A 33-year-old woman, immunocompetent, gravida 2, para 1 (natural birth), with a followed-up pregnancy (five regular prenatal check-ups) of 22 weeks of gestation, consulted for intermittent contractions inappropriate for the gestational age, with 4 days of duration. She had also experienced an episode of fluid loss that lasted 3 h. At physical examination active foetal movements and normal foetal heartbeat values were observed. Other parameters evaluated did not evidence alterations in the evolution of pregnancy, including negative uterine dynamics, closed internal cervical os, negative amenorrhoea and negative genitorrhagia both at rest and valsalva. Stable vital signs were observed with normal levels of blood pressure. On superficial and deep palpation of the abdomen, it was soft, depressible and not painful with normal air-fluid noises and without resistance or peritoneal reaction. Ultrasound monitoring showed the presence of hydrops fetalis with foetal ascites and oedema of the subcutaneous cellular tissue (SCT), although amniotic fluid index (AFI) was within normal values (AFI 13). Immunological, cardiac and chromosomal causes were discarded, as well as other possible infectious causes, including Epstein Barr virus, Cytomegalovirus, syphilis and toxoplasmosis. Serological determination of anti-B19V IgM resulted positive in maternal serum, confirming an acute infection by this agent.
The following day, a Doppler ultrasonography revealed foetal anaemia (Doppler of the middle cerebral artery: 78 cm sec-1, representing 2.4 multiples of the median) and generalized hydrops, with pleural and pericardial effusion, oedema of the SCT>6 mm, and foetal heart failure. Placenta and amniotic fluid both appeared normal. Foetal haemoglobin (fHb) determined from umbilical cord blood evidenced severe anaemia (3 g dl-1).
In the next day, intrauterine blood transfusion was performed by channelling the umbilical cord at the level of the placental insertion. Foetal parameters at this time were: weight 530 g, blood type group A Rh positive, haemoglobin 1.6 g dl-1, haematocrit 4.7 %, erythrocyte sedimentation rate 134. Twenty-three cubic centimetres of inactivated, leukocyte-free blood, type 0 Rh negative, were transfused. After treatment, good tolerance was observed together with incipient recovery of fHb levels and haematocrit. Post-transfusion control showed fHb 6.3 g dl-1, haematocrit 18.7 %. The patient evolved without post-cordocentesis complications.
A second transfusion was scheduled 48 h after the first intervention, transfunding 23 cc of inactivated, leukocyte-free blood, type 0 Rh negative. During this procedure foetal bradycardia was observed and pericardial effusion occurred. Puncture was performed draining 4 cc of fluid. However, bradycardia persisted followed by foetal death. The mother evolved without post-cordocentesis complications. After labour induction, expulsion of the dead foetus occurred within 48 h, and the patient was subsequently discharged.
Two weeks later, a blood sample was taken from the patient for further serological studies. At this time, anti-B19V IgM was negative, while anti-B19V IgG was positive, as well as B19V DNA by end-point PCR. Furthermore, viral DNA remained detectable in two subsequent determinations in serum samples obtained at intervals of 6 months, totalling a detection period of 12 months since the diagnosis. In the next serum sample, after 18 months of foetal death, no viral DNA was detected. Viral loads were determined, remaining at the limit of detection while DNA was positive (Table 1). According to the registry in the clinical history, the patient remained asymptomatic throughout the gestation period prior to the episode of the consultation due to contractions. When revising the medical records, no classical signs of suspicion of B19V infection were noted -such as fever, rash, anaemia, or arthropathies. The only epidemiological risk factor was the presence of a school age-child at home (her son); there were no other remarkable risks of exposure to B19V infection (occupational, social or drug history).
Taking into account the previous data, we can hypothesize a possible course of the infection in this case as shown in Fig. 1.