Regular scans were arranged in order to monitor fetal growth and identify the development of intracranial haemorrhage. of the IIbCIIIa platelet glycoprotein within the platelet surface. This deficiency confers abnormal main haemostasis and a bleeding phenotype. Her partner was non-consaguinous and as such paternal genotyping was not performed. Her medical history included a earlier myomectomy (uterine cavity not breached), chronic hypertension and hypothyroidism. During pregnancy, she developed two obstetric issues: gestational diabetes (stable on treatment with Metformin) and intrauterine growth restriction. The patient was regularly examined from the Haematology and Maternal Medicine teams. She offered to the Emergency Division in the 1st trimester with epistaxis and haematuria. As expected with this disorder, the maternal platelet count was normal throughout pregnancy (161C254??109/L), and at booking screening for platelet-specific antibodies was bad. Screening for platelet-specific antibodies was carried out every four to six weeks, and she tested positive for anti Human being Platelet Antigen (HPA) IIbCIIIa antibodies at 29 weeks, with titres of 1 1 in 8. A multidisciplinary meeting between the Haematology, Obstetric and Anaesthetic teams was arranged for 32 weeks. It was experienced that instrumental delivery should be avoided due to the risk of NAIT and intracranial haemorrhage, and the mother was counselled concerning this risk. The safest mode of delivery for the baby was deemed to be by caesarean section due to the combination of intrauterine growth restriction and potential risk of neonatal alloimmune thrombocytopenia (NAIT); timing would be dictated by fetal growth, but a desire to early delivery was motivated, given the late complications reported in such cases. A general anaesthetic was planned due to the risk of bleeding with regional anaesthesia. A definite strategy was made for haemostasis and postpartum monitoring in the Obstetric HDU. The fetus was mentioned to be small in the anomaly scan. No structural or placental abnormalities were mentioned. Regular scans were arranged in order to monitor fetal growth and identify the development of intracranial haemorrhage. Her final scan at 35?+?3 weeks showed consistent growth, normal liquor volume and Dopplers and an estimated fetal weight of 1729?g. Delivery was arranged for 36 weeks, by elective caesarean section, and intramuscular NBMPR steroids were administered beforehand. Prior to her caesarean, HLA-matched platelets were given to reduce the risk of bleeding given the maternal poor platelet function characteristic of Glanzmann thrombasthenia. Novoseven was also given due to the presence of maternal anti-HPA antibodies, which can reduce the effectiveness of platelet transfusions. The caesarean was theoretically hard, with multiple adhesions. Estimated blood loss was 1.5 litres; she received four devices of HLA-matched platelets, a further dose of Novoseven, 487?ml of blood via cell salvage and tranexamic acid. NSAID use was avoided. She was transfused with a further unit of blood and platelets on day time 1 post-operatively. She was discharged NBMPR home on day time 7 postoperatively having a two week supply of tranexamic acid. The baby weighed 1700?g at birth, and the platelet count was 33 within the wire blood sample. This fallen to 16 on day time four of existence, and the baby received intravenous platelets and immunoglobulins, in order to reduce the immune-mediated clearance of circulating platelets. NBMPR The babys count was 40??109/L about discharge. A cranial ultrasound performed on day time 0 of existence showed no evidence of intracranial bleeding. The mother will require preconception counselling for subsequent pregnancies, as the risk of a future fetus with NAIT is definitely greater than 75%.1 In such cases, non-invasive treatment with intravenous immunoglobulins can be administered in the antenatal period. Management of subsequent pregnancies should be multidisciplinary, between Haematology, Fetal and Maternal Medicine teams, and she will require regular monitoring of IIbCIIIa antibodies. Literature review Glanzmann thrombasthenia is an autosomal recessive haemorrhagic disorder, 1st explained in 1918. It has IMPG1 antibody an estimated prevalence of less than 1 in 1,000,000 and predominates among particular ethnic groups, such as Southern Indians, as with our patient.2 It is.