Any patient who receives a blood transfusion may develop compli-cations from that transfusion. When explaining the reasons for the transfusion, it is important to include the risks and benefits and what to expect during and after the transfusion. Patients must be informed that the supply of blood is not completely risk-free al-though it has been tested carefully. Nursing management is di-rected toward preventing complications, promptly recognizing complications if they develop, and promptly initiating measures to control any complications that occur. The following sections de-scribe the most common or potentially severe transfusion-related complications.
The nonhemolytic reaction, caused by antibodies to donor WBCs that are still present in the unit of blood or blood compo-nent, is the most common type of transfusion reaction, account-ing for more than 90% of reactions. It occurs more frequently in patients who have had previous transfusions (exposure to multi-ple antigens from previous blood products) and in Rh-negative women who have borne Rh-positive children (exposure to an Rh-positive fetus raises antibody levels in the mother). These reac-tions occur in 1% of PRBC transfusions and 20% of platelet transfusions. More than 10% of patients with a chronic transfu-sion requirement develop this type of reaction.
The diagnosis of a febrile, nonhemolytic reaction is made by excluding other potential causes, such as a hemolytic reaction or bacterial contamination of the blood product. The signs and symptoms of a febrile, nonhemolytic transfusion reaction are chills (absent to severe) followed by fever (more than 1°C eleva-tion). The fever typically begins within 2 hours after the transfu-sion is begun. Although not life-threatening, the fever and particularly the chills and muscle stiffness can be frightening to the patient.
These reactions can be diminished, even prevented, by further depleting the blood component of donor WBCs; this is accom-plished by a leukocyte reduction filter. The blood product may be filtered during processing, which achieves better results but is more expensive, or during the actual transfusion by adding the filter to the blood administration tubing. Antipyretics can be given to prevent fever, but routine premedication is not advised because it can mask the beginning of a more serious transfusion reaction.
The most dangerous, and potentially life threatening, type of trans-fusion reaction occurs when the donor blood is incompatible with that of the recipient. Antibodies already present in the recipient’s plasma rapidly combine with antigens on donor RBCs, and the RBCs are hemolyzed (destroyed) in the circulation (intravascular hemolysis). The most rapid hemolysis occurs in ABO incompati-bility. This reaction can occur after transfusion of as little as 10 mL of RBCs. Rh incompatibility often causes a less severe reaction. The most common causes of acute hemolytic reaction are errors in blood component labeling and patient identification that result in the administration of an ABO-incompatible transfusion.
Symptoms consist of fever, chills, low back pain, nausea, chest tightness, dyspnea, and anxiety. As the RBCs are destroyed, the hemoglobin is released from the cells and excreted by the kidneys; therefore, hemoglobin is present in the urine (hemoglobinuria). Hypotension, bronchospasm, and vascular collapse may result. Diminished renal perfusion results in acute renal failure, and DIC may also occur.
The reaction must be recognized promptly and the transfu-sion discontinued immediately. Blood and urine specimens must be obtained and analyzed for evidence of hemolysis. Treatment goals include maintaining blood volume and renal perfusion and preventing and managing DIC.
Acute hemolytic transfusion reactions are preventable. Meticulous attention to detail in labeling blood samples and blood components and identifying the recipient cannot be overemphasized.
Some patients may develop urticaria (hives) or generalized itching during a transfusion. The cause of these reactions is thought to be a sensitivity reaction to a plasma protein within the blood com-ponent being transfused. Symptoms of an allergic reaction are ur-ticaria, itching, and flushing. The reactions are usually mild and respond to antihistamines. If the symptoms resolve after adminis-tration of an antihistamine (eg, diphenhydramine [eg, Benadryl]), the transfusion may be resumed. Rarely, the allergic reaction is se-vere, with bronchospasm, laryngeal edema, and shock. These re-actions are managed with epinephrine, corticosteroids, and pressor support, if necessary.
Giving the patient antihistamines before the transfusion may prevent future reactions. For severe reactions, future blood com-ponents are washed to remove any remaining plasma proteins. Leukocyte filters are not useful, because the offending plasma proteins can pass through the filter.
If too much blood infuses too quickly, hypervolemia can occur. This condition can be aggravated in patients who already have in-creased circulatory volume (eg, those with heart failure). PRBCs are safer to use than whole blood. If the administration rate is suf-ficiently slow, circulatory overload may be prevented. For pa-tients who are at risk for, or already in, circulatory overload, diuretics are administered after the transfusion or between units of PRBCs. Patients receiving fresh frozen plasma or even platelets may also develop circulatory overload. The infusion rate of these blood components must also be titrated to the patient’s tolerance.
Signs of circulatory overload include dyspnea, orthopnea, tachycardia, and sudden anxiety. Neck vein distention, crackles at the base of the lungs, and a rise in blood pressure can also occur. If the transfusion is continued, pulmonary edema can de-velop, as manifested by severe dyspnea and coughing of pink, frothy sputum.
If fluid overload is mild, the transfusion can often be continued after slowing the rate of infusion and administering diuretics. How-ever, if the overload is severe, the patient is placed in an upright po-sition with the feet in a dependent position, the transfusion is discontinued, and the physician is notified. The intravenous line is kept patent with a very slow infusion of normal saline solution or a saline or heparin lock device to maintain access to the vein in case intravenous medications are necessary. Oxygen and morphine may be needed for severe dyspnea.
The incidence of bacterial contamination of blood components is very low; however, administration of contaminated products puts the patient at great risk. Contamination can occur at any point dur-ing procurement or processing. Many bacteria cannot survive in the cold temperatures used to store PRBCs (platelets are at greater risk for contamination because they are stored at room tempera-ture), but some organisms can survive cold temperatures.
Preventive measures include meticulous care in the procure-ment and processing of blood components. When PRBCs or whole blood is transfused, it should be administered within a 4-hour pe-riod, because warm room temperatures promote bacterial growth. A contaminated unit of blood product may appear normal, or it may have an abnormal color.
The signs of bacterial contamination are fever, chills, and hypotension. These signs may not occur until the transfusion is complete, occasionally not until several hours after the transfu-sion. If the condition is not treated immediately with fluids and broad-spectrum antibiotics, shock can occur. Even with aggres-sive management, including vasopressor support, the mortality rate is high.
As soon as the reaction is recognized, any remaining trans-fusion is discontinued and the intravenous line is kept open with normal saline solution. The physician and the blood bank are notified, and the blood container is returned to the blood bank for testing and culture. Septicemia is treated with intra-venous fluids and antibiotics; corticosteroids and vasopressors also may be necessary.
This is a potentially fatal, idiosyncratic reaction that occurs in fewer than 1 in 5000 transfusions. Plasma antibodies (usually in the donor’s plasma) that are present in the blood component stim-ulate the recipient’s WBCs; aggregates of these WBCs form and occlude the microvasculature within the lungs. This lung injury is manifested as pulmonary edema; it can occur within 4 hours after the transfusion.
Signs and symptoms include fever, chills, acute respiratory dis-tress (in the absence of other signs of left ventricular failure, such as elevated central venous pressure), and bilateral pulmonary infiltrates. Aggressive supportive therapy (oxygen, intubation, diuretics) may prevent death.
Delayed hemolytic reactions usually occur within 14 days after transfusion, when the level of antibody has been increased to the extent that a reaction can occur. The hemolysis of the RBCs is ex-travascular, via the RES, and occurs gradually.
Signs and symptoms of a delayed hemolytic reaction are fever, anemia, increased bilirubin level, decreased or absent haptoglobin, and possibly jaundice. Rarely is there hemoglobinuria. Generally, these reactions are not dangerous, but it is useful to recognize them, because subsequent transfusions with blood products con-taining these antibodies may cause a more severe hemolytic reac-tion. However, recognition is also difficult, because the patient may not be in a health care setting to be tested for this reaction, and even if the patient is hospitalized, the reaction may be too mild to be recognized clinically. Because the amount of antibody present can be too low to detect, it is difficult to prevent delayed hemolytic reactions. The reaction is usually mild and requires no intervention.
Despite the advances in donor screening and blood testing, cer-tain diseases can still be transmitted by transfusion of blood components. The diseases in Chart 33-18 are examples of this phenomenon.
The complications that have been described represent a real risk for any patient any time a unit of blood is administered. How-ever, patients with long-term transfusion therapy (eg, those with MDS, thalassemia, sickle cell anemia) are at greater risk for in-fection transmission and for becoming more sensitized to donor antigens, simply because they are exposed to more units of blood and, consequently, more donors. Iron overload is a complication unique to those individuals with long-term PRBC transfusions. A summary of complications associated with long-term transfusion therapy is depicted in Table 33-11.
Iron Overload. One unit of PRBCs contains 250 mg of iron.Patients with chronic transfusion requirements can quickly acquire more iron than they can use, leading to iron overload. Over time, the excess iron deposits in the tissues and can cause organ damage, particularly in the liver, heart, testes, and pancreas. Promptly initiating a program of iron chelation therapy (eg, with deferoxamine [Desferal]) can prevent end-organ damage from iron toxicity (Giardina & Grady, 1995).
If a transfusion reaction is suspected, the transfusion must be im-mediately stopped and the physician notified. A thorough patient assessment is crucial, because many complications have similar signs and symptoms. The following steps are taken to determine the type and severity of the reaction:
• Stop the transfusion. Maintain the intravenous line with normal saline solution through new intravenous tubing, administered at a slow rate.
• Assess the patient carefully. Compare the vital signs with those from the baseline assessment. Assess the patient’s res-piratory status carefully. Note the presence of adventitious breath sounds, use of accessory muscles, extent of dyspnea
• (if any), and changes in mental status, including anxiety and confusion. Note any chills, diaphoresis, complaints of back pain, urticaria, and jugular vein distention.
• Notify the physician of the assessment findings, and imple-ment any orders obtained. Continue to monitor the patient’s vital signs and respiratory, cardiovascular, and renal status.
• Notify the blood bank that a suspected transfusion reaction has occurred.
• Send the blood container and tubing to the blood bank for repeat typing and culture. The identifying tags and numbers are verified.
If a hemolytic transfusion reaction or bacterial infection is sus-pected, the nurse should do the following:
• Obtain appropriate blood specimens from the patient.
• Collect a urine sample as soon as possible for a hemoglobin determination.
• Document the reaction, according to the institution’s policy.
Pharmacologic agents to stimulate production of one or more types of blood cells by the marrow are commonly used. Chart 33-19 pre-sents examples of such pharmacologic agents.
Researchers continue to seek a blood substitute that is prac-tical and safe. Blood substitutes previously tried have not been successful. However, newer blood substitutes focus solely on oxygen delivery, as an RBC substitute (Rabinovici, 2001). Cur-rent blood substitutes in clinical trials have distinct advantages and disadvantages compared with human RBCs. They are man-ufactured hemoglobin solutions that can be sterilized without destroying the blood substitute. They require no refrigeration and appear to have a long shelf-life (possibly 1 year, versus lit-tle more than 1 month for PRBCs). Perhaps more importantly, they require no cross-matching, because there is no RBC mem-brane to interact with antibodies in the recipient’s serum. The most significant disadvantage stems from the blood substitutes extremely short life within human circulation—approximately 1 day, instead of the 30-day life span of a conventionally transfused RBC. Therefore, the use of these products would likely be limited to situations in which the need is short-term (eg, surgery, trauma). Finally, the blood substitutes are likely to be extremely expensive.
PBSCT and BMT are therapeutic modalities that offer the pos-sibility of cure for some patients with hematologic disorders such as severe aplastic anemia, some forms of leukemia, and thal-assemia. Because most hematologic disease states arise from some form of bone marrow dysfunction, an autologous trans-plantation (receiving one’s own stem cells) is not as common an option as is allogeneic transplantation. A patient receives inten-sive chemotherapy (sometimes with radiation therapy as well), with the goal being complete ablation of the patient’s bone mar-row. Stem cells from the donor (ideally, from a matched sibling), or actual marrow from the donor, is then infused into the patient using a process similar to an RBC transfusion. The stem cells travel to the marrow and slowly begin the process of resuming hematopoiesis. The advantage of autotransplantation is the re-duced likelihood of complications and mortality; however, the risk of relapse is also higher.
A relatively new strategy is based on transplantation for adop-tive cell therapy using certain immune mechanisms derived from the donor’s lymphocytes (Slavin et al., 2001; Margolis, Borrello, & Flinn, 2000). In nonmyeloablative stem cell or marrow transplantation, also referred to as a “minitransplant,” the conditioning regimen involves much less myelosuppression than in conventional regimens, rendering the patient immuno-suppressed but for a shorter period of time. Consequently, the procedure is less toxic to the patient, and there is a significant decrease in morbidity.
After the deconditioning regimen (ie, during the time the pa-tient is immunosuppressed), the allotransplantation is performed, using either marrow or stem cells. The goal is for the donor’s lym-phocytes to react against any residual malignant cells within the patient and destroy them. This process is typically augmented byinfusion of the donor’s lymphocytes as well (referred to as donor lymphocyte infusion, or DLI). If relapse occurs, repeated DLI has been effective in reestablishing remission in many patients. This approach has great promise, particularly in the setting of hema-tologic malignancy, and may provide a mechanism to increase the utility of transplantation for more patients than is possible with conventional methods.
Success of transplantation depends on tissue compatibility and the patient’s tolerance of the immunosuppression that re-sults from the ablative therapy. Patients require intensive nurs-ing care that is directed toward preventing infection and assessing for early signs and symptoms of complications. One common complication involves the formation of lymphocytes that respond to their new host (ie, the patient) as foreign and mount a reaction against the body. This process, known as graft-versus-host disease (GVHD), can involve the skin, gastrointesti-nal tract, and liver and can be life-threatening. In hematologic malignancies, some GVHD is actually desirable in that the donor lymphocytes can also mount a reaction against any lin-gering tumor cells; this process is referred to as graft-versus-malignancy. GVHD is a significant complication in nonmye-loablative transplantation therapy, as well as in conventional al-lotransplantation. Late complications (occurring more than 100 days after transplantation) are frequent; these patients, particu-larly those who receive an allogeneic transplant, require careful follow-up for years after transplantation.
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