Intraplacental Hematoma: A Rare Cause Of Non-Immune Hydrops

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

1. 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.
2. 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.
3. Désilets V, Audibert F. Investigation and management of non-immune fetal hydrops. J ObstetGynaecol Can. Oct 2013; 35(10):923-38.
4. [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