Author
Information
Parekh
NA*, Agrawal A**, Badade A***, Satoskar P****.
(* Assistant Professor, *** Honorary
Ultrasonologist, Nowrosjee Wadia Maternity Hospital; ** Senior Resident, **** Professor Department of Obstetrics and Gynecology, Seth GS Medical College &, Nowrosjee
Wadia Maternity Hospital, Mumbai, India.)
Abstract
We present a case of an
incidental intraplacental hematoma that was discovered when the placenta was
examined post-delivery in order to identify the cause of a non-immune hydrops.
Introduction
Hydrops fetalis is
defined as the presence of excessive fluid accumulation in at least two fetal
body cavities. Two major groups can
be differentiated: immune and nonimmune hydrops fetalis. Nonimmune hydrops fetalis occurs in 1 in 1500- 4000 pregnancies.With the routine
immunization of Rh negative pregnancies, the percentage of immune hydrops has
significantly decreased. Presently about 80% of cases of hydrops are due to
nonimmune causes.
Case
Report
A 32 year old
Primigravida with spontaneous conception was referred at 31 weeks of gestation
with ultrasonography report suggestive of fetal hydrops [figure 1]. She did not
have any complaints in this pregnancy. On examination, she weighed 100 kg with
an abdominal girth of 126 cm. She was normotensive. She had an overdistended
uterus, abdominal wall edema and oozing pedal edema. Fetal heart rate was
140/min. USG showed generalized fetal edema with no malformations and placental
thickness of 8 cm. Amniotic fluid index was 35 cm with estimated fetal weight
of 2.029 kg. Color Doppler showed increased middle cerebral artery peak
systolic velocity (MCA PSV) of 57 cm/sec, >1.5 MoM. Fetal echocardiography
showed a thin rim of pericardial effusion with no structural abnormalities.
Figure 1. Figure 1. USG
suggestive of generalized fetal anasarca- skin edema, ascites with polyhydramnios.
The patient’s blood
group was AB positive and the indirect Coomb’s test negative. VDRL and, serology
for toxoplasmosis, parvovirus B19 and cytomegalovirus were negative. Her glucose tolerance test with 75 g glucose values were 89/150/137 mg/dl. Hepatic viral markers were negative. SGOT (66 IU/ml), SGPT (85
IU/ml), Serum Creatinine (1.2 mg/dl) and serum uric acid (9.3 mg/dl) were
elevated. Her hemoglobin was 12.2 g/dL, white blood cell and platelet count, and serum electrolytes were normal normal. Urine culture did not show any growth. The patient was given steroids
for fetal lung maturation and 3 doses of vitamin K (10 mg).
Fetal anemia with
non-immune hydrops with maternal mirror syndrome was diagnosed. Fetal
transfusion was planned. On cordocentesis fetal hemoglobin was low (10 g/dL).
60 ml of double packed O Negative blood was transfused. On repeat Doppler MCA
PSV declined to 40 cm/sec. Cord blood sample testing revealed normal fetal
karyotype and was negative for thalassemia.
The patient continued to
have severe polyhydramnios with severe discomfort. Hence USG guided
amnioreduction was done (1.1 L drained). At 32 weeks, the patient had preterm
premature rupture of membranes with footling presentation. Emergency cesarean
delivery was performed. At delivery, female baby weighed 2.5 kg and had an
Apgar score 2/10 at 1 minute and 5/10 at 5 minutes The baby was immediately
intubated and ventilated in neonatal intensive care unit. During cesarean
delivery, significant maternal atrial ectopic beats were noted. For hyperkalemia
(6.2 mEq/l) neutral human insulin in dextrose and diuretics were given, which
corrected it within 2 days. The baby had generalized edema and abdominal distension.
Pleural effusion had resolved. She was ventilated and started on diuretics and inotropes.
Hemoglobin at birth was 13 g/dL. Gradually the baby was weaned off from ventilator.
No exchange transfusion was required.
The placenta weighed 1.2
kg and had a diameter of 21 cm. It was congested with pale areas and thickened
membranes. There was no hematoma on gross examination. Microscopy showed mild deciduitis, intervillous fibrin, marked
intervillous hemorrhage and intraplacental hematoma with infarcts (figure 2).
Figure 2. Histopathological
slide showing intraplacental hematoma.
Healthy mother with
healthy baby were discharged on day 15 of delivery; on discharge the baby
weighed 1.7 kg.
Discussion
Hydrops fetalis is
defined as the presence of excessive fluid accumulation in at least two fetal
body cavities; including ascites, pleural effusion, pericardial effusion, and skin edema; often associated with polyhydramnios and placental edema.
Ascites is the most common finding on ultrasonography.[1] Normal mechanism for the distribution of interstitial
fluid is through lymphatic return. Imbalance in this basic mechanism is
postulated as the cause of fetal hydrops. The causes of non-immune hydrops can
be grouped in broad categories like cardiovascular
(21.7%), chromosomal (13.4%), hematologic (10.4%), infections (6.7%), placental
(5.6%), syndromic, skeletal conditions, lymphatic dysplasia, inborn errors of
metabolism, thoracic, urinary tract malformations, extra-thoracic tumors, gastrointestinal
causes, Prune belly syndrome, CNS anomalies, infant of diabetic mother, feto-maternal
hemorrhage and twin-twin transfusion (donor).[2] In fetal anemia the
peak systolic velocity of the middle cerebral artery on color Doppler exceeds 1.5
MoM. Early diagnosis is important because prompt intrauterine transfusion is
highly effective and long term outcome is unimpaired in these babies. Parvovirus
infection and fetomaternal hemorrhage are self-limited causes of fetal anemia. Intra-placental hematoma is an indicator of feto-maternal hemorrhage (FMH). FMH can begin anytime from the mid-first trimester onward. It is presumed to result from a breach in the integrity of the placental circulation. The cause of FMH is unknown in 82% of cases. In most spontaneous FMH cases, microscopic areas of placental capillary damage may result from third-trimester uterine activity. Hydrops fetalis is associated with severe FMH. Diagnosis of fetomaternal
hemorrhage could have been made by Kleihauer-Betke Test in the case presented.
Disruptions of the fetomaternal circulation may be spontaneous or related to
tumors (choriocarcinoma, chorioangioma), trauma, or partial placental abruption.
The perinatal mortality rate of non-immune hydrops is high, treatment options
are limited and thus the need for precise diagnosis. Establishing the cause is
also helpful in treating the infant at birth. If prenatally diagnosed, mother
should be referred to a high-risk center with a good neonatal intensive care
unit for further management and multidisciplinary counseling.[3,4] Aggressive
management of fetal anemia in non-immune hydrops is associated with an
excellent prognosis for baby. Resuscitation of hydrops fetalis poses difficulties.
Amniotic fluid and/or fetal cells for future genetic testing, as well as
autopsy in case of fetal/ neonatal death, should be offered.
References
- Lin SM, Wang CH, Zhu XY, Li SL, Lin SM, Fang Q. [Clinical study on 156 cases with hydropsfetalis].Zhonghua Fu Chan KeZaZhi. Dec 2011; 46(12):905-10.
- Bellini C, Hennekam RC. Non-immune hydropsfetalis: a short review of etiology and pathophysiology. Am J Med Genet A. Mar 2012; 158A(3):597-605.
- Désilets V, Audibert F. Investigation and management of non-immune fetal hydrops. J ObstetGynaecol Can. Oct 2013; 35(10):923-38.
- [Guideline] Leduc L, Farine D, Armson BA, et al. Stillbirth and bereavement: guidelines for stillbirth investigation. J ObstetGynaecol Can. Jun 2006;28(6):540-52.
Citation
Parekh
NA, Agrawal A, Badade A, Satoskar P. Intraplacental Hematoma: A Rare Cause Of
Non-Immune Hydrops. JPGO 2015. Volume 2 No. 3. Available from: http://www.jpgo.org/2015/03/intraplacental-hematoma-rare-cause-of.html