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 Table of Contents  
CASE REPORT
Year : 2019  |  Volume : 4  |  Issue : 1  |  Page : 87-89

Oblivious of the yellow world – A newborn's telltale: ABO hemolytic disease of newborn


1 Department of Transfusion Medicine, All India Institute of Medical Sciences, Rishikesh, Uttarakhand, India
2 Department of Neonatology, Max Superspecialty Hospital, New Delhi, India
3 Department of Paediatrics, Max Superspecialty Hospital, New Delhi, India

Date of Web Publication22-Apr-2019

Correspondence Address:
Dr. Daljit Kaur
Department of Transfusion Medicine, All India Institute of Medical Sciences, Rishikesh, Uttarakhand
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/GJTM.GJTM_45_18

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  Abstract 


The increased destruction of fetal red cells can be immune (allo- or autoantibodies) or nonimmune (hemoglobinopathies, enzyme defects, and membrane defects) in nature and can cause shortened life span of red cells leading to hemolytic disease of the fetus and newborn. Maternofetal ABO incompatibility is common but rarely leads to severe anemia due to poorly developed A or B antigens on fetal red blood cells and neutralization of antibody by tissue and soluble ABO blood group substances in plasma, while RhD hemolytic disease of newborn (HDN) occurring due to D-antigen sensitization in D-negative mothers may lead to severe HDN. Here, we report a case of an inborn neonate who was admitted in neonatal intensive care unit of our hospital at day 1 of life with severe hyperbilirubinemia and needed exchange transfusion.

Keywords: ABO incompatibility, hemolytic disease, hyperbilirubinemia


How to cite this article:
Kaur D, Sidana P, Mandhan G, Kanodia K. Oblivious of the yellow world – A newborn's telltale: ABO hemolytic disease of newborn. Glob J Transfus Med 2019;4:87-9

How to cite this URL:
Kaur D, Sidana P, Mandhan G, Kanodia K. Oblivious of the yellow world – A newborn's telltale: ABO hemolytic disease of newborn. Glob J Transfus Med [serial online] 2019 [cited 2019 May 21];4:87-9. Available from: http://www.gjtmonline.com/text.asp?2019/4/1/87/256758




  Introduction Top


Hemolytic disease of newborn (HDN) resulting from ABO incompatibility occurs due to immunoglobulin G (IgG) antibody crossing placentally only in offspring of women of blood Group O who have IgG anti-A and anti-B and is limited to 1%, with high antepartum titers of IgG antibodies.[1] The frequency of anti-A related hemolytic disease of the fetus and newborn (HDFN) is only 0.66%, while anti-B is even lower.[2] ABO HDN causes mild postpartum jaundice with or without anemia which is detected at 24 h after delivery rarely requiring exchange transfusion.[3] We hereby report a case of an inborn neonate who was shifted to neonatal intensive care unit of our hospital at day 1 of life with severe hyperbilirubinemia and needed one double-volume exchange transfusion (DVET).


  Case History Top


The female baby, 3.8 kg, appropriate for age was delivered vaginally to a second gravida mother at 40+3 week at a tertiary care hospital in North India. The baby was found to be icteric at 16 h of life and transcutaneous bilirubin was 19 mg/dl. The baby was transferred to neonatal intensive care unit for further management and was planned for double-surface phototherapy (PT) and intravenous Ig (IVIg). The total serum bilirubin (TSB) valued 20.5 mg/dl (direct = 0.8 mg/dl and indirect = 19.7 mg/dl) at 21 h of life, and the baby was advised DVET if no further fall in TSB is observed [Figure 1].
Figure 1: The total serum bilirubin trend and neonatal management at the hospital

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On examination, the baby was hemodynamically stable, was accepting feeds, had soft abdomen, tone was normal, shrill cry was present, no cephalhaematoma was observed and the chest was clear. After 24 h of life, the TSB rose to 21.7 mg/dl (direct = 0.8 mg/dl and indirect = 20.9 mg/dl). The hemogram revealed haemoglobin of 14.8gm/dl, packed cell volume (PCV) as 44.3%, reticulocyte count as 20%, and the peripheral blood picture showed red cells with anisocytosis, poikilocytosis, and predominantly normochromic and normocytic with the presence of polychromatophilic cells and few schistocytes. The baby was treated with multiple surface PT and IVIg at 1 g/kg was started. The serum bilirubin was still showing increasing trend (at 27 h, TSB = 22.6 mg/dl; direct = 1.0 mg/dl and indirect = 21.6 mg/dl) and was in exchange zone.

A request for DVET was received in the Department of Transfusion Medicine with neonate and mother's blood sample. The ABO blood grouping performed on both revealed neonate to be B RhD positive and mother as O RhD positive. The direct antiglobulin test (DAT) for neonate was positive (2+) for IgG and negative for complement C3d. The red cell antibody screening done by commercially available three cell panel (using 0.8% Surgiscreen, Ortho-Clinical Diagnostics Limited, USA) for maternal serum was negative. The father's blood group was BRhD positive.

The crossmatch-compatible O RhD-positive packed red cell unit reconstituted with AB blood group plasma was issued for exchange transfusion at 30 h of life.

Meanwhile, the possibility of ABO HDN due to ABO incompatibility between mother and neonate was kept. The eluate so obtained after heat elution for the DAT-positive neonatal red cells was found to react with B-cells, indicating anti-B antibody-coating neonatal red cells. The maternal anti-B IgG titers (by conventional tube technique) were found to be 1:1024 (in antihuman globulin phase) and IgM to be 1:512, thus confirming the possibility of ABO-HDN. The inherited causes such as G6PD deficiency or infections were excluded in the index case.

The baby underwent one DVET under aseptic conditions. Post-DVET, the TSB at 2 h was 13.3 mg/dl and PCV was 46.3%. Multiple surface PT was continued, and another dose of IVIg was given over 4 h. The following day TSB was 12.1 mg/dl, and on day 4, it was 10.9 mg/dl. The baby was discharged on day 4 of life with danger signs explained to mother and to report back if any present.


  Discussion Top


The universal use of Rh Ig has led to a decline in Rh HDN, and as a result, the ABO incompatibility is the most common cause of HDN in high human development index countries, while Rh HDN is still a matter of great concern in low development countries.[4] The ethnicity also plays a great role in the prevalence of maternofetal ABO incompatibility, and various studies highlight the prevalence in different races suggesting 50% in Asians, 31% in Europeans, and the overall incidence of ABO HDN being higher among African ancestry.[5],[6] The higher frequencies reported from Africa and Saudi Arabia could be related to more potent anti-A and anti-B (caused by environmental factors) and a relatively strong expression of A and B antigens.[2] In our case, the maternal anti-B (IgG) titers were severe enough to cause hyperbilirubinemia and with positive DAT in neonate similar to a case reported by Kumawat et al.[7] Unlike non-ABO HDFN, the first ABO-incompatible infant is at risk for significant hemolysis, because anti-A and anti-B antibodies are already developed before pregnancy. The elder sibling (blood group not known) of index case had a history of physiological jaundice after birth and required PT, but no details of maternal anti-A/anti-B titers were available.

In the present case, neonate was diagnosed to have hyperbilirubinemia at 16 h of life and was treated with PT and IVIg at 21 h of life but needed one exchange transfusion as the baby had already reached exchange zone of hyperbilirunimea. The baby was discharged on the 4th day of life with no signs of bilirubin encephalopathy or hemolysis.

IVIG has been shown to reduce the need for exchange transfusion and the complications associated with exchanges if started well on time. It is a safe and effective treatment for HDN and is in vogue over the last decade.[8] A systematic review by Gottstein and Cooke presented an evidence of the available randomized controlled trials showing a significant effect of IVIG when administered in the postnatal period in HDN.[9] However, studies have shown that the use of IVIg in Rh HDN has reduced the need for exchange transfusion, but there is no consensus for the routine use in ABO-HDN and multicentric randomized controlled trials are required.[10],[11],[12]


  Conclusion Top


Concluding with the suggestion that obstetricians must be aware of such high risk mothers, should foresee the situation and get maternal titers evaluated and to warn the parents and paediatricians on time for high titres. Close monitoring of affected neonates is important, as high-dose IVIG adjuvant therapy and occasionally even exchange transfusion can be required. Although ABO-HDN is not common, strict monitoring of such neonates should be done and early discharge of babies born to high-titer O mothers should be avoided. A special attention is needed for the successive pregnancies if a history of previously ABO-HDN affected baby is found.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Chen JY, Ling UP. Prediction of the development of neonatal hyperbilirubinemia in ABO incompatibility. Zhonghua Yi Xue Za Zhi (Taipei) 1994;53:13-8.  Back to cited text no. 1
    
2.
Murray NA, Roberts IA. Haemolytic disease of the newborn. Arch Dis Child Fetal Neonatal Ed 2007;92:F83-8.  Back to cited text no. 2
    
3.
Klein HG, Anstee DJ, editors. Haemolytic disease of the fetus and newborn. In: Mollison's Blood Transfusion in Clinical Medicine. 12th ed. Oxford: Wiley Blackwell; 2005. p. 496-545.  Back to cited text no. 3
    
4.
Solheim BG, Gronn M. Hemolytic disease of fetus and newborn. In: Simon TL, McCullough J, Synder EL, editors. Rossi's Principles of Transfusion Medicine. 5th ed. Willey Blackwell; 2016. p. 530.  Back to cited text no. 4
    
5.
Ziprin JH, Payne E, Hamidi L, Roberts I, Regan F. ABO incompatibility due to immunoglobulin G anti-B antibodies presenting with severe fetal anaemia. Transfus Med 2005;15:57-60.  Back to cited text no. 5
    
6.
Stiller RJ, Herzlinger R, Siegel S, Whetham JC. Fetal ascites associated with ABO maternal-infant incompatibility in Asians, Blacks, Hispanics and Caucasians. Vox Sang 1988;54:181-3.  Back to cited text no. 6
    
7.
Kumawat V, Kulkarni K, Goyal M, Lokadas V. ABO hemolytic disease of fetus and newborn; still a diagnostic dilemma: A case report. Indian J Hematol Blood Transfus 2018;34:183-4.  Back to cited text no. 7
    
8.
Mundy CA, Bhatia J. Immunoglobulin transfusion in hemolytic disease of the newborn: Place in therapy. Int J Clin Transfus Med 2015;3:41-5.  Back to cited text no. 8
    
9.
Gottstein R, Cooke RW. Systematic review of intravenous immunoglobulin in haemolytic disease of the newborn. Arch Dis Child Fetal Neonatal Ed 2003;88:F6-10.  Back to cited text no. 9
    
10.
Beken S, Hirfanoglu I, Turkyilmaz C, Altuntas N, Unal S, Turan O, et al. Intravenous immunoglobulin G treatment in ABO hemolytic disease of the newborn, is it myth or real? Indian J Hematol Blood Transfus 2014;30:12-5.  Back to cited text no. 10
    
11.
Nasseri F, Mamouri GA, Babaei H. Intravenous immunoglobulin in ABO and Rh hemolytic diseases of newborn. Saudi Med J 2006;27:1827-30.  Back to cited text no. 11
    
12.
Zwiers C, Scheffer-Rath ME, Lopriore E, de Haas M, Liley HG. Immunoglobulin for alloimmune hemolytic disease in neonates. Cochrane Database Syst Rev 2018;3:CD003313.  Back to cited text no. 12
    


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