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Maternal flo 
or infarct 
intrauteri 
i 
tion: A ra 
ine fetal d 
are cause 
demise 
of sudden
a pol 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 Registrar, Indraprastha Apollo Hospitals, New Delhi, India 
b Head of Department, Holy Family Hospital, New Delhi, India 
a r t i c l e i n f o 
Article history: 
Received 14 March 2013 
Accepted 22 June 2013 
Available online 6 July 2013 
Keywords: 
Maternal 
Infarction 
Placenta 
IUFD 
Labor 
a b s t r a c t 
Introduction: Maternal floor infarction is a rare placental lesion in which large amounts of 
fibrin are deposited along the basal plate, which becomes avascular and sclerotic. The rate 
of fetal salvage is very poor as the lesion develops rapidly. 
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 
course with reactive NST in last 2 visits at 37 and 38 weeks respectively. Routine NST 8 h 
prior to admission was reactive. She had no complaints. Patient was admitted for elective 
IOL. NST reactive at the time of admission. Routine FHR monitoring by Doppler after 2 h of 
admission just prior to induction of labor showed absent FHR. Urgent USG done, confirmed 
sudden IUFD. Patient and her family counseled. IOL done. She had normal vaginal delivery 
of fresh stillborn male baby. Liquor was normal. Baby had no gross congenital anomaly. 
Placenta had yellowish discoloration of a remarkably smooth maternal surface. Histopa-thology 
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 histopatho-logical 
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 (inci-dence 
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
298 a p o l l o me 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 cervi-prime 
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. His-tology 
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 histopath-ological 
examination to rule out this rare cause of sudden 
IUFD. 
4. Discussion 
Maternal floor infarction of the placenta is a relatively rare 
disorder that leads to sudden IUFD2 (incidence: 40%) and IUGR. 
Thepathophysiologyofthe lesionremainsunclear.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 distin-guished 
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 un-known 
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 sud-den 
intrauterine fetal demise at term in subsequent preg-nancies. 
Hence delivery should be considered when 
pulmonary maturity has been established.2 
Conflicts of interest 
All authors have none to declare. 
r e f e r e n c e s 
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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Maternal floor infarction: A rare cause of sudden intrauterine fetal demise

  • 1. Maternal flo or infarct intrauteri i tion: A ra ine fetal d are cause demise of sudden
  • 2. a pol 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 Registrar, Indraprastha Apollo Hospitals, New Delhi, India b Head of Department, Holy Family Hospital, New Delhi, India a r t i c l e i n f o Article history: Received 14 March 2013 Accepted 22 June 2013 Available online 6 July 2013 Keywords: Maternal Infarction Placenta IUFD Labor a b s t r a c t Introduction: Maternal floor infarction is a rare placental lesion in which large amounts of fibrin are deposited along the basal plate, which becomes avascular and sclerotic. The rate of fetal salvage is very poor as the lesion develops rapidly. 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 course with reactive NST in last 2 visits at 37 and 38 weeks respectively. Routine NST 8 h prior to admission was reactive. She had no complaints. Patient was admitted for elective IOL. NST reactive at the time of admission. Routine FHR monitoring by Doppler after 2 h of admission just prior to induction of labor showed absent FHR. Urgent USG done, confirmed sudden IUFD. Patient and her family counseled. IOL done. She had normal vaginal delivery of fresh stillborn male baby. Liquor was normal. Baby had no gross congenital anomaly. Placenta had yellowish discoloration of a remarkably smooth maternal surface. Histopa-thology 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 histopatho-logical 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 (inci-dence 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 me 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 cervi-prime 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. His-tology 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 histopath-ological examination to rule out this rare cause of sudden IUFD. 4. Discussion Maternal floor infarction of the placenta is a relatively rare disorder that leads to sudden IUFD2 (incidence: 40%) and IUGR. Thepathophysiologyofthe lesionremainsunclear.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 distin-guished 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 un-known 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 sud-den intrauterine fetal demise at term in subsequent preg-nancies. Hence delivery should be considered when pulmonary maturity has been established.2 Conflicts of interest All authors have none to declare. r e f e r e n c e s 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.
  • 4. Apollo hospitals: http://www.apollohospitals.com/ Twitter: https://twitter.com/HospitalsApollo Youtube: http://www.youtube.com/apollohospitalsindia Facebook: http://www.facebook.com/TheApolloHospitals Slideshare: http://www.slideshare.net/Apollo_Hospitals Linkedin: http://www.linkedin.com/company/apollo-hospitals BBlloogg:: http://www.letstalkhealth.in/