Maternal floor infarction leads to sudden fetal demise
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This case report describes a rare placental lesion called maternal floor infarction that resulted in sudden intrauterine fetal demise. A 29-year old pregnant woman at 39 weeks gestation with a normal pregnancy was found to have an absent fetal heart rate on routine monitoring prior to induction of labor. Ultrasound confirmed sudden intrauterine fetal demise of a male baby. Histopathological examination of the placenta found maternal floor infarction, which is characterized by heavy fibrin deposition along the basal plate that becomes avascular and sclerotic. Maternal floor infarction has a high recurrence rate of 39% in subsequent pregnancies and can develop rapidly, resulting in poor fetal outcomes.
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Maternal floor infarction leads to sudden fetal demise
- 1. Maternal floor infarction: A rare cause of sudden Intrauterine fetal demise
- 2. a p o l l o m e d i c i n e 1 0 ( 2 0 1 3 ) 2 9 7 e2 9 8 Available online at www.sciencedirect.com journal homepage: www.elsevier.com/locate/apme Case Report Maternal floor infarction: A rare cause of sudden intrauterine fetal demise Astha Agarwal a,*, Shanti Jeyaseelan b a b Registrar, Indraprastha Apollo Hospitals, New Delhi, India Head of Department, Holy Family Hospital, New Delhi, India article info abstract Article history: Introduction: Maternal floor infarction is a rare placental lesion in which large amounts of Received 14 March 2013 fibrin are deposited along the basal plate, which becomes avascular and sclerotic. The rate Accepted 22 June 2013 of fetal salvage is very poor as the lesion develops rapidly. Available online 6 July 2013 Case report: Booked G3P1L1A1 at 39 weeks gestation with obstetric history of an uneventful FTNVD followed by a first trimester MTP. In this pregnancy she had a normal antenatal Keywords: course with reactive NST in last 2 visits at 37 and 38 weeks respectively. Routine NST 8 h Maternal prior to admission was reactive. She had no complaints. Patient was admitted for elective Infarction IOL. NST reactive at the time of admission. Routine FHR monitoring by Doppler after 2 h of Placenta admission just prior to induction of labor showed absent FHR. Urgent USG done, confirmed IUFD sudden IUFD. Patient and her family counseled. IOL done. She had normal vaginal delivery Labor of fresh stillborn male baby. Liquor was normal. Baby had no gross congenital anomaly. Placenta had yellowish discoloration of a remarkably smooth maternal surface. Histopathology was compatible with maternal floor infarction. Conclusion: Placental dysfunction in maternal floor infarction appears late in the process of the disease and the lesion develops rapidly within hours. Recurrence rate is as high as 39% in subsequent pregnancies. In all cases of IUFD placenta should be sent for histopathological examination to rule out this rare cause of sudden IUFD at term. Copyright ª 2013, Indraprastha Medical Corporation Ltd. All rights reserved. 1. Introduction Maternal floor infarction is a rare placental lesion (incidence 0.09%e5%)1 in which large amounts of fibrin are found deposited along the basal plate, which becomes avascular and sclerotic. The findings are often associated with fetal demise or premature delivery. The rate of fetal salvage is very poor and the lesion may recur in subsequent pregnancies (incidence 39%).2 2. Case report We report a case of booked 29 years old G3P1L1A1 who was admitted for induction of labor at 39 weeks of gestation. Her obstetric history was a full term normal vaginal delivery of a healthy female baby at term 5 years back, followed by a first trimester MTP for missed abortion. In this pregnancy she had a normal antenatal course. All the routine ultrasound were normal. Routine NST done for * Corresponding author. E-mail address: dr_astha_agarwal@yahoo.co.in (A. Agarwal). 0976-0016/$ e see front matter Copyright ª 2013, Indraprastha Medical Corporation Ltd. All rights reserved. http://dx.doi.org/10.1016/j.apme.2013.06.001
- 3. 298 a p o l l o m e d i c i n e 1 0 ( 2 0 1 3 ) 2 9 7 e2 9 8 fetal surveillance at 37 and 38 weeks were reactive with a baseline fetal heart rate of 140 beats/min and variability of 8e10 beats/min. She was advised admission for IOL at 39 weeks. 8 h prior to admission NST done in OPD was also reactive. Routine NST on admission was reactive. 2 h after admission just prior to IOL routine fetal heart rate monitoring was done with Doppler. The fetal heart sound could not be localized and hence an urgent USG was done. Urgent USG confirmed sudden intrauterine fetal demise. Patient and her family were counseled. IOL done with cerviprime gel and the patient delivered fresh stillborn male baby weighing 3.010 kg. Liquor was clear and not foul smelling. Baby had no gross congenital anomaly. Placenta appeared to be abnormal on gross examination. There was yellowish discoloration of a remarkably smooth maternal surface. Placenta was sent for histopathological examination. Histology was compatible with maternal floor infarction of the placenta. 3. Conclusion Maternal floor infarction is a rare placental lesion of unknown etiology and is often associated with sudden intrauterine fetal demise and intrauterine growth restriction. Placental dysfunction appears late in the process of the disease and the lesion develops rapidly within hours. In all cases of sudden IUFD the obstetrician should sent the placenta for histopathological examination to rule out this rare cause of sudden IUFD. 4. The pathophysiology of the lesion remains unclear. Maternal floor infarction frequently recurs in successive pregnancies (rate 39%)2 and there is evidence that it develops rapidly.3 It is a disorder, characterized by heavy deposition of fibrin in the region of the basal villi immediately adjacent to the decidua basalis. The fibrin extends into the intervillous space where it envelops the basal villi, which becomes avascular and sclerotic. It is not an infarct and is most directly distinguished from a placental infarct by the fact that, the affected villi are widely separated by fibrin; whereas in infarcts the villi are typically crowded together. Grossly, the maternal surface of the placenta is thickened; firm and yellow.1 Given the risk of recurrence to be as high as 39%, the identification of maternal floor infarction (by either a history of sudden IUFD of unknown etiology at term or a confirmed report of maternal floor infarction in previous pregnancy) should alert the clinician to the potential for growth retardation, preterm birth and sudden intrauterine fetal demise at term in subsequent pregnancies. Hence delivery should be considered when pulmonary maturity has been established.2 Discussion Maternal floor infarction of the placenta is a relatively rare disorder that leads to sudden IUFD2 (incidence: 40%) and IUGR. Conflicts of interest All authors have none to declare. references 1. Blaustein’s Pathology of the Female Genital Tract. 5th ed. 1135. 2. Andres Robert L, Kryper William, Resnik Robert. The association of maternal floor infarction of the placenta with adverse perinatal outcome. Am J Obstet Gynecol. July 1990;163:935e958. 3. Clewell William H, Manchester David K. Recurrent maternal floor infarction e a preventive cause of fetal death. Am J Obstet Gynecol. Sept 1983;1:346.
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