Platelet Transfusions

Chapter 465 Platelet Transfusions

Guidelines for platelet (PLT) support of children and adolescents with quantitative and qualitative PLT disorders are similar to those for adults (see Table 465-1 on the Nelson Textbook of Pediatrics website at www.expertconsult.com), in whom the risk of life-threatening bleeding after injury or occurring spontaneously can be related to the severity of thrombocytopenia. PLT transfusions should be given to patients with PLT counts < 50 × 10⁹/L when they are bleeding or are scheduled for an invasive procedure, and the PLT count should be maintained > 50 × 10⁹/L until bleeding ceases or the patient is stable after the procedure.

Studies of patients with thrombocytopenia resulting from bone marrow failure indicate that the risk of spontaneous bleeding increases markedly when PLT levels fall to < 20 × 10⁹/L, and hemorrhagic risk factors (infection, organ failure, clotting abnormalities, mucosal lesions, severe graft versus host disease, or anemia) are present. In this high-risk setting, prophylactic PLT transfusions are given to maintain a PLT count > 20 × 10⁹/L. This threshold has been challenged by studies of adult patients, who in many instances were selected to be in relatively good clinical condition without hemorrhagic risk factors. Consequently, a lower PLT transfusion trigger of 5-10 × 10⁹/L is recommended for stable (i.e., low-risk) patients. In practice, however, severe thrombocytopenia is commonly associated with the development/occurrence of risk factors, including fever, antimicrobial therapy, active bleeding, need for an invasive procedure, disseminated intravascular coagulation, and liver or kidney dysfunction with clotting abnormalities. In these situations, PLT transfusions are given to maintain relatively high PLT counts. Despite the desire by some physicians to elevate the blood PLT count to 80 × 10⁹/L or 100 × 10⁹/L or even higher, there are no definitive data to justify a true benefit of PLT transfusions given at a PLT count > 50 × 10⁹/L, unless bleeding is active with a PLT count between 50 and 100 × 10⁹/L and thrombocytopenia seems to be the only cause.

Qualitative PLT disorders may be inherited or acquired (in advanced hepatic or renal insufficiency or when blood flows through an extracorporeal circuit, such as during extracorporeal membrane oxygenation [ECMO] or cardiopulmonary bypass). In patients with such disorders, PLT transfusions are justified only if the risk of significant bleeding is quite high or actually occurs. Because inherited PLT dysfunction often is lifelong and repeated transfusions may lead to alloimmunization and refractoriness (i.e., poor response to PLT transfusions), prophylactic PLT transfusions are rarely justified, unless an invasive procedure is planned. In these cases, an abnormal result with the use of a modern PLT function device or, historically, a bleeding time more than twice the upper limit of laboratory normal may be taken as diagnostic evidence of PLT dysfunction. However, an abnormal bleeding time or any other abnormal laboratory test result is poorly predictive of hemorrhagic risk or the need to transfuse PLTs. Alternative therapies, particularly desmopressin acetate, should be considered to avoid PLT transfusions. Antiplatelet medications (nonsteroidal anti-inflammatory drugs) should be avoided in these patients.

In neonates, hemostasis is quantitatively and qualitatively different from that in older children, and the potential exists for either serious hemorrhage or thrombosis. Blood PLT counts ≥150 × 10⁹/L are present after 17 wk gestational age. Approximately 1% of term infants demonstrate PLT counts <150 × 10⁹/L, but bleeding in such infants is rare. In contrast, 25% preterm of neonates treated in intensive care units exhibit blood PLT counts < 150 × 10⁹/L at some time during admission, with about 4% overall and 50% of those < 1.0 kg birth weight receiving PLT transfusions. Multiple pathogenetic mechanisms underlying thrombocytopenia are involved in these sick neonates, predominantly accelerated PLT destruction plus diminished PLT production, as evidenced by decreased numbers of megakaryocyte progenitors and relatively low upregulation of thrombopoietin levels during thrombocytopenia, compared with thrombocytopenic children and adults.

Blood PLT counts < 100 × 10⁹/L pose significant clinical risks for premature neonates. Bleeding time may be prolonged at PLT counts < 100 × 10⁹/L in infants with birth weight < 1.5 kg; PLT dysfunction is suggested by bleeding times that are disproportionately long for the degree of thrombocytopenia. The risk of hemorrhage may be increased in thrombocytopenic infants. However, in a randomized trial, transfusing PLTs prophylactically whenever the PLT count fell to < 150 × 10⁹/L (i.e., below the lower limit of normal) to maintain the average PLT count at > 200 × 10⁹/L, in comparison with transfusing PLTs only when the PLT count fell to < 50 × 10⁹/L to maintain the average PLT count at approximately 100 × 10⁹/L, did not result in a lower incidence of intracranial hemorrhage (28% vs. 26%, respectively). Thus, there is no documented benefit to prophylactic transfusion of PLTs for modest thrombocytopenia (PLT count > 50 × 10⁹/L) to sustain a blood PLT count in the normal range. As an exception, infants with inherited PLT dysfunction disorders and bleeding, and those at high risk of bleeding owing to acquired PLT dysfunction, such as during ECMO, commonly receive transfusions to keep their PLT counts > 100 × 10⁹/L. Although basic questions about the relative risks of different degrees of thrombocytopenia in various clinical settings are only partially answered, guidelines acceptable to many neonatologists are listed in Table 465-1. For optimal PLT transfusion practices, each hospital should develop guidelines that satisfy local practices and should attempt to avoid violations of the practices.

The goal of most PLT transfusions is to raise the PLT count above 50 × 10⁹/L and to increase that for neonates to ≥ 100 × 10⁹/L. These increases can be achieved consistently in children weighing up to 30 kg by infusion of 5 to 10 mL/kg of standard (unmodified) PLT concentrates, obtained either from processing whole blood units or by plateletpheresis. For larger children, the appropriate dose is 3-4 pooled whole blood–derived PLT units or 1 apheresis unit. Because PLT concentration varies in different PLT products made available for transfusion, each hospital should monitor post-transfusion PLT counts and determine the dose that works best locally. PLT concentrates should be transfused as rapidly as the patient’s overall condition permits, certainly within 2 hr. Patients requiring repeated PLT transfusions should receive leukocyte-reduced blood products, including PLT concentrates, to diminish alloimmunization and PLT refractoriness and to reduce the risk of transfusion-transmitted cytomegalovirus infection.

Routinely reducing the volume of PLT concentrates for infants and small children by additional centrifugation steps is both unnecessary and unwise. Transfusion of 10 mL/kg of an unmodified PLT concentrate is adequate because it adds 10 × 10⁹ PLTs to 70 mL of blood (the blood volume of a 1-kg neonate), a number calculated (taking the usual hematocrit and post-transfusion PLT recovery values into account) to increase the PLT count by 100 × 10⁹/L. This calculated increment has been validated because it is consistent with the actual increment reported. Moreover, 10 mL/kg is not an excessive transfusion volume, provided that the intake of other IV fluids, medications, and nutrients is monitored and adjusted. It is important to select PLT units for transfusion with the ABO group identical to that of the recipient and to avoid repeated transfusion of group O PLTs to group A or B recipients, because passive anti-A or anti-B in group O plasma can lead to hemolysis. Although proven methods exist to reduce the volume of PLT concentrates when truly warranted (e.g., many transfusions are anticipated, in which the quantity of passive anti-A or anti-B might lead to hemolysis, or failure of 10 mL/kg of unmodified PLT concentrate to increase the PLT count), additional processing should be performed with great care because of probable PLT loss, clumping, and dysfunction caused by the additional handling, all of which could diminish the efficacy and increase the toxicity of PLT transfusions.

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