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NeoReviews Vol.7 No.2 2006 e69
© 2006 American Academy of Pediatrics

Hazards of Neonatal Blood Transfusion

Susan A. Galel, MD^*
Magali J. Fontaine, MD, PhD

^* Associate Professor, Department of Pathology, Stanford University School of Medicine; Director of Clinical Operations, Stanford Blood Center, Palo Alto, Calif
Assistant Professor, Department of Pathology, Stanford University School of Medicine; Associate Director, Transfusion Service, Stanford Hospital and Clinics, Stanford, Calif

	Objectives

Top Objectives Introduction Noninfectious Complications of... Infectious Risks Of Transfusion Conclusion References

 
After completing this article, readers should be able to:

1. Describe acute immune-mediated transfusion reactions seen in neonates, their treatment, and their prevention.
   
2. Describe acute nonimmune-mediated transfusion reactions seen in neonates, their treatment, and their prevention.
   
3. Describe delayed transfusion complications.
   
4. Delineate the steps involved in the blood donor screening process in the United States.
   

	Introduction

Top Objectives Introduction Noninfectious Complications of... Infectious Risks Of Transfusion Conclusion References

 
The safest blood transfusion is the one not administered. When a transfusion is needed, it is important for both physicians and nursing staff to be aware of its potential acute and delayed adverse effects. Adverse consequences may be minimized through early recognition and prompt therapeutic intervention.

	Noninfectious Complications of Transfusion

Top Objectives Introduction Noninfectious Complications of... Infectious Risks Of Transfusion Conclusion References

 
Noninfectious complications may be either acute (occurring within hours of transfusion) or delayed. Acute reactions may be categorized further according to their pathogenesis: immunologic versus nonimmunologic.

Patients should be monitored closely during the transfusion. For all suspected transfusion reactions, the ordering physician and the nursing staff should be trained to stop the transfusion immediately, keep the intravenous line open, check that the blood component was given to the correct patient, and assess and treat symptoms. A posttransfusion blood specimen and the blood bags should be sent to the Transfusion Service (TS) along with a transfusion reaction report form that includes patient diagnosis, history of previous reactions, date and time of reaction with associated symptoms, and vital signs before and after the transfusion. The TS technologist performs a clerical check, inspects posttransfusion blood samples for hemolysis, and repeats ABO/Rh testing on both the transfused unit and the patient’s sample along with a direct antiglobulin (Coombs) test. Further testing is guided by the nature of the patient’s symptoms. Suspected delayed complications of transfusion also should be reported to the TS so the appropriate investigation may be initiated.

     Acute Immune-mediated Transfusion Reactions
Acute hemolytic transfusion reactions are the second most common cause of transfusion-related fatality in adult patients, but these are rare in neonates. Neonates do not produce red blood cell (RBC) antibodies; any antibodies present are of maternal origin. (1) Prior to the first transfusion, neonates must be screened for passively transferred RBC antibodies, including ABO antibodies if non-O RBCs are to be given. (2) If the initial screen result is negative, no further testing is needed for the first 4 postnatal months. Compared with adult patients, infants are at increased risk of passive immune hemolysis from infusion of ABO-incompatible plasma. Although small quantities of ABO-incompatible plasma (eg, 5 mL/kg) typically are well tolerated, the quantity of plasma in the supernatant of platelet or RBC transfusions ordered for neonates may exceed this volume, particularly in the surgical setting. TSs should have procedures in place to limit the quantities of ABO-incompatible plasma transfused; platelets containing incompatible plasma can be volume reduced, and RBCs may be washed.

The symptoms of hemolysis typically seen in older patients, such as fever, hypotension, and flank pain, usually are not identified in the neonatal patient. In the neonate, an acute hemolytic event may be characterized by increased plasma free hemoglobin, hemoglobinuria, increased potassium concentration, and decreased pH. Results of the direct antiglobulin (Coombs) test may confirm the presence of an antibody on the RBC surface. Treatment is supportive to maintain blood pressure and renal perfusion with intravenous normal saline at 10 to 20 mL/kg and diuresis with furosemide. Prevention is aimed at minimizing human errors and improving patient safety by strict regulations on patient identification before blood is drawn or administered.

Febrile nonhemolytic transfusion reactions (FNHTR) are suspected in the absence of hemolysis with an increase in body temperature of less than 2°C. FNHTR occur in 0.1% to 1% of transfusions in adults but rarely are reported in neonates. (3) The temperature rise is mediated by inflammatory cytokines (interleukin [IL]-1, IL-6, IL-8, tumor necrosis factor) released from white blood cells (WBCs) during storage of the blood component or caused by preformed recipient antibodies reacting with WBCs in the infused component. Prestorage leukoreduction of RBCs and platelets reduces the incidence of FNHTR. Volume reduction of platelets also may reduce the incidence of these reactions. (3)(4) For reactions associated with a temperature rise of greater than 2°C or with hypotension, bacterial contamination also should be suspected and a Gram stain and microbial culture performed on the remaining blood product.

Allergic reactions are rare in neonates. They occur when a patient has preformed immunoglobulin (Ig)E antibody against an allergen in the donor plasma. Residual cytokines or chemokines (eg, RANTES) released by stored platelets also may contribute to allergic reactions. (5) Most reactions respond to antihistamines. Severe anaphylactic reactions are rare; some are related to anti-IgA antibodies. These severe reactions are treated with epinephrine, steroids, or both as well as intubation and vasopressors if needed. Patients who have a history of anti-IgA antibodies or anaphylaxis to blood transfusion should receive washed cellular products.

Transfusion-related acute lung injury (TRALI) is the most common cause of transfusion-related fatality but often remains unrecognized. (6) Two working groups recently published case definitions and descriptions of the syndrome. (7)(8) The recommended diagnostic criteria for TRALI are the acute onset of hypoxemia with bilateral infiltrates on chest radiograph within 6 hours of a blood transfusion and no evidence of circulatory overload. Patients who have circulatory overload respond to diuresis, but those who have TRALI do not. The treatment of TRALI is oxygen support and mechanical ventilation, resulting in recovery within 96 hours for most patients.

It is hypothesized that TRALI may be the result of two cumulative events: the first linked to the patient, such as underlying sepsis, trauma, hematologic disease, or postsurgical status, and the second event related to the transfusion of potential neutrophil primers, such as inflammatory cytokines, active lipids, or alloantibodies. (9) Anti-neutrophil and anti-human leukocyte antigen (HLA) antibodies in the donor plasma have been implicated most commonly. It is believed that these antibodies bind to the patient’s WBCs, which then adhere to and alter the pulmonary capillary endothelium, resulting in fluid leak into the alveoli. Although donor HLA antibodies have been implicated in TRALI, most products containing these antibodies do not cause TRALI. (10) Indeed, blood components from postpartum women commonly contain anti-HLA antibodies reactive with the infant, but there has been only one report of TRALI associated with a maternal-infant transfusion. (11) Furthermore, HLA or neutrophil antibodies are not detectable in every case of TRALI. Until the pathogenesis of this disorder is more clearly understood, it will be difficult to determine the most appropriate method of prevention.

Hemolysis related to T-antigen activation is a rare complication of sepsis and necrotizing enterocolitis (NEC) in infants. Enzyme sialidases released by bacteria can alter RBC membranes by cleaving sialic acid residues, thereby exposing ("activating") the T antigen. Most plasma-containing components contain naturally occurring anti-T agglutinins that can cause hemolysis of T-activated cells. Although T activation has been detected on the RBCs of up to 30% of neonates who have NEC, clinical hemolysis rarely is observed. (12)(13)

     Acute Nonimmune-mediated Transfusion Reactions
Neonates are at increased risk of fluid overload from transfusion because the volume of the blood component issued by the TS may exceed the volume that may be transfused safely into neonates. Care should be taken to ensure that, in the absence of blood loss, volumes infused do not exceed 10 to 15 mL/kg.

Metabolic complications are encountered primarily with massive transfusions (>15 to 20 mL/kg) or exchange transfusions. Hypocalcemia can result from large infusions of citrate, which prevents clotting in blood components by binding calcium. The most feared symptom of hypocalcemia is myocardial depression. A prolonged QT interval may be observed on electrocardiography. Cardiac monitoring or regular checks of ionized calcium level are recommended in neonatal patients receiving massive transfusions. Hyperkalemia can occur with rapid or massive infusion of stored RBCs. (14) Washing to reduce supernatant potassium may be appropriate in massive transfusions in neonates. The quantity of free potassium is not clinically important for small-volume transfusions administered slowly (eg, 3 to 5 mL/kg per hour). (14) Hypoglycemia and hyperglycemia both have been reported in association with neonatal transfusions. An inadequate infusion rate of glucose may result if other sources of glucose are discontinued during transfusion. Hypoglycemic episodes occur more commonly with transfusion of CPDA-1 RBCs rather than additive RBCs, which contain larger quantities of glucose. Large-volume transfusions of additive RBCs may cause transient hyperglycemia followed by rebound hypoglycemia from the insulin induced by the glucose load. (15)

The infusion of cold blood components in surgery or massive transfusion may cause hypothermia, which may be associated with hypoglycemia, apnea, and arrhythmia complicated by cardiac arrest. This can be prevented by using a monitored blood warming system with alarms. (16)

Nonimmune hemolysis of blood components can occur from overheating, use of intravenous solution other than normal saline and exposure to hypo-osmotic conditions, bacterial contamination, irradiation combined with prolonged storage, and mechanical damage from rapid infusions through small-gauge needles (<24 gauge). Blood negative for sickle cell hemoglobin should be used when a neonate undergoes massive transfusion, although clinical sickling appears rare.

     Delayed Transfusion Complications
Blood components can stimulate production of RBC and WBC alloantibodies. Although alloimmunization is rare before 4 months of age, highly immunogenic RBC antigens, such as Rh D, could stimulate antibodies. (17) Therefore, administration of Rh immune globulin to Rh-negative female infants who receive Rh D-positive platelets may be appropriate.

Transfusion-associated graft versus host disease (TA-GVHD) results from the proliferation of donor-derived lymphocytes in response to histocompatibility antigens. Typically, TA-GVHD occurs in the severely immunocompromised patient. Neonates at risk include those who have congenital immunodeficiency syndromes, those who received intrauterine or exchange transfusions, and low-birthweight infants. No effective therapy is available for TA-GVHD, which is often fatal. TA-GVHD can be prevented by irradiating cellular products with at least 2,500 cGy. Because immunocompetent patients receiving products that are HLA-similar are also at increased risk of TA-GVHD, blood products donated by relatives of the recipient are irradiated. (18)(19)

Alloantigens and cytokines in blood components not only trigger immune stimulation of transfusion recipients, but also have been linked to possible immunosuppressive effects such as immune tolerance, increased postoperative infections, and increased cancer recurrence. Whether blood transfusion causes clinically significant immunosuppression and whether leukoreduction of blood components reduces this effect remains controversial. (20)(21)

	Infectious Risks Of Transfusion

Top Objectives Introduction Noninfectious Complications of... Infectious Risks Of Transfusion Conclusion References

 
     Donor Screening for Infectious Diseases and Current Risks
In the United States, potential donors are subjected to two phases of screening. First, questioning is used to select a low-risk population. Potential donors are questioned regarding exposures to specific agents, to blood, and to sexually transmitted diseases. Donations are collected only from individuals who pass questioning. Donations then are tested for specific agents as well as for surrogate markers of blood exposure or high-risk sexual activity (eg, antibodies to hepatitis B core protein and antibodies to syphilis). Residual transmission of human immunodeficiency virus (HIV) and hepatitis has been linked to donors who have recently acquired infection and whose tests are not yet positive. These are referred to as "window period" donations. Over the past 2 decades, the risk of transfusion-transmitted infection has been reduced progressively by shortening the window period through more sensitive tests. Recently, the addition of nucleic acid testing (NAT) for HIV and hepatitis C virus RNA has reduced the window period for these agents to 10 days. NAT is performed most commonly on minipools of 6 to 24 specimens; reactive pools are resolved to the individual donation. Table 1 lists the tests currently performed on blood donations in the United States. Table 2 shows the current estimated transmission rates for HIV and hepatitis, which are now so low that they can be estimated only by mathematical modeling. (22)(23) The risk of hepatitis B virus (HBV) is higher because of its relatively long window period of 59 days. NAT testing may not substantially improve HBV risk because DNA levels in early HBV infection are usually too low to be detected in the current minipool NAT format. (24)

Table 1. Testing Performed on United States Blood Donations

Agent Tests Designed to Detect Human immunodeficiency virus (HIV) Antibody to HIV-1/2 (IgM and IgG) RNA* Hepatitis B virus (HBV) Antibody to hepatitis B core protein (IgM and IgG) Hepatitis B surface antigen DNA** Hepatitis C (HCV) Antibody to HCV peptides (IgG only) RNA* Human T-lymphotrophic virus (HTLV) Antibody to HTLV-I/II (IgG only) Syphilis Rapid plasma reagin or antitreponemal antibody West Nile virus (WNV) RNA (investigational)*

^* Testing for HIV, HCV, and WNV RNA is performed on minipools of 6 to 24 samples. WNV RNA testing is performed on individual donations when the disease prevalence is high.

^** Testing for HBV DNA is currently not required by the United States Food and Drug Administration and not widely implemented.

Table 2. Estimated Risk of Transmitting Human Immunodeficiency Virus and Hepatitis (Per Unit Transfused)

Human Immunodeficiency Virus 1/1,779,000 Hepatitis C Virus 1/1,613,000 Hepatitis B Virus 1/171,000

Estimates are based on the measured incidence of new infections in repeat donors and the estimated duration of the window period as described by Dodd, et al (22), adjusted as recommended by Glynn, et al (23) to reflect a blood supply derived from 80% repeat donors and 20% first-time donors with a two-fold increased incidence of new infections in first-time donors.

It is important to note that donors are tested for only a limited number of infectious agents. Donor questioning is the only method of screening for some agents. For example, questioning regarding travel to or residence in endemic areas is the only means available to reduce transfusion transmission of malaria and variant Creutzfeldt-Jakob disease.

     Relative Safety of Designated Versus Community Donations
Most blood components in the United States are derived from volunteer community donors. A minority of components are donated by friends, family, or acquaintances of a patient and reserved for use by that patient (designated or directed donations). The evidence indicates that designated donations are not safer than those from volunteer community donors. Designated donors have a higher prevalence of positive tests for hepatitis B and C. These increased marker rates have been attributed to a different demographic composition of the directed versus nondirected donor populations. (25)(26) Another concern is that directed donors may be more reluctant than community donors to admit to deferrable risks during the donor interview. It is critical that families understand that donor testing does not detect every infection and that donor honesty during the interview process is critical. Individuals should not be pressured unduly to donate. Screening for infectious diseases is equally important for mothers donating for their newborns. Some families mistakenly believe that the infant already would have been exposed to any infectious agent in the mother’s blood. In fact, most infections, including HIV, are transmitted relatively poorly across the placenta but highly efficiently by transfusion.

     Other Infections
Bacterial contamination is the third most common cause of transfusion-related fatality. Bacteria in blood products are derived either from donor skin or from asymptomatic bacteremia in blood donors. Low-level bacterial contamination is reported to occur in 1 in 2,000 to 1 in 3,000 blood components. Bacteria multiply readily in platelet products, which are stored at room temperature, and less readily in RBC products, which are stored in the refrigerator. Bacterial contamination of blood components has been reported to cause febrile reactions with transfusion of 1 in 10,000 platelets and 1 in 30,000 RBCs. (27)(28) In a large study, fatal septic reactions were reported in about 1 in 500,000 platelet units and 1 in 8 million RBC units, but this has been suggested to be an underestimate. (29) Although most product contaminants are skin flora, most fatalities are due to gram-negative organisms. Since March 2004, a process to screen platelet products for bacteria has been required in the United States. This testing has intercepted some, but not all, bacterially contaminated platelets. Bacterial contamination of blood components must remain in the differential diagnosis of febrile transfusion reactions or sepsis following a transfusion.

There are currently no donor screening tests for parasites in the United States. To prevent transfusion-transmitted malaria, potential donors are questioned regarding residence in and travel to malarious regions. This screening is highly effective, with only 0 to 3 malaria transmissions per year in the United States. Other parasites can be transmitted by transfusion. (30) Dozens of cases of transfusion-transmitted babesiosis have been reported in the United States. This intraerythrocytic parasite can cause clinically significant hemolysis, although many infections are asymptomatic. Transmission rates of Babesia are not yet defined because there are no serologic tests of proven sensitivity or specificity. Trypanosoma cruzi, the causative agent of Chagas disease, is endemic to Mexico and Central and South America. T cruzi antibodies have been found in 1 in 7,500 to 1 in 25,000 United States blood donors. Only a few cases of transfusion-transmitted T cruzi have been documented in this country, but it is likely that this is underrecognized. Donor screening tests for T cruzi antibody are under development.

West Nile Virus (WNV) was identified first in the United States in 1999. Initially appearing in the northeast, disease activity has progressed westward through the United States, with annual epidemics each summer and autumn. In 2002, 23 cases of transfusion-transmitted WNV were identified and attributed to donors whose blood contained WNV RNA but no detectable WNV antibody. By the summer of 2003, investigational donor screening tests for WNV RNA were developed and implemented throughout the United States. These assays continue in use today. This screening method has successfully interdicted more than 1,000 potentially infectious donations, although donations that contain low-level RNA still may be missed. (31)(32)

In 1981, Yeager and associates (33) documented that transfusion-transmitted cytomegalovirus (CMV) was associated with significant morbidity in low-birthweight infants of seronegative mothers and that transmission risk was reduced by using blood products from CMV-seronegative donors. Other studies have demonstrated that transfusion-mediated CMV transmission is reduced by leukoreduction of blood components. (34) There is controversy as to the equivalence of these two methods, but a recent consensus conference concluded that either method is acceptable for the neonatal population. (35)

There are no donor screening tests for prions. Variant Creutzfeldt-Jakob disease (vCJD) is a devastating neurologic disease caused by the same prion that causes bovine spongiform encephalopathy (BSE). This prion may be transmitted by transfusion. (36)(37) Individuals who resided in the United Kingdom and Europe during periods of BSE epidemics are prohibited from donating blood in the United States. Classic CJD does not appear to be transmitted by transfusion. Nevertheless, current policies also prohibit donation by individuals at increased risk for this disorder.

     Pathogen Inactivation (PI)
It never will be possible to screen blood donations for every potential infectious contaminant. Therefore, a treatment that could inactivate residual pathogens in blood components would be beneficial. Most commercial plasma derivatives are subjected to PI treatments such as heat or solvent/detergent that inactivate some, but not all, residual pathogens. PI systems proposed for fresh blood components involve agents that cross-link DNA. Currently, no PI treatments are approved in the United States for fresh blood products, although some fresh frozen plasma and platelet PI treatments have been approved for use in Europe. (30) PI systems that cross-link DNA may also prevent TA-GVHD.

	Conclusion

Top Objectives Introduction Noninfectious Complications of... Infectious Risks Of Transfusion Conclusion References

 
Although transfusion may be lifesaving, like all medical interventions, it is not without risk. An understanding of the potential risks of transfusion in neonates can help neonatologists make the most appropriate clinical care decisions and counsel the families of their patients. Suspected complications of transfusion, both acute and delayed, should be reported to the transfusion service to allow appropriate investigation. The medical director of the transfusion service should be consulted directly if additional information and support are needed.

	Footnotes

 
Author Disclosure

Drs Galel and Fontaine did not disclose any financial relationships relevant to this article.

	References

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This Article Extract Full Text (PDF) Take the CME quiz: Vol. 7 No. 2, February 2006 E-Letters: Submit a response Alert me when this article is cited Alert me when E-Letters are posted Alert me if a correction is posted Citation Map Services E-mail this article to a friend Similar articles in this journal Alert me to new issues of the journal Add to My File Cabinet Download to citation manager Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Galel, S. A. Articles by Fontaine, M. J. Search for Related Content PubMed Articles by Galel, S. A. Articles by Fontaine, M. J.