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Latar belakang: Protein Kidd merupakan transporter urea pada sel darah merah. Walaupun jarang, adanya antibodi terhadap antigen ini dapat menyebabkan reaksi transfusi dan hemolytic disease of the newborn. Keberadaan anti-Jka dan anti-Jkb cukup jarang ditemukan pada pemeriksaan identifikasi antibodi pasien. Studi ini melaporkan kasus pasien dengan keberadaan anti-Jka and anti-Jkb, yang mendapat darah dengan kadar aglutinasi terendah pada kondisi dimana darah kompatibel sulit didapat sementara tindakan transfusi sangat dibutuhkan segera. Penyajian Kasus: Wanita, 36 tahun, G4P3A0, datang dengan perdarahan vaginam sejak sebulan terakhir. Dari hasil pemeriksaan USG, didapatkan adanya mola hidatidosa. Pasien memerlukan terapi kuret segera setelah anemia terkoreksi (Hb 8.3 g/dL). Pada uji kecocokan pre-transfusi dengan prosedur skrining antibodi yang dilanjutkan dengan identifikasi antibodi, ditemukan anti-Jka dan anti-Jkb. Dari setidaknya 50 darah donor yang dilakukan uji kecocokan, tidak ditemukan darah yang kompatibel, sehingga pasien diputuskan untuk mendapat transfusi menggunakan darah inkompatibel dengan derajat aglutinasi terendah (level 2) dari 5 level, disertai dengan pemantauan ketat terhadap potensi terjadinya reaksi transfusi. Demam dan pruritus dilaporkan dalam 24 jam setelah transfusi, dan membaik setelah pemberian injeksi difenhidramin, deksametason, dan parasetamol. Kesimpulan: Transfusi dengan darah yang inkompatibel merupakan pilihan terakhir bila tidak ditemukan darah donor yang kompatibel. Reaksi transfusi merupakan efek yang sulit dihindari, tetapi dapat dilakukan pemantuan ketat. Pemilihan darah dengan level aglutinansi terendah adalah keputusan terbaik, mengingat tindakan medis diperlukan segera untuk menyelamatkan nyawa. Pada kasus ini, pasien mendapat tatalaksana optimal dari aspek tindakan operasi dan respon transfusi, yang ditunjukkan melalui kenaikan nilai Hb yang bermakna. Sementara itu, efek samping reaksi transfusi yang muncul hanya ringan dan dapat ditanggulangi dengan pemberian obatobatan. (Health Science Journal of Indonesia 2019;10(2):137-9) Kata kunci: reaksi transfusi, inkompatibilitas, kelompok darah Kidd Abstract Background: Kidd protein is red blood cell’s (RBC) major urea transporter. Albeit rare, the presence of antibodies against Kidd antigen may cause significant hemolytic transfusion reaction and hemolytic disease of the newborn. Yet, anti-Jka and anti-Jkb are rare to be discovered during antibody identification. This paper reported “bestmatched” transfusion practice in a patient with anti-Jka and anti-Jkb, where compatible PRC cannot be found, but transfusion is urgently needed. Case Presentation: A 36 years old, G4P3A0 female, came with continuous vaginal bleeding for the past one month before admission. USG revealed hydatidiform mole. She needed immediate curettage following correction of her anemia (Hb 8.3g/dL). After antibody screening procedure followed by antibody identification, we found a positive anti-Jka and anti-Jkb in her blood sample. At least 50 blood donors were tested for compatibility and none was a match. She was then transfused with the lowest agglutination blood available (level 2 of 5 levels), with a closed monitoring to anticipate the possibility of transfusion reaction development. Fever and pruritus transpired within 24 hours post transfusion and it resolved following diphenhydramine, dexamethasone, and paracetamol injection. Conclusion: Incompatible blood transfusion is the last option when compatible blood cannot be found. The development of transfusion reaction is inevitable, but it can be anticipated by closed monitoring. In restricted setting, blood transfusion with the lowest level of agglutination is acceptable when transfusion is imperative. In this case, the patient got optimal treatment in term of the medical surgery and transfusion response, which was shown by the significant increase of Hb level. Meanwhile, the adverse transfusion reaction was only mild, and could be treated with medicine. (Health Science Journal of Indonesia 2019;10(2):137-9) Keywords: Transfusion reaction, incompatibility, Kidd blood group

ABO-incompatible blood transfusion is potentially a life-threatening event. A 74-year-old type O Rh-positive male was accidentally transfused with 280 mL type B Rh-positive red blood cells during open right hemicolectomy, causing ABO-incompatible blood transfusion. Immediately after the transfusion, the patient experienced a hypotension episode followed by acute hemolytic reaction, disseminated intravascular coagulation and acute kidney injury. Plasma exchange therapy was performed to remove anti-B antibody and free hemoglobin because they caused acute hemolytic reaction, disseminated intravascular coagulation, and acute kidney injury. Free hemoglobin levels decreased from 13 to 2 mg/dL for 2 h. Continuous hemodiafiltration was used to stabilize hemodynamics. The patient was successfully treated for acute hemolytic reaction, disseminated intravascular coagulation, and acute kidney injury. Plasma exchange therapy and continuous hemodiafiltration are likely to be effective treatments for ABO-incompatible blood transfusion, and further studies are required to assess this effectiveness in future.

Red blood cell (RBC) transfusion is a critical component of optimal management for a broad range of conditions. Regardless of the indication, pretransfusion testing is required to appropriately match RBC donors and recipients to provide immunologically compatible blood. Although this approach is effective in the vast majority of situations, occasionally, patients will inadvertently receive an incompatible RBC transfusion, which can result in a hemolytic transfusion reaction (HTR). In addition, patients with life-threatening anemia and a complex alloantibody profile, which precludes rapid procurement of compatible RBCs, may also receive incompatible RBCs, placing them at risk for an HTR. Despite the rarity of these clinical situations, when incompatible blood transfusion results in an HTR, the consequences can be devastating. In this review, we will explore the challenges associated with actively preventing and treating acute HTRs following incompatible RBC transfusion. In doing so, we will focus primarily on the role of complement, not only as a key player in HTRs, but also as a potential target for the prevention and treatment of HTRs.

BackgroundAcute haemolytic transfusion reactions due to ABO incompatible blood transfusion remain a leading cause of transfusion-associated morbidity and mortality in the USA. Erroneous patient identification and specimen labelling account for many errors that lead to ABO mistransfusions; these errors are largely preventable.MethodsOur hospital requires a two-sample process of ABO/Rh typing prior to transfusion. Both samples must be drawn independently. To prevent simultaneous sample draw, our second sample tube has a unique pink top that is only available from the blood bank and can only be sent to the patient’s floor once the first sample arrives in the lab. We performed an audit of this process from 19 March to 30 July 2014 and 19 March to 30 July 2015.ResultsWe reviewed type and crossmatch orders for 2702 new patients during the audit period and 824 patients (30.5%) required transfusion. All patients evaluated received compatible blood, and no mistransfusions were recorded using this method. Three per cent of testing was performed incorrectly, which safely defaulted to giving type O blood.ConclusionsThe two-sample protocol used by our institution can decrease the risk of mistransfusion. Our protocol was relatively inexpensive, safe, efficient and practical for adaptation by other hospitals.

Background and Aim: Autoimmune hemolytic anemia (AIHA) is characterized by the production of autoantibodies directed against red cell antigens. Most patients of AIHA arrive in the emergency or out-patient department (OPD) with severe anemia requiring urgent blood transfusion. Here we share our experience of managing these patients with incompatible blood transfusions and suggest the minimal test required to assure patient safety. Materials and Methods: A total of 14 patients admitted with severe anemia, diagnosed with AIHA and requiring blood transfusion urgently were included in the study. A series of immunohematological investigations were performed to confirm the diagnosis and issue "best match" packed red blood cells (PRBC) to these patients. Results: A total of 167 PRBC units were crossmatched for 14 patients of which 46 units (28%) were found to be best match ones and 26 (56.5%) of these units were transfused. A mean turn around time of 222 min was observed in issuing the ′best match′ blood. Severe hemolysis was observed in all patients with a median hemoglobin increment of 0.88 g/dl after each unit PRBC transfusion. Conclusion: Decision to transfuse in AIHA should be based on the clinical condition of the patient. No critical patient should be denied blood transfusion due to serological incompatibility. Minimum investigations such as direct antiglobulin test (DAT), antibody screening and autocontrol should be performed to ensure transfusion safety in patients. All transfusion services should be capable of issuing "best match" PRBCs in AIHA.

O presente trabalho objetivou estudar a frequência dos grupos sanguíneos identificados como antígenos eritrocitários caninos (AEC) 1, 1.1 e 7 em cães da região metropolitana da cidade de São Paulo-SP, Brasil, e calcular o risco de administração de sangue incompatível tanto em uma primeira quanto em uma segunda transfusão. Para tanto, 300 cães não aparentados foram divididos igualmente em seis grupos de acordo com as raças: Pastor Alemão (PA); Rottweiler (R); Poodle (P); Cocker Spaniel Inglês (CS); raças definidas diversas (RDD) e mestiços (M). Avaliou-se a relação entre a frequência dos AEC e os grupos raciais. A frequência geral de AEC 1 na população foi de 71% (AEC 1.1 – 53,35%) e houve variações de acordo com as raças: PA- 32% (AEC 1.1 – 20%), R- 98% (1.1 – 80%), P- 76% (1.1 – 54%), CS- 84% (1.1 – 50%), RDD- 62% (1.1 – 56%) e M- 74% (1.1 – 60%). A frequência geral de AEC 7 foi de 39,33% e não houve diferenças significativas entre as raças. O risco de um cão negativo para o AEC 1 receber sangue positivo foi de 0,6 a 66,6% em uma primeira transfusão e de 0,21 a 65,3% do mesmo cão receber sangue incompatível em uma segunda transfusão. O risco quanto ao AEC 7 foi de 23,86% na primeira transfusão e 9,4% numa segunda transfusão. Este estudo concluiu que houve variação na frequência de AEC1 e AEC 1.1, mas não quanto ao AEC 7 entre raças. Esta variação na porcentagem de animais positivos quanto ao AEC 1 se refletiu na grande variação no risco de uso de sangue incompatível. Portanto, conhecer a frequência dos AEC na população tem impacto direto no manejo entre cães doadores e receptores, mas a utilização conjunta de teste de tipagem sanguínea e reação cruzada reduz a possibilidade de transfusão de sangue incompatível.

To prevent delays in transfusion and the development of hemolytic transfusion reactions at the emergency room of a local hospital, we implemented a Type O blood usage program for life-threatening bleeding patients in August 2001 according to Japanese government guidelines for transfusion. To better understand actual conditions for urgent blood transfusion before and after implementation of this program, we surveyed the time between ordering to the start of transfusion, shock index at the start of transfusion, total volume of transfused blood, causes of death, irradiation of blood, side effects, and reasonable adaptation of transfusion. Results showed the time between ordering to the start of transfusion shortened to 9.3 minutes from 62.2 minutes after implementation. There was no case in which non-irradiated blood unit, was transfused, nor of incompatible blood transfusion following cross matching. Further, there was no increase in workload following implementation of the Type O blood usage program. In conclusion, Type O blood usage programs can dramatically save time between ordering to the start of transfusion. However, they carry risks such as Rh-positive blood transfusion to Rh-negative patients (about 0.5%) and antigen-positive blood transfusion to patients positive for irregular antibodies (about 1.3%). Adaptation of this transfusion must be carefully controlled. All patients receiving type O blood transfusion should be investigated for suitability after transfusion.

Background The inherent risks of blood transfusion have led to concerted efforts to find alternatives to allogeneic blood transfusion. Among these alternatives are supplementation with iron and treatment with erythropoietin, autologous pre-donation before major elective surgery, intraoperative blood salvage (particularly for emergency cases or when major blood loss is unanticipated), acute normovolemic hemodilution, and artificial blood substitutes. Methods Review of pertinent English-language literature. Results Autologous pre-donation of the patient's own blood, even if supplemented with iron and erythropoietin, is increasingly out of favor for several reasons. Autologous pre-donation is an added out-of-pocket expense for the patient. The major cause of incompatible blood transfusion, namely clerical error, is not eliminated. Moreover, autologous pre-donated blood is not released to the general blood supply; therefore, autologous blood that is not returned to the patient by infusion is wasted. Acute normovolemic hemodilution is a safe alternative that eliminates the risk of mistransfusion, minimizes the shed red cell mass when bleeding occurs, and reduces the risk of perioperative transfusion as shown in patients undergoing radical prostatectomy. Conclusions Acute normovolemic hemodilution achieves equivalent outcomes at lower cost compared with autologous pre-donation. Patient safety is increased, and if pharmacologic strategies are combined with acute normovolemic hemodilution, allogeneic blood transfusion may be eliminated entirely.

The triggers of secondary thrombotic thrombopcytopenic purpura (TTP) include drug toxicity, radiation and high-dose chemotherapy, angioinvasive infections, surgery and acute graft versus host disease. TTP secondary to surgery have been reported in a number of cases. Most of the cases have been occurred after open heart surgery. Extensive endothelial damage is held responsible as the initiating mechanism in postoperative TTP cases. However, there is no report of secondary TTP describing development owing to ABO incompatible blood transfusion. Here, we describe a patient who developed TTP after transfusion of ABO incompatible blood during hospitalization for bypass surgery. We also propose a hypothesis which may account for the possible underlying mechanism.

Here we report the results of the National (Fact-finding) Survey on the present state of ABO-incompatible blood transfusions in Japan performed by the Japanese Society of Blood Transfusion. The targets of the survey were 777 hospitals with more than 300 beds, which have transfused more than 3, 000 units of blood products per year. The survey was performed in the style of anonymous questionnaire-based survey.The questionnaire focused on the presence or absence of ABO-mismatched transfusions in the 5-year period, between January 1995 and December 1999. The target blood products included whole blood, red cell concentrates and fresh-frozen plasma (FFP), the platelet concentrates being excluded. Among the 777 hospitals, answer could be obtained from 575, and 20% of them have experienced ABO-mismatched transfusion at least once in the period of the study. The frequency of ABO-mismatched transfusion increased with increasing the number of beds and the units of transfused blood. Approximately 50% of the hospitals with more than 700 beds and/or with more than 40 thousand units of transfused blood per year have experienced it. ABO-incompatible transfusion was performed in 166 cases (115 hospitals), and the blood products used were red cell concentrates in 90 cases, whole blood in 5 and FFP in 71. The main causes of transfusion error were change of blood bags in 71 cases (42.8%), incorrect blood typing in 25 (15.1%), and failure to identify patient in 19 (11.5%). The transfusion errors were caused by nurses in 78 cases (44.6%), doctors in 72 (41.1%), and laboratory technicians in 18 (10.3%). The evolution of the patients transfused ABO-incompatible blood was recorded as deceased in 6, among them 1 died of hemorrhage due to severe trauma. Additional 3 cases have deceased, but the cause could not be defined as either the ABO-incompatible transfusion or the basic disease.

緊急手術患者においてA1Bm血液型患者への不適合輸血を経験した。A1Bm型はB型抗原決定基数が非常に少ないBm型抗原と,A型抗原決定基数が非常に多いA1型抗原とからなるAB型の亜型であり,血液型検査では「おもて・うら」試験が不一致となる。本症例の緊急検査結果は「おもて」試験でA型であったが,「うら」試験のB血球に凝集が認められず,精査必要と報告された。患者は大量出血が続き,精査結果を待つ余裕もなく,大量のA型血液が輸血された。患者はショック状態が続いていたが,患者血液型がA1Bm型であるという精査結果が報告され,直ちに輸血血液をAB型新鮮凍結血漿,AB型濃厚血小板液,A型洗浄赤血球液に変更し,集中治療を続けた結果,重篤な臓器不全を合併することなく回復した。Bm型抗原と抗B抗体との反応性が低いことが不適合輸血による重篤な後遺症を回避できたおもな要因であると思われる。

Human error has been identified as a major source of ABO-incompatible blood transfusion which most often results from blood being given to the wrong patient. We present a case of inadvertent administration of ABO-incompatible blood to a 6-mo-old child who underwent congenital heart surgery and discuss the use of invasive therapeutic approaches. Invasive techniques included total circulatory arrest and large-volume exchange transfusion, along with conventional ultrafiltration and plasmapheresis, which could all be performed rapidly and effectively. The combination of standard pharmacologic therapies and alternative invasive techniques after a massive ABO-incompatible blood transfusion led to a favorable outcome in our patient.

Objectives & Background Patient Identification is fundamental to the success of safe transfusion. ABO incompatible blood transfusion has been classed as a Never Event by the Department of Health. In 2014, 680 Wrong Blood in Tubes (WBIT9s) were reported nationally to SHOT (Serious Hazards of Transfusion). National Guidelines have changed (2013) to improve accuracy in sample labeling (two sample rule) but SHOT reports prove on going noncompliance with this procedure. Blood samples are rejected if ANY aspect of the labeling is incorrect. This can generate rejection rates for transfusion specimens >10%. Over 3000 samples were rejected in 2014 at RCHT. This results in loss of patient confidence due to repeated clinical procedures, delay to treatment, loss of staff time, and increased cost of equipment and reagents. Llama Safe is a unique application that enables healthcare professionals to guarantee positive patient identification and accurate transfusion sample labeling at the bedside. The decision to pilot the application in the Emergency Department (ED), beginning Jan 2015, was due to: ▸Above average Tx samples rejected; ▸Large multidisciplinary teams with high staff rotation; ▸Unpredictable workload and stressful environment; ▸60–70 thousand patients per year; ▸Poor adherence to labelling at the patient9s bedside, including Wrong Blood in tube events annually; Methods Prior to the pilot, two months were spent shadowing a multitude of clinical staff in the ED to fully understand the sampling processes and the problems that arise. A simple system was designed in collaboration with ED staff, containing minimal steps, ensuring all safety measures had been considered and satisfied. Llama posters and stickers were placed throughout the department to remind staff to use the new labelling system. Results Staff were extremely invested and supportive in the Llama implementation allowing the pilot to be smooth and successful. ED very quickly took it upon themselves to cascade training and encourage the implementation on other wards. No WBITs have been identified in ED since the introduction of Llama (18 months). Rejections in ED have reduced 10 fold with Llama labelled samples, consequently improving patient care and proving concept for full roll out. Conclusion With appropriate planning and collaboration, introducing new technology into an acute environment can be easily achieved. Staff pressure has been relieved from a tense clinical environment. Llama was very positively received in the ED.

A fatal incident of an ABO incompatible erythrocyte transfusion in a 75-year-old male patient who suffered from dilated cardiomyopathy with cardiac failure is reported. Blood group A red cells were transfused to the unintended recipient who had blood group O. The patient died 45 min after the incompatible erythrocyte transfusion. The way the incident happened remained unclear and the immunohistochemical detection of ABO incompatible erythrocytes in formaldehyde-fixed paraffin-embedded kidney, lung, liver and spleen tissue provided the only material evidence of the transfusion error.

Summary. A male patient of blood group A was accidentally given two units of group B blood when operated upon because of injury. This resulted in an immediate haemolytic transfusion reaction. The patient was treated with exchange transfusions in order to remove the incompatible red cells and thus prevent renal damage. Two weeks after the transfusion, an anti-B humoral immune response appeared. The antibodies were mainly IgG and IgA types, of IgG3 and IgA1 subclasses. The anti-B antibodies seemed specific for the B trisaccharide [Galα1–3(Fucα1–2)Gal] as tested by radioimmunoassay and chromatogram binding assay. No antibodies recognizing part of the core saccharide chain could be detected, i.e. antibodies capable of differentiating between B type 1 and B type 2 chains did not occur. An unsuspected finding was that the patient had IgG antibodies recognizing glucosylceramide (and weakly also galactosylceramide) before and after the transfusion. These antibodies were still present 9 years after the ABO-incompatible blood transfusion.

Sir, The recent report on thrombotic thrombocytopenic purpura (TTP) after transfusion of ABO incompatible blood is very interesting.[1] Solak et al. hypothesized that the TTP might be due to “transfusion of ABO incompatible blood” or “open cardiac surgery.”[1] Solak et al. also noted that “TTP secondary to ABO incompatible blood transfusion has never been reported in the literature until date.”[1] What the exact mechanism in the present case is still a myth and the data on confounding morbidity (such as occult cancer) in the present case is not well presented. In fact, it is no doubt that ABO incompatibility can induce TTP. The previous reports on TTP after ABO mismatched liver and renal transplantations are good example.[2,3] Hence, the cases of ABO blood transfusion should be no doubt for the pathogenesis of TTP.

PERITONEAL irrigation as a means of treating a patient with uremia resulting from acute renal damage following sulfathiazole therapy has been reported by Frank, Seligman and Fine. 1 These same workers had previously observed the results of this technic on animals. 2 Recently we utilized this method of peritoneal irrigation on a patient with uremia resulting from an incompatible blood transfusion. The procedure was effective and directly associated with improvement and subsequent recovery of the patient. The patient was not expected to survive, since grave sequelae of uremia existed. Moreover, certain complications related to the peritoneal irrigation were encountered. A report of the case therefore seems warranted. REPORT OF A CASE A white woman aged 36 years entered the hospital for a pelvic operation. A transfusion of whole blood was ordered prior to operation as a corrective measure for a moderate degree of anemia (red blood cell count 3,600,000 per

Background and Objectives Morbidity and mortality from ABO-incompatible transfusion persist as consequences of human error. Even so, insufficient attention has been given to improving transfusion safety within the hospital. Materials and Methods National surveys of ABO-incompatible blood transfusions were conducted by the Japanese Society of Blood Transfusion, with support from the Ministry of Health, Labor and Welfare. Surveys concluded in 2000 and 2005 analysed ABO-incompatible transfusion data from the previous 5 years (January 1995 to December 1999 and January 2000 to December 2004, respectively). The first survey targeted 777 hospitals and the second, 1355 hospitals. Data were collected through anonymous questionnaires. Results The first survey achieved a 77·4% response rate (578 of 777 hospitals). The second survey collected data from 251 more hospitals, but with a lower response rate (61·2%, or 829 of 1355 hospitals). The first survey analysed 166 incidents from 578 hospitals, vs. 60 incidents from 829 hospitals in the second survey. The main cause of ABO-incompatible transfusion was identification error between patient and blood product: 55% (91 of 166) in the first survey and 45% (27 of 60) in the second. Patient outcomes included nine preventable deaths from 1995 to 1999, and eight preventable deaths from 2000 to 2004. Conclusion Misidentification at the bedside persists as the main cause of ABO-incompatible transfusion.

The transfusion of rhesus positive (D+) red blood cells to a rhesus negative (D-) person usually induces the development of an irregular anti-D antibody in the recipient. This can lead to a hemolytic reaction in subsequent transfusions, and, in women of childbearing age, can lead to fetal erythroblastosis in any future pregnancy. The recommended interventions to avoid the immunization of the recipient include the administration of intravenous rhesus immune globulin within 72 h after the transfusion. We report the case of a D- woman who received one unit of D+ red blood cells and a total of 40 units of D- red blood cells after severe trauma. In spite of treatment with rhesus immune globulin, the patient developed anti-D antibodies.

Unfortunately, transfusion errors continue to pose a major clinical problem. In practice there is a remarkable lack of understanding of the reasons behind transfusion medicine, a worrying disregard for protocol and an offhand attitude to bedside checking. Clearly transfusion medicine education, as often said, must be more extensively incorporated into the core curriculum of medical, nursing and laboratory staff. In this immunological case report, following accurate pre-transfusion procedures and routine laboratory testing, we highlight, once more, that it would be better for the patient to rely on proper bedside checking rather than on their own immune system in order to avoid serious side effects related to transfusions. Albeight this case we had "a happy ending", we must always bear in mind that one cannot compromise on safety and the quality care of patients.

A 50-year old man with blood type 0, Rh +, experienced disseminated intravascular coagulation (DIC) with massive bleeding and post-transfusion hemolytic reaction (PTHR) following transfusion of incompatible blood type AB Rh + (7000 mL) during an operation of pharyngeal carcinoma with lymphoid metastases. DIC (PLT count 54, APTT 51 s, PT 27%, fibrinogen level 0.5 g/L, TT 21 s, fibrin monomers ethanol test ++) was treated with standard therapy, massive PTHR (RBC 1.57, Hb 55, htc 0, 16, RTC 0.107, bilirubine 345 micromol/L, LDH 1560 IU/L, haptoglobin very low, free hemoglobin high, hemoglobin and hemosiderin in urine positive) was treated with plasmapheresis. The patient developed acute renal failure (creatinine clearance 18 mL/min) and nosocomial sepsis (Acinetobacter sp.). This case report present clinical and laboratory features of complications due to incompatible blood transfusion and answer the following questions: 1. Why was the clinical feature of PTHR and DIC considered to be clinical feature of DIC and hemorrhagic shock? 2. Why were the cross-match reactions of patients serum and AB Rh + erythrocytes negative? 3. Why did massive intravascular hemolysis appear on the sixth day of the illness? 4. Is plasmapheresis the right choice for treatment of PTHR? The patient is alive and fully recovered. Laboratory studies are normal.

Hemolytic reactions such as immune complications of incompatible blood transfusion are described. Characteristics of the immediate intravascular and extravascular antibody mediated red cell destruction are presented with particular attention to delayed hemolytic transfusion reactions. Moreover, the most frequent causes of incompatible blood transfusion are summarized. A general strategy to assure the immunologic safety in blood transfusion is suggested.

Irregular antibodies were identified in 1.3% of obstetric patients who were delivered at the Royal women's Hospital, Melbourne. The most common antibodies found were anti-P1 and anti-Lewis, but, although these antibodies may cause difficulty in obtaining compatible blood if transfusion is required, they were not associated with haemolytic disease of the newborn. Immunization with other irregular antibodies, especially Rhesus subtype and Kell, may occur due to pregnancy alone or follow the combination of pregnancy and incompatible blood transfusion. Irrespective of the initial cause of immunization, these antibodies are often associated with haemolytic disease of the newborn which may be severe enough to result in perinatal death. As most irregular antibodies are found in patients with Rh-positive blood, the need for screening of all antenatal patients in each pregnancy must be recognized.

Applicability of the mixed cell agglutination reaction (MGAR of Davidsohn) in histological examination was tested in a case of ABO incompatible blood transfusion, who had died of severe head injury two days after an accident. Massively disseminated intravascular aggregation of erythrocytes was identified as immune agglutination by the modified method of MGAR (Ishiyama & Okada) with precise knowledge of topographic isoantigen localization in tissues. The immune specific agglutination mimics intravascular changes such as hyperemia, stagnation and hemorrhage derived from various circulatory disturbances obtained in routine autopsy materials. ACTA PATH. JAP. 27: 729 ˜ 738, 1977.

For the purpose of adoption to the type and screen in our hospital, we investigated some problems on daily blood transfusion service for last 2 years. Main problems were 0.027% of order mistake, 0.03% of blood collection error, and 0.03% of serological technical error in our blood bank. Serological technical problems were also found 0.018% of blood derivered from red cross blood center.Presently, ABO incompatible blood transfusion will be done 1 per 1000 un-crossmatched transfusion, but it will be reduced 1 per 1, 000, 000 after crossmatched transfusion. Also irregular antibody incompatible blood transfusion will be reduced 1 per 500 to 1 per 100, 000.In our hospital, patients information were registrated to personal computer for prevent clerical management error.Under the strict quality control of reagents and technical methods, selected patients control, we could applied un-crossmatched blood transfusion and partically addreviated crossmatch test on type and screen.

1. 1. The hemorrhagic diathasis following an incompatible blood transfusion reaction is associated with thrombocytopenia, prolongation of the coagulation time, prolongation of the prothrombin time, a decrease in the circulating white blood cells, the appearance of fibrinolytic activity and of a “heparinoid” anticoagulant. 2. (2) The reaction is somewhat different in dogs inasmuch as the fibrinogen level does not decrease as markedly as in the human case, nor does fibrinolytic activity appear. 3. 3. It is suggested that the management of these cases be a complete immediate estimate of all the major blood clotting factors with a subsequent replacement of fibrinogen or the use of an antiheparin agent wherever indicated.

Intravascular thrombosis follows the injection of incompatible blood into the aorta of the dog. The thrombi form quickly and may disappear quickly. Under different experimental conditions thrombi persist in different locations. The organ or organs through which the coagulating blood circulates first receive and retain the majority of the thrombi. The functional and pathologic consequences of the injection of incompatible blood depend upon the organ or organs which are most severely involved by the clotting process. The localization of thrombi is dependent on the site and speed of injection, and the condition of the vascular bed at the time of the clotting episode. The most likely source of the clotting agent in these experiments is the hemolyzed human red blood cell.

Summary: 1. A 10-year study of 120 patients with massive, primary post partum haemorrhage is presented. 2. The aetiological factors were as follows: retained placenta, 54 patients; birth canal trauma, 43 patients; coagulation defect, 11 patients; and uterine “atony”, 12 patients. 3. Although a major degree of control has been obtained over haemorrhages resulting from uterine atony and coagulation defect, the other 2 groups may fully tax the obstetrician's resources (as a result of morbid placental adherence and major vessel damage). 4. There were 5 maternal deaths in the series, 4 from birth canal trauma and 1 from an incompatible blood transfusion.

This is a report of a case which developed acute hemolytic reaction due to incompatible blood transfusion of anti-D and anti-C Rh antibody.1) The case had received massive blood transfusion in the previous gastrectomy which, it is construed, probably gave rise to production of anti-Rh antibody and induced an antigen-antibody reaction in the concurrent blood transfusion. In order to prevent such complications it is advisable to test anti-D and anti-E antibody on those patients with histories of blood transfusion, stillbirth or abortion and if it is negative Coomb's test should be performed.2) Shock due to incompatible blood transfusion under general anesthesia is evasive to detection, and so need of its careful detection cannot be over-emphasized.3) As for the treatment plasma, plasma expander, massive administration of hydrocortisone and transfusion of Rh negative blood showed remarkable effects.

Twenty maternal deaths resulting from acute renal failure (anuric uraemia) are reported. Three of these were caused by incompatible blood transfusion. Each, of the remaining 17 suffered from accidental haemorrhage. The communication covers 150,000 hospital deliveries. In no case did fatal suppression follow eclampsia (350 cases) or non-convulsive toxaemia (5,122 cases) unaccompanied by accidental haemorrhage. Death from renal failure occurred once in association with placenta praavia (1,131 cases) and once with postpartum haemorrhage. The failure resulted from mismatched transfusions in both. There was no case of fatal anuria following haemorrhage, shock or trauma of any other nature. Thirty-five cases of accidental haemorrhage died and the cause of death in 17 was acute renal failure (excluding one mismatched blood transfusion).

A patient with pheochromocytoma was a 55-year-old Japanese female. Anti-E antibody was detected in her serum. Its titer measured by indirect antiglobulin test was 4. She was transfused with 2 units of incompatible (E antigen positive) blood, which was judged to be compatible by an inexperienced technician, late in the night in December, 1988. The immediate posttransfusion period was uneventful. Three days later, she developed a slight fever and hypertension, but these symptoms disappeared without special treatment after several hours. No elevation of anti-E antibody titer was observed during a month after the incompatible transfusion.