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Objective: To describe the hematological profile in cord blood of late preterm and term newborns and compare blood indices according to sex, weight for gestational age and type of delivery. Methods: Cross-sectional study with late preterm and term newborns in a second-level maternity. Multiple gestation, chorioamnionitis, maternal or fetal hemorrhage, suspected congenital infection, 5-minute Apgar

Lesão pulmonar aguda associada à transfusão (transfusion-related acute lung injury, TRALI) é uma complicação clínica grave relacionada à transfusão de hemocomponentes que contêm plasma. Recentemente, TRALI foi considerada a principal causa de morte associada à transfusão nos Estados Unidos e Reino Unido. É manifestada tipicamente por dispnéia, hipoxemia, hipotensão, febre e edema pulmonar não cardiogênico, que ocorre durante ou dentro de 6 h, após completada a transfusão. Embora o exato mecanismo não tenha sido totalmente elucidado, postula-se que TRALI esteja associada à infusão de anticorpos contra antígenos leucocitários (classes I ou II ou aloantígenos específicos de neutrófilos) e a mediadores biologicamente ativos presentes em componentes celulares estocados. A maioria dos doadores implicados em casos da TRALI são mulheres multíparas. TRALI, além de ser pouco diagnosticada, pode ainda ser confundida com outras situações de insuficiência respiratória aguda. Um melhor conhecimento sobre TRALI pode ser crucial na prevenção e tratamento desta severa complicação transfusional. Transfusion-related acute lung injury (TRALI) is a serious clinical syndrome associated with the transfusion of plasma-containing blood components. Recently, TRALI has come to be recognized as the leading cause of transfusion-related death in the United States and United Kingdom. This complication typically presents as shortness of breath, hypoxemia, hypotension, fever and noncardiogeneic pulmonary edema, all occurring during or within 6 h after transfusion. Although the mechanism of TRALI has not been fully elucidated, it has been associated with human leukocyte antigen antibodies (class I, class II or neutrophil alloantigens) and with biologically active mediators in stored cellular blood components. Most of the donors implicated in cases of TRALI are multiparous women. Rarely diagnosed, TRALI can be confused with other causes of acute respiratory failure. Greater knowledge regarding TRALI on the part of clinicians could be crucial in preventing and treating this severe complication of blood transfusion.

Avaliamos a ocorrência da hemorragia feto-materna entre 343 puérperas que receberiam profilaxia da aloimunização Rh com emprego de imunoglobulina anti-D. Realizamos o teste de roseta para triagem dos casos que necessitariam determinação quantitativa do volume de sangue fetal transferido para circulação materna, que foi então apurado pelo teste de Kleihauer-Betke (K-B). O teste de roseta apresentou resultado positivo em 22 casos (6,4%). Em cinco dessas amostras o teste de K-B não apontou hemorragia feto-materna (falso positivo do teste de roseta de 1,45%) e noutra a leitura do teste não foi conclusiva. Tivemos oito casos com volume apurado de hemorragia feto-materna < 10ml (2,3%), seis com hemorragia feto-materna entre 10 e 30ml (1,7%) e duas puérperas apresentaram transferência sangüínea feto-materna maior que 30ml (0,58%), necessitando suplementação além da dose padrão de anti-D. O teste de roseta dispensou 93,6% das pacientes da avaliação adicional da hemorragia feto-materna por método quantitativo. This study evaluated fetomaternal hemorrhage (FMH) in 343 postpartum patients who required prophylaxis of Rh alloimmunization with anti-D immunoglobulin. The rosette test was applied to screen for patients needing quantitative determination of fetal blood transferred from the maternal circulation, which was then measured by the Kleihauer-Betke test (K-B). The rosette test was positive in 22 cases (6.4%). In five of these cases, K-B did not show fetomaternal hemorrhage (a 1.45% false-positive rate for the rosette test), and in one case the test was inconclusive. There were 8 cases with FMH < 10ml (2.3%), 6 cases with FMH from 10 to 30ml (1.7%), and two cases with FMH > 30ml (0.58%), requiring a supplementary dose of anti-D. The study concludes that following the rosette test, additional evaluation of FMH using a quantitative test was unnecessary in 93.6% of the cases.

White cell (WBC)-reduction filters have been shown to be effective in removing infectious agents from infected blood products. In this study, the mechanisms of Trypanosoma cruzi (T. cruzi) retention by WBC-reduction filters were assessed. Human packed red blood cell (PRBC) and platelet concentrate (PC) samples were contaminated with T. cruzi organisms (Y strain; 3.4 x 10(6)/ml), and then filtered using WBC-reduction experimental filters that provided about 3 log10 WBC removal. Transmission electron microscopy sections showed that T. cruzi parasites were removed from contaminated PRBC and PC samples primarily by mechanical mechanism without interacting with filter fibbers or blood cells. In addition, we found that T. cruzi parasites were also removed by a direct fibber adhesion. These data indicate that T. cruzi parasites are removed from infected blood not only by mechanical mechanism but also by biological mechanism probably mediated by parasite surface proteins. Os filtros de leucócitos são eficazes em remover agentes infecciosos de hemocomponentes infectados. Neste estudo, foram avaliados os mecanismos de retenção de Trypanosoma cruzi (T. cruzi) por filtros de leucócitos. Amostras de concentrado de glóbulos vermelhos (CGV) e concentrado de plaquetas (CP) foram contaminados com parasitas T. cruzi (cepa Y, 3,4 x 10(6)/ml), e filtrados com filtros experimentais de leucócitos, com capacidade de remoção de aproximadamente 3 log10 leucócitos. A análise das fibras dos filtros através de microscopia eletrônica de transmissão mostrou que os parasitas T. cruzi foram removidos dos CGV e CP contaminados por mecanismo físico, sem interação com células sangüíneas. Além disso, foi demonstrado que os parasitas T. cruzi foram também removidos por adesão direta às fibras dos filtros, sugerindo um mecanismo biológico, provavelmente mediado por proteínas da superfície do parasita.

CONTEXT: Patients with sickle cell anemia (SCA) are frequently transfused with red blood cells (RBC). Recently, we reported that the calculated risk of RBC alloimmunization per transfused unit in Brazilian patients with SCA is 1.15%. We describe a delayed hemolytic transfusion reaction (DHTR) presenting as a painful crisis in a patient with SCA. CASE REPORT: A 35-year-old Brazilian female with homozygous SCA was admitted for a program of partial exchange transfusion prior to cholecystectomy. Her blood group was O RhD positive and no atypical RBC alloantibody was detected using the indirect antiglobulin technique. Pre-transfusional hemoglobin (Hb) was 8.7 g/dL and isovolumic partial exchange transfusion was performed using 4 units of ABO compatible packed RBC. Five days after the last transfusion she developed generalized joint pain and fever of 39°C. Her Hb level dropped from 12.0 g/dL to 9.3 g/dL and the unconjugated bilirrubin level rose to 27 mmol/L. She was jaundiced and had hemoglobinuria. Hemoglobin electrophoresis showed 48.7% HbS, 46.6% HbA1, 2.7% HbA2, and 2.0% HbF. The patient’s extended RBC phenotype was CDe, K-k+, Kp(a-b+), Fy(a-b-), M+N+s+, Le(a+b-), Di(a-). An RBC alloantibody with specificity to the Rh system (anti-c, titer 1:16.384) was identified by the indirect antiglobulin test. The Rh phenotype of the RBC used in the last packed RBC transfusion was CcDEe. The patient was discharged, asymptomatic, 7 days after admission. CONTEXTO: Pacientes com anemia falciforme recebem com freqüência concentrados de glóbulos vermelhos (CGV). Recentemente, nós relatamos que o risco de alo-imunização eritrocitária por unidade transfundida em pacientes brasileiros com anemia falciforme é 1,15%. RELATO DE CASO: Nós descrevemos uma reação transfusional hemolítica tardia (RTHT) apresentando-se como uma crise dolorosa em um paciente com anemia falciforme.

The present measures adopted to prevent transfusion-associated Chagas' disease include screening of blood donors. and/or the inactivation of T. cruzi in collected blood using gentian violet (GV) as a trypanocidal agent. In this study, we investigated the efficacy of the combined use of AMT and UV-A in inactirating T. cruzi in infected human platelet cuncentrates. Human platelet concentrates were infected with T. cruzi (2x10/ml) of the Y strain transfered to PL 269 (Fenwal Laboratories) containers and treated with GV (250řg,/ml). and ascorbic acid (1 mg/ml); GV. ascorbic acid and UV-A; GV and UV-A; AMT (40/tG/ml) and ascorbic acid; AMT, ascorbic acid and UV-A; AMT and UV-A; UV-A alone; and untreated (control). All UV-A treated platelet concentrates were exposed to UV-A doses of 24, 92, 184, 276, 368 and 644 kj/m². and the microscopical research of active T. cruzi was performed, using the microhematocrit technique, 1, 6 and 24 hours after each treatment. A high number of active forms of T. cruzi was observed in all condictions, except when GV was used as the trypanocidal agent, providing evidence of the failure of AMT and UV-A in inactivating T cruzi in infected human platelet concentrates. As medidas adotadas atualmente para prevenir a doença de Chagas transfusional incluem a seleção dos doadores de sangue e/ou a inativação do T. cruzi no sangue coletado através do uso da violeta de genciana (VG) como agente tripanosomicida. Neste estudo, nós investigamos a eficácia do uso combinado do AMTe da UV-A para a neutralização do T. cruzi em concentrados de plaquetas humanas infectados. Os concentrados de plaquetas infectados com cepa Y de T. cruzi (2x10/ml) foram transferidos para recipientes PL. 269 (Fenwal Laboratories) e tratados com VG (250/ml) e ácido ascórbico (1mg/ml) VG. ácido ascórbico e UV-A; GV e UV-A; AMT (40 G/ml) e ácido ascórbico; AMT, ácido ascórbico e UV-A; AMT e UV-A; somente UV-A; e não tratado (controle). Todos os concentrados de plaquetas foram expostos a doses de 24, 92, 184, 276, 368 e 644 kJ/m² de UV-A, e a pesquisa microscópica do T. cruzi foi realizada pela técnica do microbematócrito, 1, 6 e 24 horas após cada tratamento. Grande número de formas ativas de T. cruzi foi observado em todos os experimentos, exceto quando foi usada a VG como o agente tripanosomicida, evidenciando a ineficácia do AMT e da luz ultravioleta em inativar o T. cruzi nos concentrados de plaquetas humanas infectados.