Deepti Sachan

Sudden increased incidence of transfusion reactions reported from a ward: root cause analysis

The transfusion medicine department of a teaching hospital in north India was inundated with reports of transfusion reactions with red blood cells (RBCs) seen in patients admitted to the hematology ward (seven adverse transfusion reactions in a <2-week period). Buffy coat–removed RBCs were routinely being transfused to these patients without frequent reactions previously. The transfusions had to be stopped immediately after initial 10 to 20 mL of blood infusion in most cases. Patients presented with chills, rigors, fever, dyspnea, and wheezing but no red-colored urine. The RBC units with the attached blood administration (BA) set and patients’ blood samples were collected immediately after the reactions as per departmental standard operating procedure. No ABO and Rh blood group discrepancy or incompatible crossmatch with preand posttransfusion samples from the patients could be demonstrated using gel cards (DiaMed-ID, Cressier, Switzerland) and standard tube methods. Immunohematologic workup including direct and indirect anti-human globulin tests by gel cards was also negative. The posttransfusion blood samples from recipients showed no hemolysis. There was no evidence of any hemolysis in the bag, no clots, and no evidence of any compromise in integrity of the

RhD blocking phenomenon implicated in an immunohaematological diagnostic dilemma in a case of RhD-haemolytic disease of the foetus

Of all red blood cell antigens, RhD is second only to the ABO antigens in importance in blood transfusion. The Rh antigens are fully expressed at the time of birth unlike the weak expression of ABO antigens in neonates1. Immunisation to D antigen can occur in reaction to less than 0.1 mL of foetal blood, resulting in anti-D alloantibody in the maternal circulation2. Haemolytic disease of the foetus and newborn (HDFN) occurs when there is a destruction of foetal/neonatal red cells by IgG antibodies produced by the mother. When Anti-D is the cause of HDFN, the severe anaemia can cause foetal hydrops, tissue hypoxia and even foetal death in utero3. Sensitised pregnant women require close monitoring for early detection of foetal anaemia and to decide whether and, if so, when intrauterine transfusion is required. As a key part of any pre-transfusion testing, the ABO and RhD groups of recipient samples are determined. It has been reported that if a neonate’s red cells are heavily saturated with IgG antibodies, RhD typing with anti-D reagents may give either false negative or false positive results3. We report here the case of blocked RhD in a cord blood sample in a suspected case of RhD-HDFN which was detected in our hospital blood bank laboratory.

Error reporting in transfusion medicine at a tertiary care centre: a patient safety initiative.

Abstract Background: Errors in the transfusion process can compromise patient safety. A study was undertaken at our center to identify the errors in the transfusion process and their causes in order to reduce their occurrence by corrective and preventive actions. Methods: All near miss, no harm events and adverse events reported in the ‘transfusion process’ during 1 year study period were recorded, classified and analyzed at a tertiary care teaching hospital in North India. Results: In total, 285 transfusion related events were reported during the study period. Of these, there were four adverse (1.5%), 10 no harm (3.5%) and 271 (95%) near miss events. Incorrect blood component transfusion rate was 1 in 6031 component units. ABO incompatible transfusion rate was one in 15,077 component units issued or one in 26,200 PRBC units issued and acute hemolytic transfusion reaction due to ABO incompatible transfusion was 1 in 60,309 component units issued. Fifty-three percent of the antecedent near miss events were bedside events. Patient sample handling errors were the single largest category of errors (n=94, 33%) followed by errors in labeling and blood component handling and storage in user areas. Conclusions: The actual and near miss event data obtained through this initiative provided us with clear evidence about latent defects and critical points in the transfusion process so that corrective and preventive actions could be taken to reduce errors and improve transfusion safety.

Passenger Lymphocyte Syndrome Following Minor ABO Mismatch Liver Transplantation

Non-ABO identical liver transplantation (LT) is in growing trend in India due to limited availability of organ donors and the growing number of patients awaiting orthotopic liver transplantation. Recipients of minor ABO mismatched organ transplantation may experience delayed hemolysis mediated by donor lymphocytes contained in the graft. Donor lymphocytes produce iso-agglutinins capable of destroying the recipient’s red cells, resulting in varying degree of hemolysis known as passenger lymphocyte syndrome (PLS) [1]. PLS is not an uncommon cause of anemia in non-ABO identical LT but often goes undiagnosed and not yet reported in India in ABO mismatch LT. We present a case of 48 years old male, AB positive, with ethanol related end stage liver disease who underwent live donor liver transplant from a O positive donor without any intraoperative complications. He had history of multiple transfusions in past 2 years during episodes of gastrointestinal bleeds but no history of haemolytic transfusion reaction or red cell immunization. Intraoperatively, the patient was transfused with AB positive 4 packed red cells (PRC), 2 fresh frozen plasma (FFP), 3 units of cryoprecipitate and 1 unit of single donor platelets (SDP) and 2 units of FFP postoperatively. Injection Methylprednisolone 500 mg was given intravenously in the anhepatic phase and then was changed to oral prednisolone. Cap tacrolimus 0.5 mg twice daily was started 12 h after the surgery and was adjusted as per tac levels during postoperative period. The postoperative course of the patient was uneventful and graft function was normal by postoperative day (POD) 5. However, POD 7 onwards, patient showed decline in hemoglobin (Hb) level from 10 to 6.9 g%. As per liver transplant transfusion policy, Crossmatch compatible O positive PRC was issued and transfused. However, the Hb was not raising in spite of transfusion of O positive PRC. There was no evidence of bleeding or sepsis and by POD12, investigations showed peak bilirubin levels 14.53 gm/ dl, reticulocyte count 9%, Serum LDH 708 IU/ml and peripheral smear suggestive of hemolytic anemia. On immune-hematological workup, repeat ABO and Rh typing (Gel method) showed AB positive with mixed field reaction with anti-A and anti-B in forward grouping, the reverse grouping showed no discrepancy in saline phase. On performing polyspecific direct anti-globulin test (DAT) using the LISS Coombs column agglutination technique (Bio-Rad GmbH, Cressier-sur-Morat, Switzerland), the patient’s red cells were found to be positive (2?). Elution was performed using commercial acid elution kit (Diacidel, Bio-Rad GmbH, Cressier-sur-Morat, Switzerland) and the eluate showed the presence of anti-A antibody. Indirect antiglobulin test of the patient’s serum and eluate using 3-cell panel of O group (Diacell, Biorad GmbH, Cressiersur-Morat, Switzerland) was negative, ruling out the presence of any unexpected antibody. Anti-A antibody was probably IgG type as it was detectable in the serum only in AHG phase and was also confirmed by presence in RBC eluate. Serial titration of liver donor serum showed IgG anti A and anti B titres of 256 and 128 respectively. Hemolysin test was positive. A provisional diagnosis of PLS was made. Autoimmune hemolytic anemia was ruled & Deepti Sachan deepti.vij@gmail.com

Delayed Serological Transfusion Reaction After Platelet Transfusion Due to Anti-e

Abstract Delayed serological transfusion reaction (DSTR) is defined as absence of clinical signs of hemolysis and demonstration of new, clinically-significant antibodies against red blood cells after a transfusion, by either positive direct antiglobulin test or positive antibody screen with newly identified RBC alloantibody. Various delayed hemolytic transfusion reaction cases are reported after red cell transfusions. However, the incidence of DSTR after platelet transfusion due to non-Rh(D) antibodies is not much documented. We report here a case of DSTR due to anti-e Rh antibody in a multiply red cell alloimmunized female patient after single donor platelets transfusion.

Delayed hemolytic transfusion reaction due to anti-D in Rh (D) positive patient

1. Singh A, Dubey A, Sonker A, Chaudhary R. Evaluation of various methods of point‐of‐care testing of haemoglobin concentration in blood donors. Blood Transfus 2015;13:233‐9. 2. Goldman M, Uzicanin S, Yi QL, Acker J, Ramirez‐Arcos S. Validation and implementation of a new hemoglobinometer for donor screening at Canadian Blood Services. Transfusion 2012;52 (7 Pt 2):1607‐13. 3. Tayou Tagny C, Kouam L, Mbanya D. The new HemoCue system Hb 301 for the haemoglobin measurement in pregnant women. Ann Biol Clin (Paris) 2008;66:90‐4. 4. HemoCueHb 301 Operating Manual. Angelholm, Sweden. Available from: www.hemocue.com. [Last accessed on 2014 Dec 16]. Access this article online

Rapid diagnosis of heparin-induced thrombocytopenia using a particle gel immunoassay in at-risk cardiac surgery patients

Department of Transfusion Medicine, Global Health City, Chennai, India Department of Cardio Vascular and Thoracic Surgery, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India Department of Transfusion Medicine, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India Correspondence to: Dr. Deepti Sachan, Department of Transfusion Medicine, Global Health City, Chennai 600 100, India. E-mail: deepti.vij@gmail.com

Late onset neonatal anaemia due to maternal anti-Kpb induced haemolytic disease of the newborn

BACKGROUND Alloanti-Kp(b) is a rare, clinically significant antibody against high frequency red cell antigen Kp(b) of Kell blood group system. We report here a case of Haemolytic disease of newborn (HDN) due to anti-Kp(b), which manifested as severe anaemia at the age of 1 month. AIM To diagnose and successfully manage anti-Kp(b) induced HDN. METHODOLOGY Direct antiglobulin test (DAT), antigen typing, irregular antibody screening and identification were done by polyspecific LISS Coombs Gel card and standard methods. RESULTS At presentation the neonate had severe anemia with reticulocytopenia. Blood group was B, Rh D positive and DAT was 2+. Anti-Kp(b) was detected in mothers serum. Due to unavailability of Kp(b) negative red cells and incompatible blood group of mother (A(1)B Rh D positive) infant was transfused group B Rh D, Kp(b) positive PRBCs under steroid cover. He was symptom free at 4 months of age and DAT became negative at 6 months. CONCLUSION Anti-Kp(b) is capable of causing severe late HDN. Infants born to irregular antibody positive mothers should be investigated and closely monitored for several weeks after birth for immune HDN even if asymptomatic at birth.

Events at blood collection area due to nonconforming blood bags and plateletpheresis kits: need for timely corrective and preventive actions

BACKGROUND: Good blood banking practice requires that every effort should be made to detect any deviation or defect in blood bank products and to identify any potential risk to blood donor or recipient(s). We report the findings of an exercise that provide an insight into why feedback from the user side is crucial.