hemolytic... read more ). The high osmotic load of blood products draws volume into the
intravascular space over the course of hours, which can cause transfusion-associated circulatory overload in susceptible patients (eg, those with cardiac or renal insufficiency). RBCs should be infused slowly. The patient should be observed and, if signs of
heart failure Heart Failure (HF)
Heart failure (HF) is a syndrome of ventricular dysfunction. Left ventricular (LV) failure causes shortness of breath and fatigue, and right ventricular (RV) failure causes peripheral and abdominal... read more Typical treatment is with a diuretic such as furosemide 20 to 40 mg IV. Occasionally, patients requiring a higher volume of plasma infusion to reverse a warfarin overdose may be given a low dose of furosemide simultaneously; however, prothrombin complex concentrate (PCC) is the first choice for such patients. Patients at high risk of transfusion-associated circulatory overload (eg, those with heart failure or severe renal insufficiency) are treated prophylactically with a diuretic (eg, furosemide 20 to 40 mg IV). Transfusion-related acute lung injury is an infrequent complication caused by anti-HLA and/or antigranulocyte antibodies in donor plasma that agglutinate and degranulate recipient granulocytes within the lung. Acute respiratory symptoms develop, and chest x-ray has a characteristic pattern of noncardiogenic pulmonary edema. This complication is the second most common cause of transfusion-related death. Incidence is 1 in 5,000 to 1 in 10,000 transfusions, but many cases are mild. Mild to moderate transfusion-related acute lung injury probably is commonly missed. General supportive therapy typically leads to recovery without long-lasting sequelae. Diuretics should be avoided. Using blood donated by men reduces the risk of this reaction. Cases should be reported to the hospital transfusion medicine service or blood bank. Allergic reactions to an unknown component in donor blood are common, usually due to allergens in donor plasma or, less often, to antibodies from an allergic donor. These reactions are usually mild and include urticaria, edema, occasional dizziness, and headache during or immediately after the transfusion. Simultaneous fever is common. Less frequently, dyspnea, wheezing, and incontinence may occur, indicating a generalized spasm of smooth muscle. Rarely, anaphylaxis Anaphylaxis Anaphylaxis is an acute, potentially life-threatening, IgE-mediated allergic reaction that occurs in previously sensitized people when they are reexposed to the sensitizing antigen. Symptoms... read more occurs, particularly in recipients with IgA-deficiency Selective IgA Deficiency Selective IgA deficiency is an IgA level 7 mg/dL ( 70 mg/L, 0.4375 micromol/liter) with normal IgG and IgM levels. It is the most common primary immunodeficiency. Many patients are asymptomatic... read more . In a patient with a history of allergies or an allergic transfusion reaction, an antihistamine may be given prophylactically just before or at the beginning of the transfusion (eg, diphenhydramine 50 mg orally or IV). NOTE: Drugs must never be mixed with the blood. If an allergic reaction occurs, the transfusion is stopped. An antihistamine (eg, diphenhydramine 50 mg IV) usually controls mild urticaria and itching, and transfusion may be resumed. However, a moderate allergic reaction (generalized urticaria or mild bronchospasm) also requires hydrocortisone (100 to 200 mg IV), and a severe anaphylactic reaction requires additional treatment with epinephrine 0.5 mL of 1:1000 solution subcutaneously and 0.9% saline IV along with investigation by the blood bank. Further transfusion should not occur until the investigation is completed. Patients with severe IgA deficiency require transfusion of washed RBCs, washed platelets, and plasma from an IgA-deficient donor. Occasionally, a patient who has been sensitized to an RBC antigen has very low antibody levels and negative pretransfusion tests. After transfusion with RBCs bearing this antigen, a primary or anamnestic response may result (usually in 1 to 4 weeks) and cause a delayed hemolytic transfusion reaction. A delayed hemolytic transfusion reaction usually does not manifest as dramatically as acute hemolytic transfusion reaction. Patients may be asymptomatic or have a slight fever. Rarely, severe symptoms (eg, low-grade fever, jaundice) occur. Usually, only destruction of the transfused RBCs (with the antigen) occurs, resulting in a falling hematocrit and a slight rise in lactate dehydrogenase and bilirubin and a positive direct antiglobulin test. Because delayed hemolytic transfusion reaction is usually mild and self-limited, it is often unidentified, and the clinical clue may be an unexplained drop in hemoglobin to the pretransfusion level occurring 1 to 2 weeks posttransfusion. Severe reactions are treated similarly to acute reactions. Bacterial contamination of packed RBCs occurs rarely, possibly due to inadequate aseptic technique during collection or to transient asymptomatic donor bacteremia. Refrigeration of RBCs usually limits bacterial growth except for cryophilic organisms such as Yersinia, which may produce dangerous levels of endotoxin. All RBC units are inspected before dispensing for bacterial growth, which is indicated by a color change. Because platelet concentrates are stored at room temperature, they have greater potential for bacterial growth and endotoxin production if contaminated. To minimize growth, storage is limited to 5 days. The risk of bacterial contamination of platelets is 1:2500. Therefore, platelets are routinely tested for bacteria. Human T-cell lymphotropic virus 1 (HTLV-1), which can cause adult T-cell lymphoma/leukemia and HTLV-1–associated myelopathy/tropical spastic paraparesis, causes posttransfusion seroconversion in some recipients. All donor blood is tested for HTLV-1 and HTLV-2 antibodies. The estimated risk of false-negative results on testing of donor blood is 1:641,000. Malaria Malaria Malaria is infection with Plasmodium species. Symptoms and signs include fever (which may be periodic), chills, rigors, sweating, diarrhea, abdominal pain, respiratory distress, confusion... read more is transmitted easily through infected RBCs. Many donors are unaware that they have malaria, which may be latent and transmissible for 10 to 15 years. Storage does not render blood safe. Prospective donors must be asked about malaria or whether they have been in a region where it is prevalent. Donors who have had a diagnosis of malaria or who are immigrants, refugees, or citizens from countries in which malaria is considered endemic are deferred for 3 years; travelers to endemic countries are deferred for 1 year. Post-transfusion purpura is a very rare complication in which the platelet count falls rapidly 4 to 14 days after an RBC transfusion, causing moderate to severe
thrombocytopenia
Thrombocytopenia Platelets are circulating cell fragments that function in the clotting system. Thrombopoietin helps control the number of circulating platelets by stimulating the bone marrow to produce megakaryocytes... read more
Patients develop purpura along with moderate to severe bleeding—usually from the surgical site. Platelet and red cell transfusions make the condition worse. Massive transfusion is transfusion of a volume of blood greater than or equal to one blood volume in 24 hours (eg, 10 units in a 70-kg adult). When a patient receives standard resuscitation fluids of packed RBCs (colloid) plus crystalloid (Ringer's lactate or normal saline) in such large volume, the plasma clotting factors and platelets are diluted, causing a coagulopathy (dilutional coagulopathy). This coagulopathy worsens the consumptive coagulopathy due to major trauma itself (ie, as a result of extensive activation of the clotting cascade) and leads to a lethal triad of acidosis, hypothermia, and bleeding.
Click here for Patient Education Can you have a blood transfusion with IgA deficiency?If anti- IgA is detected, IgA deficient blood would be safer, should a blood transfusion be required. Development of antibodies to IgA is rare but, these antibodies can lead to serious transfusion reactions.
What is the most common transfusion reaction?Febrile non-hemolytic transfusion reactions are the most common reaction reported after a transfusion. FNHTR is characterized by fever or chills in the absence of hemolysis (breakdown of red blood cells) occurring in the patient during or up to 4 hours after a transfusion.
What is the most common cause of hemolytic transfusion reaction?Human error is the most common cause of AHTRs due to ABO incompatibility. The error could be made in many places: during the initial blood draw, issuing of the blood product, and transfusing product to the wrong patient.
Which antibody is associated with hemolytic transfusion reactions?Hemolytic transfusion reactions have been reported to be caused by antibodies with varying specificities, including anti-c, anti-E, anti-Fy3, anti-Fya, anti-Fyb, anti-Jka, anti-Jkb, anti-K, anti-Kpa, anti-M, anti-N, anti-s and anti-U antibodies [13, 14].
|
