The patient had a history of meningitis at 3 years, curettage due to molar pregnancy (G1P0A1) in her first pregnancy in 2005, and smoker at 10-20 years.
No previous transfusion history.
Ultrasound performed at 35 weeks of gestation revealed bilateral fetal hydrocephalia and oligohydramnios. A cesarean section was scheduled at 36 weeks.
In the previous analytical study a positive serology (IgM) for Parvovirus B19 was highlighted.
Examination of the newborn after cesarean section revealed a good general condition, with an Apgar test of 8 and 9 points in the 1st and 5th minute, respectively, small hematomas in the left shoulder and gluephalia.
A severe bulletitis (9 x 109/L) was found in the blood count.
After a long-term clinical suspicion of TFNA, an aliquot of apheresis was maintained irradiated with apheresis platelets of unknown HPA-1a phenotype, and treatment with intravenous immunoglobulins (IGIV) was initiated.
The patient was referred to the Hematology Transfusion Center of Nava, as well as the search for platelets from a negative HPA-1a donor.
Cerebral ultrasound showed severe hydrocephalia secondary to intraventricular hemorrhage, requiring the placement of an external derivation catheter through which cerebrospinal fluid was hemorrhagic pressure.
The patient presented a subsequent torpid evolution, with ventriculomegaly and seizures, requiring treatment with antibiotics and phenobarbital, respectively, and implantation of a ventricular-peritoneal shunt.
During admission, a leukocyte depleted and irradiated aliquot was transfused.
The immunologic study performed on newborns in the Blood Transfusion Center of Navarre confirmed the maternal and positive HPA-1a phenotype, as well as the presence of antibodies with anti-HPA-1 specificity.
