Breus` mole occurs rarely, in approximately 1:1200 placentas. The author here describes a case of 38 years old diabetic and hypertensive lady who was gravida 4, parity 2, living 2, abortion 1, and presented at 26 weeks to antenatal outpatient department. On Ultrasound she was found to have a Breus` mole with Symmetrical Intrauterine Growth Retardation. She was managed conservatively with increased fetal surveillance, regular Doppler velocimetry, and medical management for her hypertension and diabetes mellitus.Her pregnancy was terminated at 33 weeks by an emergency Cesarean section in view of regular uterine contractions and oligoamnios due to Preterm Premature Rupture Of Membranes(PPROM). The 1.38 kg baby girl was discharged in good condition after 10days of Neonatal intensive care unit care. Thus a Breus` mole can lead to Intrauterine Growth Retardation and should be looked for, especially in the presence of high risk factors like hypertension, diabetes mellitus.
A 38-year-old lady, gravida 4, parity 2, living 2, abortion 1, presented for antenatal care at 26 weeks’ gestation. She was hypertensive and diabetic since the past 2 years. She was overweight, body mass index of 30, a nonsmoker with blood group A and Rh type positive with no atypical antibodies. She had family history of hypertension , diabetes mellitus and pre-eclampsia in her ﬁrst degree relatives. She had two full term normal vaginal deliveries 10 and 6 years ago and one medical abortion 2 years ago in view of her uncontrolled diabetes mellitus. She was on regular human insulin(rHI) since then and her blood sugar levels (BSL) were well controlled with the present insulin administration.At 26 weeks she had edema feet, blood pressure(BP) of 140/90 mm Hg and trace urine albumin.
Ultrasound revealed symmetrically growth retarded fetus equivalent to 21 weeks at 26 weeks’ gestation with estimated fetal weight(EFW) of 402 gms + 42 gms. It also revealed the presence of hypoechoic protuberaces on fetal surface of the placenta, with no vascularity, suggestive of old subchorionic hematomas (SH).(Fig 1a,b,c,d). The placenta was thick (more than 5cm) and located posteriorly with no retroplacental hematoma or collection. These SH were spread mainly along the upper and lower fetal surface of the placenta and also reached upto umbilical cord insertion at the lower end of placenta. The fetus showed no gross congenital anomalies. At 26 weeks, on Doppler ultrasound, she had bilateral uterine artery notching, and a fortnightly ultrasound scan for fetal growth assessment was recommended. At 28 weeks, there was persistence of the notching of both uterine arteries.
She was admitted to hospital and strict BP and BSL surveillance was done. She was monitored for premonitory symptoms of eclampsia like headache, vomiting, blurring of vision and for symptoms of hyperglycemia or hypoglycaemia like sudden palpitations, excessive sweating, giddiness. Despite administration of antihypertensives like alphamethyldopa 250 mg four times daily, at 30 weeks, the diastolic BP increased to 150/100 mmHg with mild proteinuria but biochemical proﬁle was normal.
However, her BSL was well controlled by titration with rHI. Nifedipine (5mg ) four times daily was added to alphamethyldopa and weekly Doppler studies conducted. 2 doses of intramuscular betamethasone were administered 24 hrs apart to accelerate fetal pulmonary maturity.At 32 weeks, she had persistently raised diastolic BP of above 100 mmHg and proteinuria 2+. At 33 weeks, she developed PPROM followed by regular uterine contractions. Doppler study reported absent diastolic ﬂow in Umbilical artery (Fig 2) and severe oligoamnios (AFI = 4 cm ), EFW of 1400 + 317 gms. At 33 weeks, the diastolic BP remained above 110 mmHg with premonitory symptoms of vomiting and headache, increasing uric acid levels, proteinuria. In view of the fetoplacental insufficiency and severe oligoamnios, a decision of emergency caesarean section under spinal anaesthesia was taken.
rHI was withheld, senior paediatricians on call were summoned and vacancy in Neonatal Intensive Care Unit (NICU) confirmed. A live female baby was born with Apgar scores of 7 at 1 min and 9 at 5 min, weighing 1,380 g.The placenta weighed 420 gms. Macroscopically, the placenta showed scattered areas of old hematomas on the fetal surface,some measuring up to 5 x 4 cm, and containing yellowish ﬂuid., more towards the lower and upper end of placenta.(Fig 3). There were few areas of calcification on maternal surface of placenta. Histopathological examination of the placenta revealed extensive fibrin deposition in subchorionic space with old hemorrhage.
Thus, macroscopically and microscopically diagnosis of Breus` mole was confirmed.It had compressed the umbilical cord causing fetoplacental insufficiency. Baby was transferred to the NICU where she received expert care and showed rapid improvement.The mother was transferred to the postoperative ward and antihypertensives were continued.Her diastolic blood pressure decreased to 90 mm Hg on day 2 and then became normal by day 5. Her BSL was checked regularly and decreasing doses of rHI were required to maintain satisfactory BSL.The postoperative period was uneventful and she was discharged on the postoperative day 10 along with her baby.
Since the first description of a subchorionic tuberous hematoma by Karl Breus` in 1892 in five cases of missed abortion, its etiology and pathogenesis remained a dilemma in the 18th and early 19th century. (1,2) .The term Breus` “Mole” does not actually mean molar degeneration as seen in hydatiform moles,but is related to “mass” or coagulated blood.(1) Breus` mole is a condition in which maternal blood collects and separates the chorionic plate from the villous chorion .
(2) Breus`postulated that after embryonic death , membranous growth continues which later gets filled up with hemorrhage forming the hematoma, thus concluding fetal death to be the primary factor and hematoma development as secondary. (1,3) But in the later years, after further studies, many authors contradicted Breus` postulation, most prominent among which was a report by Shanklin and Scott who studied ten placenta of 25 weeks and beyond and had seven liveborn infants, thus disapproving of the fact that fetal death is a primary event in formation of Breus` mole. Their incidence was 1:1200 placentas.(1,4) .
Despite various studies no unified etiology has emerged for development of Breus mole, however it may occur in mothers with various medical problems including disorders of circulation, complex heart disease, monosomyX (45XO -Turner syndrome),hypertension, diabetes and anticoagulation therapy, maternal thrombophilia.(1,4,5,6) Baxi and Pearlstone suggested that presence of autoantibodies increases the tendency of platelet aggregation leading to thrombosis and/ or vasculitis causing Subchorionic thrombohematoma.(2,7).
Breus` mole has been pathologically described as cystic degeneration of subchorionic intervillous thrombi.(2) There is regular formation of laminated thrombi in small quantities in the subchorionic space causing backward flow of intervillous (maternal ) blood.This eddying of intervillous blood causes small amounts of fibrin deposition in subchorionic space which is seen as white patches or as bosellations on the fetal surface of placenta.(2,8) When such large patches of subchorionic coagulation contract, fluid may be extruded from them thus forming cysts which contain old clotted blood.(2,8)A Breus mole (coagulated mass) may be large enough to cause protuberance from fetal surface of placenta and be detected by prenatal ultrasound.(8,9) .
Their significance depends not on their size, but on their site of appearance. For eg: if near cord insertion they may lead to cord compression and decreased fetal perfusion , fetoplacental insufficiency as discussed in one of the cases by Kirkinen & Jouppila where hematoma dissected into base of the umbilical cord causing umbilical venous obstruction and furcate cord insertion. (8,9) Also a massive subchorionic thrombohematoma may lead to Oligohydarmnios and Intrauterine Growth retardation as described in their case report by Naoko Nishida.(2) Thus the indepth knowledge on the pathogenesis of Breus mole concluded to its histopathological fibrinoid nature and its clinical significance of probability of causing Intrauterine growth retardation and oligoamnios.
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Springer; 2000 .
2.Naoko Nishida, Shunji Suzuki,Yukie Hamamura,Kenji Higarashi ,Zuisei
Hayashi,Rintaro Sawa, Yoshio Yoneyama,Hirobumi Asakura,Ken Kawabata,Yoshi
Shima,Sumio Shin,Tsutomu Araki:Massive Subchorionic Hematoma(Breus`mole)
complicated by Intrauterine Growth Retardation. JNipponMed Sch 2001: 68.
3. James Blake Thomas: Breus` Mole.Obstetrics & Gynecology 1964;24:794-97
4. Shanklin DR, Scott JS:Massive subchorial thrombohaematoma (Breus' mole). . Br J Obstet Gynaecol. 1975 Jun;82(6):476-87.
5. A.E.Madu: Breus’ mole in pregnancy.Journal of Obstetrics and Gynecology
6. Usta, Ihab M., Abdallah, Mazen , El-Hajj, Nassar, Anwar H: Massive
Subchorionic Hematomas Following Thrombolytic Therapy in Pregnancy.
Obstetrics & Gynecology 2004; 5:1079-82
7. Baxi LV, Pearlstone MM:Subchorionic hematomas and the presence of
autoantibodies.Am J Obstet Gynecol 1991 ;165 :1423-24.
8. Ona Marie Faye-Petersen, Debra S. Heller,Vijay V. Joshi. Handbook Of Placental
Pathology.2nd ed.United Kingdom: Taylor and Francis Group; 2006
9. P. Jouppila, P. Kirkinen, R. Puukka : Correlation between umbilical vein blood
flow and umbilical blood viscosity in normal and complicated pregnancies.
Archives of Gynecology and Obstetrics 1986 ;237
Fig 1a- Subchorionic hematoma at the upper end of placenta appearing as
protuberances on fetal surface of placenta.
Fig 1b- Large Subchorionic hematoma (4.7 x 3.1 cm) at the lower end of placenta .
Fig 1c – Colour doppler showing absent vascularity in the hypoechoic collections
on fetal surface of placenta thus excluding placental lakes .
Fig 1d- Thick posteriorly located placenta.
Fig 2 – Absent diastolic flow in umbilical artery seen on Doppler ultrasound at 33
Fig 3- Gross appearance of placenta showing areas of old hematomas on the fetal
surface,some measuring up to 5 x 4 cm, and containing yellowish ﬂuid., more
towards the lower and upper end of placenta
Dr. Baldawa Pratibha S
M.S(Obgyn),D.N.B, D.G.O,F.C.P.S,D.F.P, Assistant Professor .
Correspondence address :
Baldawa Hospital, Budhwar Peth, Near Kasturba Market, Solapur – 413002,
Phone: (+91) 217- 2324762 (home), (+91) 9745306852 [Mobile].
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