 Good morning everyone. I am Dr. Rupali Bansalpareek, fellow under Dr. Hemangini Thakkarman at KAM Hospital and my topic is complex anomalies of the body wall. Are they that complex after all? My aim is to explain by examples the definition and classification of complex body wall anomalies which is not a very well understood topic. I will be presenting four rare cases of body stock anomalies. My first case is that of a 23-year-old primary gravita who came for a routine scan at 17 weeks. The scan showed a closed neural tube defect arising from the lumbo-sacral spine, sacral agenesis and a cyst within cyst appearance that is a myelocystal cell. Liver gallbladder and few bowel loops were seen outside in a herniated sac. One kidney was not seen and one was hydronephrotic with paper thinning of its parankaima. Urinary bladder could not be identified, severe oligohydraminous was seen, bilateral club feet were also seen. This in a loop shows a very short umbilical cord, actually almost no cord was seen at all. On termination of pregnancy, the abortus showed the closed neural tube defect, the anterior abdominal wall defect and the herniated contents which included liver and bowel loops. Bilateral club feet were also seen, anal swinger was not seen, also no external genitalia was seen except for two small nubbin structures on either side. This is the edge of placenta which was seen directly flushed with the fetus with no evidence of any visible umbilical cord. Abortus ultrasound confirmed the findings of unilateral renal agenesis and controlateral hydronephrotic kidney and a myelocystocene. Final diagnosis was given as body stock anomaly type 4 along with exostrophy of cloaca. My second case is that of a 22 year old primie who came for an NTNB scan. The scan showed an 11 weeks 4 days old fetus lying continuously in the star gazing position. The spine appeared short in length, the cervical part of the spine appeared absent or deficient. There was an occipital encephalosil with herniation of posterior fossa structures, the subcutaneous tissue was thickened posteriorly. This in a loop shows the encephalosil along with the cystic hygroma. This in a loop shows the fetus stuck anteriorly to the placenta resulting in inadequate visualisation of the thoracobdominal area. Also we can see the scoliothic spine. We gave the final diagnosis as Indian kefali abortus and the parents went ahead with an MTP. Post delivery, our findings of a short spine with deficient cervical spine were confirmed. Myeloscisis was also seen at the cervical level. Abortus also showed a short umbilical cord and thoracobdomino scises, a finding that we had missed antinatally. Abortus radiograph confirmed our findings. Final diagnosis after seeing the abortus was then changed to body stock anomaly type 6. The third case is that of a 29 year old G2P1L1 who came with 16 weeks of amenorrhea for her malphoscan. A large defect with herniation of bowel loops and entrolitis was seen, herniation of liver and gallbladder, bilateral club feet, kyphoscoleotic deformity of the spine with a closed neural tube defect, terminal visceral organs appeared unformed likely suggestive of inelotrisia or cloacal malformation, genital organs and bilateral kidneys could not be appreciated, severe oligohydraminus was noted. This in a loop shows the fetus stuck anteriorly to the placenta, kyphoscoleosis, neural tube defect, abdomino scises and that's the club foot with an extremely short cut seen in the image above. On MTP the abortus showed bilateral club feet, a large umfalocele, a short umbilical cord, abscent anal complex and external genitalia, severe kyphoscoleosis and a closed neural tube defect. On ultrasound of the abortus severe kyphoscoleosis and closed neural tube defect were confirmed. The large umfalocele showed herniation of liver, spleen, gallbladder, bowel loops as well as urinary bladder, while intra-abdominal contents included normal bilateral kidneys. Final diagnosis was given as body shock anomaly type 4, we didn't think it was a case of cloacal exostrophy as both kidneys were intra-abdominal and normal. Case 4 was one which honestly took us all by complete surprise. A 30-year-old G2A1 came for her first scan at 19 weeks of amenorrhea, kyphoscoleosis with closed neural tube defect was seen, a large abdominal wall defect with bowel loops and free fluid within the sac was seen, severe oligohydraminos, a midline inter hemispheric cyst which we reported as corpus callosum dysgenesis, echogenic bilateral kidneys and only one foot was seen which showed clubfoot. Hypotelidism was also noted, however the orientation of the pharx versus the orientation of the face was not corresponding. Nevertheless, in view of neural tube defect, abdominal wall defect, one clubfoot and likely some craniofacial anomaly diagnosis of body shock anomaly was given. Post delivery we were surprised that this was a case of con joint twins that is craniotoracob domino pegas along with body shock anomaly. Here we can see the short cord, omfalocelan both, no anal complex in either along with unformed nexonal genitalia, bilateral club feet and both the fetus. This in a loop shows the abotus and here we can see the full body radiograph of the same. Abotus ultrasonic drivel kyphus calliosis and a closed neural tube defect in both the twins. There were two livers, two gallbladders both intraabdominal, while bowel loops in both twins had herniated out. We could see a total of three lungs along with a single heart. This in a loop shows the first twin cerebellum, cerebel peduncle, thalamine, common third ventricle and the second twins thalamine, cerebel peduncle and cerebellum. Here we can see the lateral ventricles of both the twins and here we can see the cerebellum of both the twins. There were four ecogenic kidneys with no obvious CMD which probably explained the severe oligo hydrimenose. Final diagnosis was given as body stock anomaly type 4 in a case of con joint twins. Body stock anomaly includes three obligatory components that is a body wall anomaly, abdominals kaisis or thoracobdominos kaisis, a spinal anomaly and an umbilical cord anomaly and two accessory components that is a structural or non-structural limb defect and anal genital or urinary defect. Lim body wall complex has two obligatory components, limb and body wall. A third component may or may not be same that is craniofacial anomalies. Actually limb body wall can just be classified as a subset of body stock anomalies but since craniofacial anomalies are additional some people consider it a different entity. OEIS complex on the other hand has all the features of BSA except short chord hence some consider it a subset. However as an obligatory criteria of BSA is not met it should not be considered in the same spectrum. Pathogenesis includes three theories the vascular disruption, the early amniol rupture and the disturbance in embryonic folding. Incidents of BSA anomalies is between 1 per 14,000 to 1 per 31,000. They are not associated with chromosomal anomalies, have no specific gender predilection, no increased risk of recurrence in X pregnancy and are invariably fatal. So I ask again complex anomalies of the body wall are they that complex after all? No they are not. As long as you have checked for all the obligatory and accessory criteria and the classification is in its place this seemingly complicated topic can also be made easy. Another thing to remember is that this is a first trimester or early second trimester diagnosis as an MTP is absolutely essential in these cases. These are my references. Thank you.