Prenatal ultrasonographic approach to skeletal dysplasia: Practical tips

What is the ideal time to look for the skeletal dysplasia?
The long bones, vertebrae and calvarium begin ossifying by 12 weeks, so the presence of certain skeletal dysplasias especially the lethal ones can be suggested as early as the first trimester.

When should we suspect for skeletal dysplasia?
Any fetus showing femoral length (FL) or humerus length (HL) measurements less than 5th centile or −2 SD from the mean at all gestations should be evaluated.

Table 1: Checklist to approach to the skeletal dysplasias.

Gestational age based on LMP or first trimesterultrasound (IUGR/Constitutional)
Long bones-Absence/Length (femurs, humerus, radius, ulna, tibia, fibula,and clavicle)
Shape (straight, curved, bilateral vsunilateral)
Appearance of the metaphyseal ends (spikes, irregularities)
Echo density(well mineralized, poorly mineralized)
Foot (size and shape)
Hands (poly/syn/oligo – dactyly, trident hand, talipes, hitchhikers thumb/toe)
Circumferences (head, abdomen, and chest)
Skull (mineralization, suture, shape like cloverleaf, size)
Thorax (champagne cork shape, barrel shaped, bell shaped)
Ribs (short, fracture/beaded, absent/disorganised)
Scapula (size and shape)
Presence of the secondary epiphyses (calcaneus >20 wk, kneeepiphyses >28 wk)
Mandibular size and shape
Fetal profile (frontal bossing, absent/flat nasal bone, micrognathia, cleft lip/palate, orbits)
Vertebral bodies (Mineralization, hemivertebrae,disorganised and shape)
Other congenital anomalies (CNS, cardiac, renal, anterior abdominal wall, genitals) Evaluation of amniotic fluid volume (hydramnios)
Hydrops

 

Table 2:Important ratios to evaluate skeletal dysplasia.

Biometric ratios Findings Interpretation
1 Short femur (FL) >4 SD below the mean Lethal(8)
Short femur (FL) < 4 SD below the mean Suggestive of a skeletal dysplasia.
2 FL: footlength <1 Suggestive of a skeletal dysplasia(9).
3 3D USG lung volume ≥5th percentile for gestational age Non-lethal
3D USG lung volume <5th percentile for gestational age Lethal(10).
4 FL:AC <0.16 lethal (With polyhydramnios mostly lethal)
FL:AC >0.16 Non-lethal(11).
5 CC:AC <0.6 Lethal
CC:AC <0.6 Non-lethal(12).
CC:AC <0.6 Non-lethal(12).
  • The femur length is more than >5 mm below 2 standard deviations (equivalent to greater than 4 standard deviations below the mean), the sonologist can be certain he or she is dealing with a significant skeletal dysplasia (Fig. 1a) (8). Femur length normalized chart is in Table
  • The femur/foot length ratio (FL: foot) nomogram appears to be a useful parameter to help differentiate fetuses that have dysplastic limb reduction from those whose limbs are short because of constitutional factors or IUGR, significant correlation was demonstrated (r = 0.98; P less than .0001) (Fig. 1b)(9).
  • 3D US calculated lung volumes compared to normal fetuses (
  • Femur length to abdominal circumference ratio (FL:AC), (Sensitivity 92–96%) whencombined with the presenceof polyhydramnios, the ability to predict lethality has been reported tobe as high as 100% (11) (Fig. 1c).
  • Chest circumference to abdominal circumference ratio (CC:AC), chest circumference to abdominal circumference ratio had the highest diagnostic accuracy for antenatal diagnosis of pulmonary hypoplasia (sensitivity: 93.5% and specificity: 90.3%) independent of gestational age (Fig. 1d) (12).

Lethality occurs in most skeletal dysplasia’s as a result of a small chest circumference and resultant pulmonary hypoplasia(13).imsgedFlowchart 1.Systematic approach to evaluate

Table 3: Ultrasound findings in Major skeletal dysplasias’s:

Diagnosis Skeletal system – Femoral length (FL) is <5th centile PLUS Other systems
1 Achondrogenesis 1 Limbs: severe shortening;Trunk: shortHead: macrocephaly with frontal bossingThorax: NarrowSkull: hypo-mineralisationSpine (vertebral bodies):
Hypo-mineralisationThorax: rib fractures
2 Achondrogenesis2 Limbs: severe shortening;Trunk: shortHead: macrocephaly with frontal bossingThorax: NarrowSkull: hypo-mineralisationSpine (vertebral bodies):
no/minimal Hypo-mineralisationThorax: no ribfractures
3 Achondroplasia Limb: short (>22 weeks),
trident hands (Fig. 2a)Head: macrocephaly with frontal bossing (Fig. 2b)Spine: lumbar lordosis.Thorax: normal
4 Campomelic dysplasia Limb: short, bowed legs, arms normal length, club feet.Thorax: narrowScapulae: hypoplasticHead: large with small faceAmbiguous genitalia +/-
5 Cleidocranial dysplasia Limb: shortSpine (vertebral bodies): poor mineralizationSkull: mild hypomineralizationClavicle: hypoplastic
6 Conradi-hunermann-
Happle syndromeLimb: rhizomelic shortening, stippled epiphysis
Spine: stippledThorax and skull: normal
Cataract, midface hypoplasia
7 Rhizomelic
Chondrodysplasia punctata
Limb: rhizomelic severe shortening
Stippled epiphyses (Fig. 2c)Head: late onset microcephaly
Skull & thorax: normal.Others: nasal hypoplasia (Fig. 2d, 2e), cataract.
8 X-linked recessive Chondrodysplasia
punctata
Limb: shortening with stippled
EpiphysesThorax: normalSkull: normalOthers: larynx and sternum
Stippled epiphyses,Face: nasal and distal phalangeal
hypoplasia
9 Diastrophic dysplasia Limb: very short & bowing,Joints: flexion contracture, talipesOthers: hitchhiker thumb/toeSpine: scoliosisThorax: normalSkull: normal
10 Ellis van Creveld
Syndrome
Limb: acromelic&mesomelic shorteningPostaxial polydactylyThorax: smallSkull/spine – normal. Cardiac anomaly- ASD >50%
Posterior fossa cyst
11 Hypophosphatasia- severe neonatal form Limb: very short, acute angulationThorax: small narrow with short ribsOther: hypomineralization of all long bones, skull, ribs, vertebrae,
talipes
Polyhydramnios
12 Hypophosphatasia- variable onset Limb: very short, acute angulation (decreases with gestation)Thorax: small narrow with short ribsOther: hypomineralization all long bones, skull, ribs, vertebrae, talipes
13 Juenes asphyxiating thoracic dystrophy Limb: short, 22weeks,
polydactyly
Thorax: narrow (Fig. 2f) and short ribs Skull
spine: normal
Renal anomalies
14 Osteogenesis imperfecta IIA/C Limb: short with fracturesThorax: small with fractured ribsSkull: hypomineralization.
15 Osteogeneis imperfecta IIB/III/IV Limb: mild shortening & bowed
long bonesSkull: mild hypomineralizationThorax: normal/slightly smallSpine: scoliosis
16 Osteogenesis imperfecta VIII Limb: very short <3rd centile with
bowed long bonesSkull: mild hypomineralizationThorax: normal/slightly small with fractured ribs
17 Roberts syndrome Limb: short/absent
Oligodactyly, talipes,Skull: normalThorax: normal
Cardiac anomalies, cleft lip/palate.
18 Thanatrophic dysplasia type I Limb: very short, trident handThorax: narrow with short ribsTrunk: normalSpine: Platyspondyly (type I>II).Head: macrocephaly with frontal bossingFemur: curved or bowing of femur (telephone receiver) (Fig. 2g). Polyhydramnios- 50%
19 Thanatrophic dysplasia type II Limb: very short, trident handThorax: narrow with short ribsTrunk: normalSpine: Platyspondyly (type I>II).Head: macrocephaly with frontal bossingFemur: straightSkull: cloverleaf- shaped
20 Spondylo-epiphyseal-dyplasia congenita Limb: shortThorax: short with normal ribsSkull: normalSpine: hypomineralised vertebral bodies
21 Short-ribbed polydactyly syndromes I (Saldino-noonan) Limb: severe micromelia (<<3rd)
Polydactyly
Thorax: smallSkull: normal
Generalized skin oedema
22 Short-ribbed polydactyly syndromes II
(Majewski)
Limb: severe shortening, polydactylyThorax: small with short ribSkull: cloverleaf (Fig. 2h)Others: exomphalos,
bladder outflow obstruction,
midline facial cleft
Generalised skin odema, CNS anomalies.
23 Short-ribbed polydactyly syndromes III
(Verma-Naumoff )
Limb: normal <10th centile,
Postaxial polydatyly
Thorax: small
Skull: normal


What is the role of 3D USG?

The overall accuracy for the diagnosis of the specific type of skeletal dysplasia using routine USG approaches only 40%-60%,which can be enhanced by the use of other imaging modalities. 3dimentional USG is helpful in differentiating the fetal facial abnormalities and in the evaluation of fetal limbs better, for example: severe flattening of the nasal bridge and craniosynostoses in thanatophoric dysplasia. Fetal MRI has been reserved for cases with suspected spinal abnormalities in the form of scoliosis or diastemetomylia. (14)

Is there any role for MRI in the diagnosis of skeletal dysplasia?

MRI has superior soft tissue contrast, better resolution, ability to examine both sides of the fetus simultaneously and also provide information about the stages of maturation of gray and white matter. Similar to USG it does not expose the fetus to ionizing radiation and has no teratogenic effect during pregnancy. (15) Echoplanar MRI may also be valuable in determining the presence or absence of ossification. Skeletal dysplasias such as osteogenesis imperfecta and hypophosphatasia, present with a generalized decrease in osseous density, which is demonstrated as lack of hypointense signal (indicative of normal ossification) on echoplanar imaging sequences. (16)

Prenatal use of CT scan in the diagnosis?

In a study conducted by Miyoko et al 3D-CT was more accurate than was 2D ultrasound in visualizing vertebral anomalies (abnormal shape of the vertebral bodies, abnormal interpedicular distance), pelvic bone malformations (delayed ossification of the pubic bones, abnormal acetabular shape) and enlarged metaphysis or synostoses in long bones. Both imaging techniques are useful in the management of fetal dysplasia; 2D ultrasound is a useful screening test and 3D-CT is a valuable complementary diagnostic tool (14). Because of the associated radiation dose, which may be similar to that of conventional fetal radiography, the use and potential impact of CT is limited. (17). There are ongoing newer studies on low dose 3D CT, where the dose is below 100mGy, reducing the overall exposure risk to mother and fetus.

What investigations are recommended in women who opt to discontinue the pregnancy?

Cases of suspected lethal skeletal dysplasia where the couple opt to discontinue the pregnancy or where there has been an antepartum stillbirth ,in order to reach a specific diagnosis a minimum post-delivery work up should include(a)external examination with photographs anterior and posterior of the appendicular and axial skeleton including hands and feet(b)post whole body radiographs/infantogram anteroposterior and lateral views (c)skin or tissue biopsy specimens for chromosome analysis or preservation of fibroblasts/DNA storage (d)if possible a complete autopsy should be performed. (18)

How to counsel the couple?

In cases where there is a previous molecular diagnosis of a childaffected by skeletal dysplasia, there is a role of prenatal diagnosis in the form of chorionic villous sampling or amniocentesis.In situations where either of the parent has a clinically identifiable skeletal dysplasia, they should be encouraged to get a molecular diagnosis before planning pregnancy.Role of Non-invasive testing in the diagnosis of Skeletal Dysplasia
There are several studies about the different techniques used for the non-invasive prenatal testing (NIPT) of achondroplasia like conventional PCR with restriction enzymes, matrix assisted laser desorption/ionization(MALDI) time of flight mass spectrometry, real time quantitative PCR, digital PCR and next generation sequencing (19-23).In 2019 Vivanti etal (24) reported the results of a novel simple non-invasive molecular analysis technique using high-resolution melting (HRM) analysis for the prenatal diagnosis of achondroplasia in a prospective multicentre cohort study. They also suggested thatcell free DNA can be advised in the first trimester in cases where there is history of an affected child with FGFR3 related skeletal dysplasia or where the father is affected but for technical reasons it cannot be applied to pregnant women who are affected by the disease, as their plasma contains a background of mutated DNA. NIPT can also be offered where neither of the parent is affected but FGFR3 related skeletal dysplasia is suspected in the fetus on the basis of USG.

How do we manage the pregnancy and labour?

The aim of antepartum care is to reach a final diagnosis as to the type of skeletal dysplasia the baby has, as that is one of the main indicators of the final outcome. The delivery should be planned in a tertiary care centre with a multidisciplinary team consisting ofan obstetrician,neonatologist, paediatric orthopedician and emergency medicine specialist. If possible, instrumentation during delivery should be avoided when fetal skeletal dysplasia is suspected due to the increased risk of intracranial and cervical spine complications.(25)Caesarean section is usually performed for obstetric indications or in cases where the biparietal diameter (BPD)>40cm.The role of elective caesarean section in women carrying a baby with suspected Osteogenesis imperfecta is controversial with newer guidelines indicating that an elective caesarean section vs a vaginal delivery does not reduce the risk of fractures(26). Postnatal genetic evaluation should be performed in order to confirm the diagnosis and also to assess the recurrence risk in future pregnancies.

References:

  • Barbosa-Buck CO, Orioli IM, da Graça Dutra M, Lopez-Camelo J, Castilla EE,Cavalcanti DP. Clinical epidemiology of skeletal dysplasias in South America. AmJ Med Genet A 2012.
  • Geert R. Mortier,Daniel H. Cohn,et al, Nosology and classification of genetic skeletal disorders: 2019 revision, Am J Med Genet. 2019.
  • Parilla BV, Leeth EA, KambichMP et al (2003) Antenatal detection of skeletal dysplasias. J Ultrasound Med.
  • Gaffney G,Manning N, Boyd PA et al (1998) Prenatal sonographic diagnosis of skeletal dysplasias–a report of the diagnostic and prognostic accuracy in 35 cases. Prenat Diagn.

Take home messages from the 4th February Journal Club meet

journal club blog banner

Prenatally diagnosed omphaloceles: Report of 92 cases and association with Beckwith Wiedemann syndrome. PND, Vol 41 (7), 798-816
Abbasi N et al

Beckwith‐Wiedemann syndrome (BWS) is the most common pediatric overgrowth syndrome, classically characterized by omphaloceles, macroglossia, and overgrowth and is associated with 2%–22% of antenatally diagnosed omphaloceles. Macrosomia, macroglossia and visceromegaly typically occur later in gestation or postnatally. The chromosomal region 11p15.5 spans ~ 1 Mb and harbors two separate imprinting control regions (ICRs):

  • The telomeric one, ICR1, includes the H19/IGF2:IG-DMR, which is methylated on the paternal allele,
  • The centromeric one, ICR2, includes the KCNQ1OT1:TSS-DMR, which is maternally methylated.

Four different types of molecular changes have been reported in BWS

  1. Imprinting due to hypomethylation at ICR2 (40-50%) or hypermethylation of ICR1
  2. Uniparental disomy
  3. Deletions/duplications
  4. Point mutations

Molecular testing of BWS involves MS-MLPA as the primary technique for detecting epigenetic and genetic variations at 11p15 including microdeletions, microduplications, alterations in gene dosage, and DNA methylation at two imprinting centers as well as UPD, followed by other techniques such as Karyotype for chromosomal rearrangements, genetic sequencing for point mutation analysis. It is important to know the mechanism of BWS to delineate the recurrence risk.

In this paper by Abbasi et al, the authors studied 92 cases (2010-2015) of prenatally diagnosed omphalocele and report association with BWS in 19 cases.  An echocardiogram and detailed fetal ultra- sound were performed, and amniocentesis was offered with karyotype/microarray analysis and BWS molecular testing. Perinatal, neonatal, and long‐term outcomes were retrieved for BWS cases.

  • Over the 15 year‐study period, the prevalence of BWS was approximately 8% among prenatally diagnosed omphaloceles
  • Two cases were part of MCDA twins which were discordant for BWS.
  • With routine implementation of BWS testing for prenatally diagnosed omphaloceles, BWS was identified in 37% and 7% of isolated and non‐isolated omphaloceles respectively, after exclusion of aneuploidy
  • Mortality was 20%, embryonal tumors were detected in 12.5% and neurodevelopment was normal in 75%
  • BWS should be considered in prenatally diagnosed isolated omphaloceles, after exclusion of chromosomal abnormalities
  • This series highlights the importance of expanded molecular analysis for BWS, and long‐ term follow‐up for malignancies and neurodevelopment.

Clinical experience with noninvasive prenatal screening for single gene disorders- ISUOG, Vol 59(1), 33-39, Mohan et al

It is now 10 years since analysis of cell free DNA (cfDNA) in maternal blood was introduced clinically as a highly specific and sensitive screening test for fetal trisomies. In this study, Mohan et al report on clinical experience with NIPT-SGD, which focuses on a specific set of dominantly inherited or de-novo gene variants in 30 genes.

Single-gene disorders (SGD) are present in approximately 1% of births. NIPT-SGD is feasible for a broad range of monogenic disorders and is most straightforward when applied for the detection of dominant conditions with a high de-novo rate OR for paternally inherited dominant gene variants. A currently available NIPT-SGD panel screens for 25 conditions that result from disease-causing variants across 30 genes which have a combined incidence of 1 in 600 (0.17%). The conditions include Noonan spectrum disorders (NSD), skeletal disorders, craniosynostosis syndromes, Cornelia de Lange syndrome (CdLS), Alagille syndrome, tuberous sclerosis, epileptic encephalopathy, SYNGAP1-related intellectual disability, CHARGE syndrome, Sotos syndrome and Rett syndrome.

Diagnostic yield is 5.7% in overall cases taken up in the study and the detection rates are higher in cases tested for fetal long-bone abnormalities (33.7%), fetal craniofacial malformations (28.6%), family history of a disorder included in the panel (15.2%), fetal lymphatic abnormalities (13.3%) and fetal cardiac abnormalities (12.9%).  No false-positive or false-negative results were found in the cases which were followed up which was limited to screen positive cases.

NIPT-SGD is in its earliest stages of development and considerable potential exists to expand its scope through the sequencing of more genes. This study demonstrates the potential value of NIPT-SGD, particularly in cases with abnormal ultrasound findings or with a relevant family history. If implemented correctly with close counselling and monitoring, NIPT-SGD offers a safe and timely prenatal screening option for at risk couples.

Successful completion of the fetal abnormalities online theory course

FMFI fetal abnormalities course

Our much awaited annual event-The Fetal Abnormality Theory Course (FMF UK Approved) made its debut on the digital platform on 6th and 7th Feb,2021.

The course was attended by nearly 250 delegates from all over the country, many of them on their way to get their certificates of competence in the midtrimester fetal scanning.

FMF India team of Rachna Gupta, Akshatha Sharma, Anita Kaul and Rakesh Rai designed, managed and ran the 2 day webinar. GE and astraia software supported the course.

The talks were presented by FMF UK approved renowned senior faculty-Dr Anita Kaul, Dr Prashant Acharya, Dr Gowrishankar Paramsivan, Dr Chinmayee Ratha, Dr Veena Acharya, Dr Tulika Tayal, etc and covered normal and abnormal views in every organ system.

FMF India firmly believes in establishing a standard of care in fetal scanning across the country which will ensure a reduction in paediatric morbidities/disabilities. Going digital has only helped us in reaching out to a larger audience and is a gratifying step in this direction. For more information on upcoming events, become an FMF India member and  keep watching the space at fmfindia.in

The attendees will be given a Theory Certificate (by email, in 10 days). The requirements for FMF UK Certificates of Competence (in Fetal abnormalities) are:

  • Submitting a logbook of images (as mentioned on the FMF UK website) to anomaly@fetalmedicine.org
  • Attending the online Fetal Abnormalities course on FMF UK website.
  • Theory Course Certificate
  • Clearing the Practical Assessment (with an FMF approved Trainer)-This will be possible only once the logbook of images has been approved by FMF UK.

 

 

 

Key takeaways from the FMFI Research webinar on fetal growth and monitoring

Fetal growth and monitoring has always been a subject of tremendous interest
for the obstetricians ,Fetal medicine specialists, neonatologists and not to forget
-the parents!

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Research from various parts of the world has provided  the much needed insight
in this aspect however published work from Indian quarters has always been a
sore point.This is especially when we have some researchers arguing that
growth is ethnicity specific with an equally vociferous disagreement.

We were however fortunate to have Dr Uma Ram and Dr Seneesh KV for the
FMFI Research Webinar on 15.01.21 who have initiated work in this field.

Dr Uma Ram presented her work on how the Diabetic foetuses have increased
subcutaneous fat at the midtrimester scan, predating the clinical diagnosis of
GDM. She also shared that these studies are now being validated as prospective
studies.

An interesting discussion by the chairpersons- Dr S Suresh, Dr Ashok
Khurana and Dr Anita Kaul was whether these findings could be integrated in
an algorithm to initiate early maternal nutrition therapy.

Dr Seneesh showcased his study, prospectively comparing different available
antenatal and postnatal growth charts.

The concluding remarks by the chaipersons emphasised the need of following up every fetus by the
drop/increase in their centiles irrespective of the growth charts that are used. In
addition, multivessel Dopplers added significant value in the decision of
delivery of a fetus that shows declining centiles.

It was a stimulating session and pushed us to think beyond the routine where a
simple additional measurement from a standard fetal plane could potentially
change the course of maternal complications. The hard work put in a
prospective study whilst doing routine clinical work to answer questions that we
come across daily but brush aside due to lack of time was equally invigorating.

We hope to collate many more such research work by Indian authors in the
times to come.

Research, such a necessity – Prof. Kypros Nicolaides

We had the history of Fetal Medicine unfolding in front of our eyes on 23rd October when Prof. Kypros Nicolaides narrated his journey over the past 30 years as part of FMF India’s research webinar series.

He gave a very personalized insight into how he observed patterns and their variations, gathered data , collaborated with like minded people and came up with algorithms for Down Syndrome screening. …and then preeclampsia, preterm births, multiple pregnancy, in utero therapy, non invasive prenatal screening ..and you name it all! His training has raised pioneers across the world and it is no surprise that his team has been at the forefront of investigating and finding solutions for almost every obstetric malady.

We feel proud that we practice evidence based medicine but he is the legend who assembled this evidence. It is his toil, hardwork and exemplary research on which the science of Fetal Medicine is based. When you hear “This one slide in my presentation is hard work of over 25 years” it makes you realise the enormity of it all.

What drives him to spend this time in research? How does he balance work, research and personal life? At the root of it all is the passion to make a difference in women’s obstetric outcome. His innovation in screening strategies using very simple markers and then motivating various research teams on finding solutions have transformed our practice.

Acknowledging the deficiencies in government’s allotment towards research activity, his charity- Fetal Medicine Foundation has donated 45 million pounds towards research in this field. He believes India has the potential and his parting words for us were “For India, the answer is collaborative research”.

Thanks to Anita Kaul for conceptualising FMF India’s Research webinar series and bringing her much beloved Professor, mentor, Kypros Nicolaides to share his passion and zeal for research and inspire others to understand why Research is such a necessity and not a luxury.

Key takeaways from the FMFI webinar on Rh isoimmunization

 – 25th September 2020.

FMFI Webinar on Rh Isoimmunization

  1. 1. Whichever lab is used for titration of Rh antibody titres, once ICT comes positive, check whether the titres are verified by Tube agglutination method rather than column method.
    Most labs have facilities for both but prefer to do the initial screening on the column method. An antibody screening panel test should be done straight away.
    Best would be that as soon as ICT comes positive to refer to a fetal medicine unit
  2. 2. The follow -up for ICT positive women is 2 weekly scans in a fetal medicine unit for MCA PSV.
    The follow-up for Rh negative, but ICT negative is ICT blood checks every 4 weeks from 20 weeks onwards, apart from the booking bloods ICT . This will avoid late referrals for blood transfusion when the fetus is already in heart failure.
  3. 3. Timing of subsequent transfusion after the initial in utero transfusion will be monitored by the cut-off of MCA PSV >1.5 MoM or rate of fall of hematocrit. Increasing the threshold to 1.69 MoMs (as suggested by a few papers) will miss a significant number of anaemic fetuses.
  4. 4. A lot of cases of isoimmunization happen even in women who have received prophylactic Anti-D injections. This could be secondary to inadequate doses, incorrect timing of prophylactic doses or faulty storage.
  5. 5. All Rh negative women who are ICT negative at 28 weeks, should receive full dose prophylaxis between 28-30 weeks and then at delivery in Rh positive babies.
  6. 6. Ideally a Kleihauer -Betke should be checked post delivery and additional doses be given if feto-maternal haemorrhage is deemed to be beyond the neutralization effects of the standard dose.
  7. 7. In peripheral areas, please check that your supplier has maintained the cold chain for Anti-D procurement and storage.

3rd Mastercourse in Neurosonography

Date: 25th & 26th April 2020
Venue: Auditorium, Indraprastha Apollo Hospitals, New Delhi

Faculty
karina
Dr. Karina Krajden Haratz
Specialist in Fetal Medicine and Fetal Neuroimaging,
Senior Consultant at the ObGyn US Unit – Lis Maternity Hospital – Tel Aviv Medical Center, Israel.
Researcher and Lecturer affiliated to the Tel Aviv University.

Target audience
Sonologists and Fetal Medicine practitioners, ObGyn Ultrasound consultants (max 20 delegates for hands-on)

Objectives
A unique 2-day intensive learning experience on Fetal Neurosonography focused on the exam technique and definition of normal imaging patterns: Hands-on training, dedicated time with expert, state-of-the art lectures, 3D practice with real-case volumes.

Programme schedule
Day 1
TIME TOPIC
8:00 Registration and opening
8:30 Physical aspects and presets for better imaging the fetal CNS
09:15 Technical aspects of the Neurosonographic exam
10:00 Neurosonoembryology
10:45 Coffee break
11:15 The lateral ventricles: developmental sonoanatomy and work-up in ventriculomegaly
12:15 Developmental sonoanatomy of the anterior complex and the CC and abnormal imaging patterns
13:45 Lunch
14:45 Live scan 1
15:15 Group hands-on training
Day 2
TIME TOPIC
8:00 Developmental sonoanatomy of midbrain-hindbrain structures and the differential diagnosis of MB-HB anomalies
09:30 3D neurosonography – tips and tricks
10:15 Coffee break
10:45 The fetal brain parenchyma and cortex – normal development and patterns of disease
12:00 The brain vasculature and congenital vascular malformations.
13:00 Lunch
14:00 Live scan 2
15:00 Alternate groups – hands on / 3D practice

 
Registration Fees :

  • 32000 INR for theory with hands-on practical
  • 17000 INR for only theory

*Delegates appearing for practical session need to submit documents of their degree, med council reg and affidavit.

PAYMENT OPTIONS:

1. Bank Transfer to A/c No: 03192560004661; HDFC Bank, South Extension Branch, New Delhi; IFSC Code: HDFC0000319
2. Post Cheque in favour of “Fetal Medicine Foundation,India” to:
Apollo Centre for Fetal Medicine,
Gate No:7, Indraprastha Apollo Hospitals , Sarita Vihar, New Delhi,110044

For Programme Queries, Contact:
Dr Rachna Gupta, General Secretary: 09899294499
Dr Akshatha Sharma, Programme Coordinator : 09891494545
Dr Anita Kaul : 9811100511 anita_kaul@apollohospitalsdelhi.com

For Registration, PCPNDT, Payment details, Contact:
Himanshi: 09560127575, 011-29873018, 011-29873056 or write to fetalmedicine@apollodelhi.com