Egyptian Maternal and Fetal Medicine Foundation

28/07/2025

Lower doses of enoxaparin(clexane) is more effective in lowering pregnancy loss rates in women with recurrent spontaneous abortion than higher doses .A recent study says:

Recurrent spontaneous abortion (RSA) is a severe concern for women's reproductive health, with an incidence of 1% to 5%.(1)
Low molecular weight heparin (LMWH)is widely recognized as an effective treatment for RSA caused by antiphospholipid syndrome (APS), post-thrombotic syndrome (PTS), autoimmune diseases, and other conditions.(2)
Recent studies have shown that LMWH, aside from its anticoagulant effects, offers immunomodulatory and other benefits. These benefits include inhibiting the immune response triggered by antiphospholipid antibodies , promoting trophoblast proliferation , invasion and differentiation, preventing trophoblast apoptosis, protecting vascular endothelium, and enhancing placental formation.(3,4)
There has been an increasing trend among clinicians that increasing the doses of clexane might be more effective in improving live birth rates and lowering prenancy loss rate (LBR). However, the current evidence antagonizes that belief.
A recent systematic review and meta-analysis (level I evidence & level A recommendation) , published by American Journal of Of Obstetrics & Gynecology in February 2025 concluded that both the 20mg and 40mg doses of enoxaparin were effective in increasing live birth rates and lowering pregnancy loss risk, among women with recurrent pregnancy loss . The study emphasized that the 20mg dose has shown superior efficacy over the 40mg dose. (5)
The research added that enoxaparin beside significantly improving live birth rates , also reduces the risks of pre-eclampsia, preterm delivery, and pregnancy loss.
The research data were collected from 22 randomized controlled trials, encompassing 4,773 participants.
It seems that increasing the doses of clexane during pregnancy as a trial to improve live birth rates and reducing pregnancy loss risk might only add more economic suffering together with higher risks of maternal side effects from the drug.

Mohamed Ali Abdelkader(MD)

References:
1) Genovese HG, McQueen DB. The prevalence of sporadic and recurrent pregnancy loss. Fertil Steril. 2023 Nov;120(5):934-936

2) Berker B, Taşkın S, Kahraman K.
The role of low-molecular-weight heparin in recurrent implantation failure: a prospective, quasi-randomized, controlled study.Fertility and Sterility, Volume 95, Issue 7, June 2011, Pages e29

3) Brenner B. Enoxaparin use in pregnancy: state of the art. Womens Health (Lond). 2007 Jan;3(1):9-14.

4) Pasquier E, de Saint Martin L, Bohec C, Chauleur C, Bretelle F, Marhic G, Le Gal G, Debarge V, Lecomte F, Denoual-Ziad C, Enoxaparin for prevention of unexplained recurrent miscarriage: a multicenter randomized double-blind placebo-controlled trial. Blood. 2015 Apr 2;125(14):2200-5.

5)Huang W, Yu Y, Chen L, Tang X, Fang X, Ou X, Du X. Comparative effectiveness of low molecular weight heparin on live birth for recurrent spontaneous abortion: systematic review and network meta-analysis. Am J Obstet Gynecol MFM. 2025 Feb;7(2):101572.

11/07/2025

Fetal Aortic Stenosis with Left Ventricular Hypoplasia and Endocardial Fibroelastosis.
By
Durr-e-Sabih.Multan-Pakistan

Fetal aortic stenosis refers to narrowing of the aorta, this is most commonly due to valvular stenosis but can very rarely be subvalvular or supravalvular. Isolated aortic stenosis is found in about 1:1000 live births[1]. Bicuspid aortic valves are the most common cause of valvular aortic stenosis, but a diagnosis of fetal bicuspid valves tends to be difficult [2]. Focused ultrasound of the aortic valve is still not part of the ISUOG guidelines.
Aortic stenosis can occur as an isolated finding or be combined with other anomalies, it can be mild, severe or critical. Ultrasound has a low sensitivity (~15%) for diagnosing isolated mild aortic stenosis [3]. This improves (~85%) when secondary signs of aortic stenosis like left ventricular hypoplasia or fibroelastosis occur [4].
Aortic stenosis is often a progressive disease and might not be apparent at the time of the routine anomaly scan in mid-second trimester.As the aortic stenosis becomes more severe it can progress to critical aortic stenosis with left ventricular dysfunction.Eventually leading to left ventricular hypoplasia and endocardial fibroelastosis in about 75% of cases of severe/critical aortic stenosis.
In this talk , I will present 2 cases of fetal aortic stenosis with left ventricular hypoplasia and endocardial fibroelastosis .

Case 1. 32 year old woman in a non-consanguinous marriage Para-4, G-3, all alive, had Gestational diabetes. She was unsure of dates. She had had a previous scan (done elsewhere) at 22 wks that was reported as normal. On a routine visit to her obstetrician, she noted cardiomegaly and sent for a repeat scan. Scan findings: ( Clip 1) Right ventricle is enlarged, and extends below the left ventricle to form the apex. The left ventricle is smaller and has a globular shape, it contracts poorly. The left ventricular walls are echogenic. The tricuspid valve shows good excursion but the mitral valve is restricted. The flap of the foramen ovale was in the right atrium andthere was left to right blood flow through the foramen ovale.

Case 2 G-2- P1, previous baby healthy, no consanguineous, non- diabetic, unsure of dates 26 weeks of pregnancy breech at the time of examination.Scan findings (clip 2). Scan showed a very small left ventricle with markedly reduced contraction and echogenic walls. Right ventricle is enlarged and forms the apex. The left ventricle is globular, contracts poorly and has echogenic walls (endocardial fibroelastosis). The aortic root and isthmus are narrow and there is reversed flow in the isthmus.
Durr-e-Sabih.Multan-Pakistan

References

1. Abnormalities seen in the great arteries view (Aortic Valve Stenosis). Available from: https://courses.fetalmedicine.com/fmf/show/809?locale=en.
2. Zheng, M., et al., Diagnostic value of selected fetal echocardiographic parameters in the prenatally suspected bicuspid aortic valve. Echo Research & Practice, 2025. 12(1): p. 1.
3. Freud, L.R., et al., Low rate of prenatal diagnosis among neonates with critical aortic stenosis: insight into the natural history in utero. Ultrasound Obstet Gynecol, 2015. 45(3): p. 326-32.
4. Respondek-Liberska, M., et al., Fetal hypoplastic left heart syndrome and neonatal follow-up in Polish Mother's Memorial Hospital Research Institute report from January 2023 to January 2024: an improvement of survival rate. Ginekol Pol, 2025.
5.Simpson, J., Z. V, and M. O, Fetal Cardiology: A Practical Approach to Diagnosis and Management 2018.

03/07/2025

03/07/2025

Master the technique of fetal cardiac examination on the machine supervised by Prof. Mohamed Ali Abdelkader.
For any Information about the workshop call:
(+2) 01223409160
(+2) 01092515830

29/05/2025

Fetal cerebral arteriovenous malformation (AVMs): Pial AVMs.

By Prof. Mohamed Ali Abdelkader.

Introduction:
Fetal cerebral arteriovenous malformations (AVMs) are congenital, high-flow low resistance arteriovenous shunts without a capillary connection.They are rare lesions mostly involving the vein of Galen and, less commonly, the dura and pia mater.(1)
In a previous article I presented a case of vein of Galen malformation (VGAM). In this article , I will present a case of massive AVMs that are located directly beneath the pia matter on the surface of the brain . This is called pial AVMs.
Case presentation:
A 25 years old woman, primigravida was referred at 35 weeks of gestation for targeted brain ultrasound because of a suspected brain lesion .A detailed fetal neurosonography revealed a large well-circumscribed hypo-echoic supratentorial left hemispherical cerebral lesion that mostly involve the parietal and temporal lobes .It measures 45x43 mm. Color Doppler revealed aliased high-flow, color signals with dilated, tubular, tortuous vascular channels. Spectral Doppler showed high-velocity, turbulent, bidirectional, blood flow. (Please review attached video clip).
The woman,who had no relevant personal or family history was delivered by Cesarean section at term .Postnatal MRI imaging confirmed the prenatal diagnosis.Palliative transarterial embolizations was planned . However extensive intracranial hemorrhage and demise of the neonate occurred before the first session .
Discussion:
Cerebral AVMs involving the vessels of the pia matter( Pial AVMs ) represent abnormal direct connections (fistulae) between pial arteries (that supply the brain surface) and draining veins, without the normal intervening capillary bed. (2)They are usually supratentorial in location.(3)
Distinguishing pial AVMs from VGAM is crucial because the approach to management differs significantly. The location of the lesion is quite important in differentiation .
VGAM malformation is subarachnoid and represents ectasia of vein of Galen at the junction of falx cerebri and tentorium cerebelli .It is central in location while pial AVMs are mostly lateral , just beneath the pia mater on the surface of the brain. They are often found in the frontal, temporal, and parietal lobes. The most common feeding artery for Pial AVMs is the middle cerebral artery (MCA), followed by the anterior cerebral artery (ACA) .(3)
In VGAM,interventions are often delayed until the child is a few months old, while in pial AVMs, prompt treatment is necessary to minimize brain tissue damage. (4)
Pial AVMs can cause significant shunting of blood, potentially leading to heart failure and pulmonary hypertension in newborns. Treatment options include endovascular embolization (using liquid embolic agents or coils) and, in some cases, surgical intervention.
Prognosis of pial AVMs is much worser than that of VGAM . Death is caused by significant shunting of blood,leading to heart failure and fetal hydrops together with pulmonary hypertension in newborns. The major cause of neonatal death is intracranial hemorrhage .(5)

Mohamed Ali Abdelkader MD
References:
1) Geibprasert S, Pongpech S, Jiarakongmun P, Shroff MM, Armstrong DC, Krings T. Radiologic assessment of brain arteriovenous malformations: What clinicians need to know. Radiographics. 2010;30:483–501.
2) Hetts SW, Keenan K, Fullerton HJ, Fullerton HJ, Cooke DL, Amans MR, et al. Pediatric intracranial nongalenic pial arteriovenous fistulas: Clinical features, angioarchitecture, and outcomes. AJNR Am J Neuroradiol. 2012;33:1710–9.
3) Medhi G, Gupta AK, Saini J, Ramalingaiah AH, Pendharkar H, Parida S. Pial arteriovenous fistula: A clinical and neuro-interventional experience of outcomes in a rare entity. Indian J Radiol Imaging. 2020 Jul-Sep;30(3):286-293.
4) Berenstein A, Ortiz R, Niimi Y, Elijovich L, Fifi J, Madrid M. Endovascular management of arteriovenous malformations and other intracranial arteriovenous shunts in neonates, infants, and children. Childs Nerv Syst. 2010;26:1345–58.
5) Madsen PJ, Lang SS, Pisapia JM, Storm PB, Hurst RW, Heuer GG. An institutional series and literature review of pial arteriovenous fistulas in the pediatric population: Clinical article. J Neurosurg Pediatr. 2013;12:344–50.

07/05/2025

Choroid plexus cysts and the risk of aneuploidy:

By prof. Mohamed Ali Abdelkader

Introduction:The choroid plexus begins to develop at approximately six to seven weeks of gestation and fills approximately 75 percent of the lateral ventricular cavity by 9 weeks of gestation.Fetal choroid plexus cysts are formed when cerebrospinal fluid is trapped in the choroid plexus and are typically identified in approximately 1% of fetuses in the first and second trimesters of pregnancy during routine prenatal ultrasound scans.(1)
The typical sonographic appearance is that of circumscribed, anechoic structures. Cysts may be unilateral,bilateral, bilobulated, or multiple and typically measure less than 10 mm in diameter.(2)
Approximately 90% of cysts disappear after 28 weeks of gestation,and only a few show progressive enlargement.(3)
Therefore, Choroid plexus cysts are not considered to be a brain anomaly.

Effect on neurodevelopment : A systematic review was conducted to examine the neurodevelopmental outcomes of children who were followed with isolated choroid plexus cysts and delivered at birth. The results demonstrated that there were no significant neurodevelopmental effects in these cases.(4)

Risk of aneuploidy:In a study in which 12,672 patientswere screened and 336 choroid plexus cysts were detected, it was reported that the presence of additional structural abnormalities was observed in all cases with aneuploidy. (5) In a separate study, in which ultrasound findings of fetuses with trisomy 18 were analyzed,choroid plexus cysts were detected in approximately half of the cases.Therefore choroid plexus cysts are more linked to trisomy 18 than other trisomies. (6)
In no case of trisomy 18 or other trisomies , isolated choroid plexus cysts were detected as a sole soft maker. When identified as a solitary finding, it is advised that choroid plexus cysts be regarded as a benign phenomenon.(7)

Conclusion : In conclusion, fetal choroid plexus cysts represent a risk factor for chromosomal abnormalities, especially trisomy 18 when associated anomalies are present. In the absence of additional anomalies choroid plexus cysts are considered a variant of normal. The shape, size, or laterality of the choroid plexus cyst is considered to be of no clinical significance.
Consequently, when such a cyst is identified, a comprehensive sonographic anatomical examination and a meticulous evaluation of the patient for other structural soft markers of aneuploidy should be conducted. If it is confirmed that the cyst is isolated, it is crucial to avoid exacerbating the distress of the family.

Mohamed Ali Abdelkader, MD.

References:

1) Demasio K, Canterino J, Ananth C, Fer-nandez C, Smulian J, Vintzileos A. Isolated choroid plexus cyst in low-risk women less than 35 years old. Am J Obstet Gynecol. 2002;187(5):1246-1249.

2) Epelman M, Daneman A, Bl**er SI, et al.Differential diagnosis of intracranial cystic lesions at head US: correlation with CT and MR imaging. Radiogr Rev Publ Radiol Soc N Am Inc.2006;26(1):173-196.

3) Lopez JA, Reich D. Choroid plexuscysts. J Am Board Fam Med JABFM.2006;19(4):422-425.

4) Bernier FP, Crawford SG, Dewey D. Developmental outcome of children who had choroid plexus cysts detected prenatally.Prenat Diagn.2005;25(4):322-326.

5) Coco C, Jeanty P. Karyotyping of fe-tuses with isolated choroid plexus cysts is not justified in an unselected population. J Ultrasound Med 2004;23(7):899-906.

6)Beke A, Barakonyi E, Belics Z, et al. Risk of chromosome abnormalities in the presence of bilateral or unilateral choroid plexus cysts. Fetal Diagn Ther. 2008;23(3):185-191.

7) Yhoshu E, Mahajan JK, Singh UB. Choroid plexus cysts-antenatal course and postnatal outcome in a tertiary hospital in North India. Childs Nerv Syst. 2018 Dec;34(12):2449-2453.

11/04/2025

For any details please call the numbers at the bottom of the announcement.
I would highly recommend this course for those who need to upgrade their sonographic skills and knowledge about fetal anatomy survey and anomaly scan .Good luck .

06/04/2025

Absent cavum septum pellucidum is not only linked to agenesis of corpus callosum :
By Professor : Mohamed Ali Abdelkader.
Introduction:
The cavum septum pellucidum ( CSP ) is a midline fluid filled structure that is situated inside the corpus callosum . It is bounded anteriorly by the rostrum and genu of the corpus callosum, superiorly by the body of the corpus callosum, and inferiorly by the columns of fornix. (Figure 1)
The CSP is typically fully formed at 17 weeks of gestation. Throughout gestation, the CSP gradually closes, and after 37 weeks of gestation, it is usually no longer detectable ultrasonographically. (1) Visualization of the CSP during prenatal ultrasound is essential for confirmation of normal brain anatomy and integrity of corpus callosum.(2)
Sonographic findings:
In the axial plane, the CSP is seen as an anechoic area interrupting the falx cerebri anteriorly in the midline that sits between 2 parallel echogenic lines (the 2 bordering of septum pellucidum laterally). (Figure 2)
Care must be taken to avoid mistaking the columns of the fornix for the CSP (3). Those appear as 3 parallel lines (Figure 3)
In agenesis of corpus callosum, there is posterior ventriculomegaly(colpocephaly). This is called tear drop sign.There is also upward displacement of third ventricle which can be seen in trans axial view at the same level of lateral ventricle. (Figure 4)
Differential Diagnosis
Although absent CSP is mostly linked to agenesis of corpus callosum (ACC),the differential diagnosis of an absent CSP includes several other CNS anomalies. Absent CSP might be associated with holoprosencephaly (HPE), ventriculomegaly, septo-optic dysplasia (SOD) and schizencephaly.(4&5)
1)Holoprosencephaly:
Signs of alobar HPE on ultrasound include a large single fused ventricle, fused thalami, and absent midline brain structures. (Figure 5).In semilobar (Figure 6) and lobar HPEs (Figure 7), CNS findings are more subtle and include fused frontal lobes but distinct occipital lobes, absent interhemispheric fissure, and partial or complete ACC.

2)Severe ventriculomegaly:
Severe ventriculomegaly can also lead to nonvisualization of the CSP.
The increased pressure within the
ventricles may cause obliteration of the CSP.(Figure 8)

3)Septo-optic dysplasia(SOD):
SOD is characterized by hypoplastic optic nerves, visual problems, and hypothalamic-pituitary dysfunction.
Prenatal ultrasound shows absent cavum septum pellucidum with communicating frontal horns. (Figure 9) .Postnatal brain MRI, along with ophthalmologic examination are used to make the clinical diagnosis of SOD.

4)Shizencephaly:
Schizencephaly is a destructive cerebral lesion in which a cortical defect extends to the subaracnoid space and the lateral ventricles .It may be unilatetal or bilateral . (Figure 10).In approximately two-thirds of cases of schizencephaly,the CSP may be absent. It is difficult to be diagnosed ultrasonographically.
Mohamed Ali Abdelkader MD.

References:
1) Falco P, Gabrielli S, Visentin A, Perolo A, Pilu G, Bovicelli L. Trans-abdominal sonography of the cavum septum pellucidum in normal fetuses
in the second and third trimesters of pregnancy. Ultrasound Obstet
Gynecol 2000;16:549–53.

2) Winter TC, Kennedy AM, Byrne J, Woodward PJ. The cavum septi
pellucidi: why is it important? J Ultrasound Med 2010;29:427–44.

3) Callen PW, Callen AL, Glenn OA, Toi A. Columns of the fornix, not to be
mistaken for the cavum septi pellucidi on prenatal sonography.
J Ultrasound Med 2008;27:25–31.

4) Malinger G, Lev D, Oren M, Lerman-Sagie T. Non-visualization of the
cavum septi pellucidi is not synonymous with agenesis of the corpus cal-
losum. Ultrasound Obstet Gynecol 2012;40:165–70

5) Malinger G, Lev D, Kidron D, Heredia F, Hershkovitz R, Lerman-Sagie T.
Differential diagnosis in fetuses with absent septum pellucidum. Ultra-
sound Obstet Gynecol 2005;25:42–9.

03/03/2025

Prenatal sonographic diagnosis of epiganthus could be life saving:

By Mohamed Elnamory. A.Professor of Ob/Gyn. Fetal medicine unit .Tanta university.

An epignathus is an extremely rare form of oropharyngeal teratoma that arises from the oral cavity, most commonly from the palate and is associated with a high mortality secondary to airway obstruction in the neonatal period.Most babies with epignathus have a poor prognosis due to late diagnosis and, subsequently, complications in securing the airway. (1)
However, with early detection and multidisciplinary healthcare teams, an adequate treatment plan to secure the baby's airway and surgically remove the lesion may improve the prognosis.(2&3)
Here’s a fascinating case of fetal epignathus,diagnosed prenatally. This condition can pose significant challenges for airway management at birth, making early detection crucial.

Key considerations:
✅ Early ultrasound for assessment
✅ Planning for EXIT (ex utero intrapartum treatment) procedure if needed
✅ Multidisciplinary approach for optimal outcomes
Mohamed Elnamoury .MD.

References:
1)Jadhav SS, Korday CS, Malik S, Shah VK, Lad SK (January 2017). "Epignathus Leading to Fatal Airway Obstruction in a Neonate". Journal of Clinical and Diagnostic Research. 11 (1): SD04 – SD05.

2)Hedrick, H. L., Flake, A. W., Crombleholme, T. M., & Johnson, M. P. (2002). Prenatal diagnosis and management of oropharyngeal teratomas: The EXIT procedure. American Journal of Perinatology, 19(2), 99-107.

3)Bats, A. S., Zerah, M., Revillon, Y., Boulat, C., Vuillard, E., & Oury, J. F. (2005). Prenatal diagnosis and management of an oropharyngeal teratoma: A case report and review of the literature. Prenatal Diagnosis, 25(10), 988–991.

26/02/2025

Maternal propranolol treatment for fetal pleural effusion:
By professor: Mohamed Ali Abdelkader

Fetal pleural effusion is rare but can be life threatening. Prenatal treatment for large symptomatic fetal pleural effusion involves thoracocentesis followed by pleuro–amniotic shunting, but these invasive procedures are associated with significant fetal risks.(1)
Propranolol is a non-selective beta blocker that is used in pregnancy for women with underlying cardiac disease and hypertension, and in fetal medicine for supraventricular tachycardia.(2)
In the last decade, propranolol has gained interest as a treatment for chylous effusion and other lymphatic malformations in infants and children.
Maternal propranolol treatment has also been used successfully for prenatal treatment of fetal congenital chylothorax .(3)
I am presenting here a case sent to me by Dr. Syed Hamdoon from Uganda .She had isolated pleural effusion at 21 week gestation. (Figure 1).After a discussion with her and her doctor , she was placed on propranolol 20 mg orally three times daily.
After 4 weeks she has resolved totally. (Figure 2)
How does propranolol acts?
Lymphatic malformations (chylothorax) are associated with increased vascular endothelial growth factor level and increased expression of beta-2 adrenergic receptors. It has been proposed that propranolol causes down-regulation of the Raf-mitogen-activated protein kinase signaling pathway, which signals decreased expression of vascular endothelial growth factor, leading to apoptosis in capillary endothelial cells(4)

In summary, propranolol may be a beneficial maternal treatment for fetal chylothorax as it avoids the risks associated with interventional procedures. Further research is needed to assess its efficacy.
Mohamed Ali Abdelkader.MD

References:
1) Wilson R, Johnson M. Prenatal ultrasound guided percutaneous shunts for obstructive uropathy and thoracic disease. Semin Pediatr Surg 2003; 12: 182–189.
2) Teuscher A, Bossi E, Imhof P, et al. Effect of propranolol on fetal tachycardia in diabetic pregnancy. Am J Cardiol 1978;2013:304–7
3) Handal-Orefice R, Midura D, Wu JK, Parravicini E, Miller RS, Shawber CJ. Propranolol therapy for congenital chylothorax. Pediatrics. 2023;151(2)
4) Ozeki M, Fukao T, Kondo N. Propranolol for intractable diffuse lymphangiomatosis. N Engl J Med. 2011;364(14):1380-1382.

24/02/2025

16/02/2025

The Egyptian maternal and fetal medicine foundation held a scientific meeting on 13th and 14th February 2025 ‘Advanced topics in fetal medicine’, in Princess Fatma academy in Nasr city.
It was attended by around 60 doctors from different specialities: fetal medicine specialists, Obstetricians, radiologists & neonatologists. Speakers were Dr. Mohamed Ali Abdelkader from Egypt - president of the EMFMF, Dr. Durr Sabih from Pakistan & Dr. Buhmika Singe from India.
The meeting was greatly successful and the scientific content was appreciated by most of the attendees.
The event was also broadcasted abroad to doctors from other countries who could not travel to Cairo.
The EMFMF would like to thank all professors and doctors who attended and shared in this success together with Cairo medical-Mindray company who sponsored the event.