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Obstetric case reports

References Arulkumaran S, Ng CS, Ingemarsson I, Ratnam SS. 1986. Medical treatment of placenta accreta with methotrexate. Acta Obstetrica Gynecologica Scandinavica 65(3):285 286. Breen JL, Neubecker R, Gregori CA, Franklin JE Jr. 1977. Placenta accreta, increta, and percreta. A survey of 40 cases. Obstetrics and Gynecology 49(1):43 47. Engelsen IB, Albrechtsen S, Iversen OE. 2001. Peripartum hysterectomy-incidence and maternal morbidity. Acta Obstetrica Gynecologica Scandinavica 80:409 412. Gorodeski IG, Bahari CM, Holzinger M, Schachter A, Neri A. 1982. Placenta previa with focal accretion. Israel Journal of Medical Science 18:277 280. Jackson N, Paterson-Brown S. 2001. Physical sequelae of caesarean section. Best Practice & Research. Clinical Obstetrics & Gynaecology 15(1):49 61. Jurcevic P, Grover S, Henderson J. 2002. A reassessment of options for the management of placenta praevia percreta. Australian and New Zealand Journal of Obstetrics and Gynaecology 42(1):84 88. Lam G, Kuller J, McMahon M. 2002. Use of magnetic resonance imaging and ultrasound in the antenatal diagnosis of placenta accreta. Journal of the Society for Gynecologic Investigation 9:37 40. OBrien JM, Barton JR, Donaldson ES. 1996. The management of placenta percreta: conservative and operative strategies. American Journal of Obstetrics and Gynecology 175(6):1632 1638. Ota Y, Watanabe H, Fukasawa I, Tanaka S, Kawatsu T, Oishi A, Yasuda S, Inaba N. 1999. Placenta accreta/increta. Review of 10 cases and a case report. Archives of Gynecology and Obstetrics 263:69 72. Otsubo Y, Shinagawa T, Chihara H, Araki T. 1999. Conservative management of a case of placenta praevia percreta. Australian and New Zealand Journal of Obstetrics and Gynaecology 39(4):518 519. Price FV, Resnik E, Heller KA, Christopherson WA. 1991. Placenta previa percreta involving the urinary bladder: a report of two cases and review of the literature. Obstetrics and Gynecology 78:508 511.

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specically focussed on percreta. Sensitivity as low as 33% for ultrasound detection and 38% for MRI detection have been reported (Lam et al. 2002). These lower values may actually be representative of fact. The study focussed on conditions less welldened (accreta). It is known that the sensitivity of medical tests deteriorate when the sample size is small and when the condition tested is not well-dened. Percreta on the other hand is much more obvious condition for tests to detect. Percreta can be managed conservatively, as in this case, with preservation of the placenta. This signicantly reduces morbidity from severe haemorrhage (OBrien et al. 1996) particularly with bladder involvement. Alternatively, percreta can be managed surgically with intrapartum hysterectomy, although this is associated with considerable morbidity and mortality (Gorodeski et al. 1982). Ultimately, the treatment needs to be tailored to the individual situation and specics of the percreta. A grossly invasive percreta with parametrial or bladder involvement seem best left in situ. However, a focal percreta may be surgically treated by attempted removal, excision and repair of the uterus. But this situation is rare. Focal disease is more common with accreta where placental removal is clearly an option (Otsubo et al. 1999). A concise review on various surgical management options is presented by Jurcevic et al. (2002). The novel approach of treating women with placenta left in situ with methotrexate, was rst reported in 1986 (Arulkumaran et al. 1986). This is claimed to reduce the risk of secondary PPH and augment the process of placental separation and resorption. This should also theoretically hasten the decline in HCG levels and reduce the risk of persistent trophoblastic disease. However as yet, these benets are unproven and the optimal methotrexate regimen is unclear. It certainly seems theoretically plausible that it may also increase the success rate of conservative management of placenta percreta.

Acknowledgement Our thanks and appreciation go to the patient for allowing us to publish her experience and to Professor Seckl (Charing Cross Hospital Gestational Trophoblastic Unit) for advice on the methotrexate regimen for treatment of persistent trophoblastic disease.

Correspondence to: V. Valayatham, Womens Health Directorate, 10th Floor North Wing, St. Thomas Hospital, London, SE1 7EH, UK.
DOI: 10.1080/01443610500135669

Bombay blood group and pregnancy: A rare clinical scenario

N. D. DEO, F. ODEJINMI, B. DAWLATLY, & A. KHAN

Department of Obstetrics and Gynacology, Whipps Cross University Hospital, London, UK

Introduction
The Bombay blood group is a rare blood group distinct from the ABO grouping. The clinical signicance lies in the fact that these individuals can only by transfused blood of the same group. The antiH present in the maternal blood can cause isoimmunisation and jaundice in the newborn. We hereby report a rare case of pregnancy in a women with the Bombay blood group.

Case report
A 35-year-old primigravida of Srilankan Tamil origin was booked for antenatal care. Due to difculty in grouping and typing of her blood and identifying the nature of irregular antibodies, her blood samples were sent to the regional blood bank. She was reported to have the Bombay blood group with the red cells being H antigen negative and blood group of the Ohh genotype. Irregular

Obstetric case reports

antibodies of the anti H type were reported, the titre being 512 IU. The difculty in diagnosing the blood group resulted in a delay in further management of her pregnancy. A chemiluminescence test was not done. The husbands blood group was Rh positive and normal H status. She was started on haematinics to ensure optimal levels of haemoglobin (Hb). Her Hb at 38 weeks was 13.8 g% and hence it was planned for her to have an autologous blood donation. Unfortunately before this could be done, she had spontaneous rupture of the membranes and went into spontaneous labour at 38 + 2 weeks and it was therefore inadvisable to subject her to an autologous blood donation. The national blood bank register identied only two known Bombay blood group donors in the country and one of them underwent a direct donation. A second unit of frozen stored blood was also arranged from the Frozen blood bank, Birmingham. Labour was augmented with syntocinon and she had a ventouse delivery for poor maternal effort, resulting in prolonged second stage. She delivered a healthy male baby weighing 3.08 kg. Her blood loss at delivery was approximately 250 ml and she thus did not require a blood transfusion. The baby did not develop jaundice and did not require exchange transfusion or phototherapy.

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Discussion
The Bombay blood group is an extremely rare blood group and the number of individuals with this blood group is unknown. Most of the individuals identied with this blood group come from the Indian subcontinent. It was rst identied in 1952 by Bhende and his colleagues in Bombay and hence the name. It results from the presence of a homozygous recessive gene that inhibits the formation of A, B and H antigens. H antigen, a precursor of A and B antigens, is found on all human red cells except those subject of phenotype Oh. In genotype hh (phenotype Oh), H antigen is not synthesized on red cells or in secretions and therefore neither A or B antigens can be synthesized (Levine et al. 1955; Moores et al. 1975). Normally, almost everyone inherits at least one H gene, which determines the production of the H substance. The H substance, or its precursor is subsequently converted to A and or B. O is the absence of A and B substances, but the presence of H substance. Normally not all of the H substance is converted, so even the A and B cells contain some H. Bombay cells are therefore produced in people who lack the H gene, and hence the H, A and B substances. The red cells of newborn infants react less strongly than those of adults with anti H and the number of H antigen sites on RBC of the newborn is one-sixth that on adult cells (Bhattacharya et al. 2002). The H antigen can be detected on red cells of 5 6 week old embryos, but even at birth they are not fully developed. Soluble A, B, and H substances are found in amniotic uid from about the 9th week gestation onwards and are derived from the fetus. Anti H is found in subjects of this very rare Bombay phenotype in addition to anti A and anti B. Oh is a haemolysin and is active at 378C and 08C. It is usually IgM and may be partly IgG.

A literature search has shown only three cases of Bombay blood group and pregnancy, and due to its rarity, the prevalence in the general population is not known (Katz et al. 1981; SchenkelBrunner 1980; Moores et al. 1994). In such patients, blood grouping may pose to be difcult and reference laboratories may be needed for conrmation of the blood group status. Early grouping in pregnancy may help towards planning an autologous blood donation. It is known to cause haemolytic disease of the newborn since IgG is active in 378C and exchange transfusion may be needed (Moores et al. 1994). Weak expression of the H antigen may result in less severe hemolysis. Hence the need to monitor the neonate for developing jaundice. An individual of the Bombay phenotype can be transfused only Bombay group blood (Devey et al. 1978). Due to the rarity of the blood and limited number of donors, planning an autologous donation would help in arranging for blood for exchange transfusion for the neonate if required and for the mother in the event of post partum haemorrhage. Fortunately, the neonate did not develop HDN. The titre of anti H was high by indirect agglutination test. But due to the fact that it was the rst pregnancy and the rst sensitization to the H antigen, HDN did not develop. The weak expression of the antigen, heterozygous status of the fetus and distribution of the H antigen in non-erythroid tissues as well (in secretions) may have contributed to the non-development of HDN. Future pregnancies will have to be monitored closely. Blood donation and freezing of donated blood in the interpregnancy period should help in the management of future pregnancies and if blood transfusion should be required at any other time, as the frozen blood can be stored indenitely.

References Bhattacharya S, Makar Y, Laycock RA, Gooch A, Poole J, Hadley A. 2002. Outcome of consecutive pregnancies in a patient with Bombay (oH) blood group. Transfusion Medicine 12:379 381. Davey RJ, Tourault MA, Holland PV 1978. The clinical signicance of antiH in an individual with the Oh (Bombay) phenotype. Transfusion 18:738 742. Katz AR, Ali V, Ross PJ, Gammon E. 1981. Management of a rare blood group: Oh Bombay in pregnancy. Obstetrics and Gynaecology 57:16S 17S. Levine P, Robinson E, Celano M, Briggs O, Falkinburg L. 1955. Gene interaction resulting in suppression of blood group substance B. Blood 10:1100 1108. Moores PP, Issitt PD, Pavone BG, McKeever BG. 1975. Some observations on Bombay bloods, with comments on evidence for the existence of two different Oh phenotypes. Transfusion 15:237 243. Moores PP, Smart E, Gabriel B. 1994. Letter. Transfusion 34:1015 1016. Schenkel-Brunner H. 1980. Blood group ABH antigen of human erythrocytes. Quantitative studies on the distribution of H antigenic sites among different classes of membrane components. European Journal of Biochemistry 104:528 534.

Correspondence to: F. Odejinmi, Department of Obstetrics and Gynaecology, Whipps Cross University Hospital, London, E11 1NR.
DOI: 10.1080/01443610500150585