|Year : 2016 | Volume
| Issue : 2 | Page : 126-128
Resolution of isolated large fetal pericardial effusion after delivery
Amar M Taksande, Rewat Meshram, Khusboo Bhatia, Amol Lohakare
Department of Pediatrics, Jawaharlal Nehru Medical College, Sawangi Meghe, Wardha, Maharashtra, India
|Date of Web Publication||14-Apr-2016|
Amar M Taksande
Department of Pediatrics, Jawaharlal Nehru Medical College, Sawangi Meghe, Wardha - 442 102, Maharashtra
Source of Support: None, Conflict of Interest: None
Pericardial effusion (PE) is detectable during routine obstetric ultrasonography. PE is the result of the same mechanism that produces fetal hydrops. Structural cardiac malformations and fetal cardiac arrhythmias are the most common cause of nonimmune hydrops. A male infant weighing 2300 g was born by through elective cesarean section. Isolated large PE was detected in a fetus at 34 weeks of gestation. The women delivered a male neonate at 37 weeks period of gestation through elective cesarean section. Baby cried immediately after birth with APGAR score 7, 9, 10 at 1, 5, and 10 min, respectively. Though the mother condition was stable. The baby was shifted to special care neonatal unit in view of for respiratory distress and severe grunt. Neonatal echocardiography showed trivial tricuspid regurgitation with no PE. Most fetal PEs resolve and fetuses with isolated PEs have a good prognosis.
Keywords: Fetal, fetal echocardiograph, pericardial effusion, pericardial fluid
|How to cite this article:|
Taksande AM, Meshram R, Bhatia K, Lohakare A. Resolution of isolated large fetal pericardial effusion after delivery. Int J Health Allied Sci 2016;5:126-8
|How to cite this URL:|
Taksande AM, Meshram R, Bhatia K, Lohakare A. Resolution of isolated large fetal pericardial effusion after delivery. Int J Health Allied Sci [serial online] 2016 [cited 2019 Sep 20];5:126-8. Available from: http://www.ijhas.in/text.asp?2016/5/2/126/180423
| Introduction|| |
Fetal pericardial effusions (PEs) refer to the accumulation of pericardial fluid in utero. Pericardial fluid thickness >2 mm is considered as abnormal., PE is the result of the mechanism that produces fetal hydrops. Structural cardiac malformations and fetal cardiac arrhythmias are the most common causes of nonimmune hydrops.,, Other conditions associated with nonimmune fetal hydrops include genetic disorders, metabolic disorders, pericardial teratoma, hematologic abnormalities, and congenital infections. We report a case of fetal PEs and developed respiratory distress soon after birth with sudden remission of PE.
| Case Report|| |
A 25-year second gravida was referred for routine screening ultrasonography for advanced maternal age was detected to have fetal PE on an obstetric ultrasound done at 34 weeks gestation. Her prior pregnancy was uneventful. No H/O pregnancy induced hypertension, no H/O gestational diabetes mellitus, exanthematous fever or jaundice. The mother's blood group was B Rh positive. A fetal echocardiogram revealed large PE but no structural heart disease. The fetal heart rate was sinus 150 beats/min. Cardiac anatomy, flow velocities, and cardiac rhythm were normal. Planned early delivery and postnatal management explaining the risk and benefits to the patient relatives.
The women delivered a male neonate at 37 weeks period of gestation through elective cesarean section. The birth weight was 2300 g, head circumference 33 cm and total body length 48 cm. Baby cried immediately after birth with APGAR score 7, 9, 10 at 1, 5, and 10 min, respectively. The baby was shifted to special care neonatal unit in view of for respiratory distress and severe grunt. He had a respiratory rate of 82/min with intercostal and subcostal retractions. Peripheral pulses were weak, and heart sounds were normal. There was no murmur. There were no obvious congenital anomalies or syndromic facies. Evaluation for sepsis was performed, and antibiotics started.
At 4 h of life, the baby was intubated and put on ventilator (pressure control mode). Antibiotics and inotropes (dopamine and dobutamine) were started. Chest radiograph showed haziness of lung field and electrocardiography was normal. Echocardiography done at 6 h of age of life showed trivial tricuspid regurgitation with no PE. There was no structural heart disease with normal biventricular ventricular function. Septic screen was positive and C-reactive protein was raised. Blood culture was suggestive of Pseudomonas. Neonate did not respond to the antibiotics. On the 8th day of life, there was a profound shock not responding to inotropic agents. The neonate succumbed in spite of aggressive resuscitation due to septicemia.
| Discussion|| |
PE is the accumulation of fluid in the pericardial space and considered as a marker of many other anomalies, eventually leading to fetal hydrops. The incidence of true PE is unknown., It may be the result of the mechanism that produces nonimmune fetal hydrops in a large number of cases, thus presenting with ascites, pleural effusion, or skin edema. In previous years, most cases of hydrops were caused by severe erythroblastosis fetalis secondary to Rh isoimmunization. Most cases of hydrops fetalis are now caused by other conditions and are known as nonimmune hydrops. Structural cardiac malformations and arrhythmias are the most common cause while other conditions associated with fetal hydrops include genetic disorders, metabolic disorders, tumors, hematologic abnormalities, and congenital infections. PE is also associated with other congenital structural abnormalities such as diaphragmatic hernia/eventration, abdominal wall defects, and also with congenital hypothyroidism  and maternal systemic lupus erythematosus, very likely related to a heart failure due to primary myocarditis or anemia. Pericardial fluid 2 mm or greater in thickness may be associated with structural anomalies or hydrops, but its clinical significance in the absence of these associated findings has not been evaluated.,
The most commonly used investigation to diagnose and evaluate fetal PE is an echocardiogram. Large PE may be drained through. Di Salvo et al. concluded that in the absence of other sonographic abnormalities, the finding of a fetal pericardial fluid collection 2-7 mm in thickness is not associated with adverse outcome. Slesnick et al. reported that large PEs are associated with a greater likelihood of structural heart disease, impaired cardiac function, and chromosomal abnormalities, and PEs with hydrops or extracardiac malformations are associated with death. Most fetal PEs resolve and fetuses with isolated PEs have a very good prognosis. If the complete diagnostic workup assessment is negative, the PE is classified as isolated. In such cases, the pathogenic mechanism is not well understood since most of the times the PE is transitional finding as in trisomy 21 fetuses and regresses spontaneously.,, The seriousness of the condition depends on the primary cause and size of the effusion and whether it can be treated effectively. Our patient was diagnosed to have fetal PE without any underlying heart defect, which was disappeared after birth.
The outlook of a fetus with PE mainly depends on the underlying cause and the association with hydrops. Isolated PE does not appear to be associated with an adverse perinatal outcome, and spontaneous resolution is a common finding. In the presence of hydrops, prenatal therapy with pericardiocentesis may be needed to avoid extreme prematurity and to improve survival. The main aim in the management of a fetus with PE is to delay the delivery until adequate lung maturity is achieved. Therefore, assessing the risk of hydrops with close monitoring of the fetal hemodynamics is mandatory. If the PE is associated with other disorders, some situations will need a prenatal therapeutic approach, such as serial intrauterine transfusions in fetal anemia or antiarrhythmic drug administration, which may be life-saving. In cases of PE with hydrops and/or cardiac tamponade, pericardiocentesis may be life-saving.,,, Postnatally, the majority of the disorders associated with PE have to be treated after an assisted delivery. Intensive care of the neonate including the use of inotropes, diuretics, vasodilators, assisted ventilation, prostaglandins, and other measures, as pericardiocentesis and surgery, may be necessary.
| Conclusion|| |
This case report has highlighted a large fetal PE had spontaneous resolution after the birth of the neonate. PE is a manifestation of a chromosomal or a genetic disease. Therefore, a complete diagnostic work-up is mandatory comprising fetal ultrasonography, Doppler fetal echocardiography, amniocentesis, and when necessary cord sampling and pericardiocentesis.
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Conflicts of interest
There are no conflicts of interest.
| References|| |
Shenker L, Reed KL, Anderson CF, Kern W. Fetal pericardial effusion. Am J Obstet Gynecol 1989;160:1505-7.
Di Salvo DN, Brown DL, Doubilet PM, Benson CB, Frates MC. Clinical significance of isolated fetal pericardial effusion. J Ultrasound Med 1994;13:291-3.
Jauniaux E, Van Maldergem L, De Munter C, Moscoso G, Gillerot Y. Nonimmune hydrops fetalis associated with genetic abnormalities. Obstet Gynecol 1990;75:568-72.
Santolaya J, Alley D, Jaffe R, Warsof SL. Antenatal classification of hydrops fetalis. Obstet Gynecol 1992;79:256-9.
Steiner RD. Hydrops fetalis: Role of the geneticist. Semin Perinatol 1995;19:516-24.
Sagristà-Sauleda J, Angel J, Permanyer-Miralda G, Soler-Soler J. Long-term follow-up of idiopathic chronic pericardial effusion. N Engl J Med 1999;341:2054-9.
Dizon-Townson DS, Dildy GA, Clark SL. A prospective evaluation of fetal pericardial fluid in 506 second-trimester low-risk pregnancies. Obstet Gynecol 1997;90:958-61.
Stevens RL, Mathers A, Hollman AS, MacKenzie JR, Galea P, Macdonald PD, et al.
An unusual hernia: Congenital pericardial effusion associated with liver herniation into the pericardial sac. Pediatr Radiol 1996;26:791-3.
Daftary AS, Patole SK, Whitehall JS. Association of pericardial effusion with gastroschisis. Intensive Care Med 1999;25:422-3.
Rondanini GF, de Panizza G, Bollati A, Manzoni P, Terenghi A, Mutinelli MR, et al.
Congenital hypothyroidism and pericardial effusion. Horm Res 1991;35:41-4.
Fox R, Hawkins DF. Fetal-pericardial effusion in association with congenital heart block and maternal systemic lupus erythematosus. Case report. Br J Obstet Gynaecol 1990;97:638-40.
Slesnick TC, Ayres NA, Altman CA, Bezold LI, Eidem BW, Fraley JK, et al.
Characteristics and outcomes of fetuses with pericardial effusions. Am J Cardiol 2005;96:599-601.
Kyeong KS, Won HS, Lee MY, Shim JY, Lee PR, Kim A. Clinical outcomes of prenatally diagnosed cases of isolated and nonisolated pericardial effusion. Fetal Diagn Ther 2014;36:320-5.