 Hello, everyone. I'm Dr. Sonil Kalwani, third-year resident in Holy Spirit Hospital, Mumbai. I'm presenting a rare obstetric case report. A bunch of grapes always mowl, let's say. A 29-year-old female, Prami Gravada with spontaneous conception, was referred to ultrasound department in Holy Spirit Hospital for routine ultrasound at 27 weeks of gestation. She had no complaint of bleeding per vagina, no pain in the abdomen, no comorbidities. Her routine hematological and biochemical parameters were within normal limits. The NIPT reveals low risk for eneuploidies, serum alpha-fetoprotein and beta-SCGs were mildly high. Ultrasonic ultrasound done at 27.3 weeks reveals a single viable fetus, which was corresponding to the age of gestation. The placenta was unusually thickened, extending from funders, inferiorly completely covering the ores, suggestive of placenta previa. The maximum thickness of placenta was approximately 8.9 centimetre. The placenta showed multiple varying size and equi-cystic lesions within. On colour Doppler, there was mild peripheral vascularity. So, the first differential which came into our mind was the partial mola pregnancy because of the snowstorm appearance of the multi-cystic lesions. But the fetus was corresponding to the age of gestation. There was no gross structural anomaly noted in the fetus. The beta-SCG which was done prior was not unusually or moderately on the higher side. Therefore, the second differential which we considered was the diabetes, but the blood sugar were normal. And the rare differential which we considered was the placenta mesenchymal dysplasia, which has a similar ultrasound appearance, that is the placenta migale with multi-cystic lesions, and the alpha-fetoprotein done was also mildly raised. So, we advised patient for repeat beta-SCG and carotyping to rule out the partial mola pregnancy. However, because of some cost issues, the carotyping was not done and the beta-SCG came out to be mildly high. So, we went retrospectively and saw the few initial ultrasoundography which were done elsewhere. So, the first time is to reveal single-life intrauterine fetus with optimal cardiac activity. NLNB scan was normal, there was no gross anomaly. At 18.3 weeks, level 2 was done and the placenta appeared thickened that time and was completely covering the internal ores, but no fetal anomalies were detected. Now, the ultrasound repeated in our department after 2 weeks at 29.5 weeks revealed progressive increase in the thickness of the placenta to approximately 9.8 to 10 centimeter and the planes between the placenta and the myometriums were preserved. There was no myometrial invasions. These findings were more inclined, we were inclined towards the placental mesenchymal dysplasia but now the fetus started showing early growth lag which can be seen in the trending graphs. The ultrasound done after 2 weeks at 31 weeks reveals diffusely thickened placenta with further progressive increase in the maximum diameter to 11.9 to 12 centimeter. But the Doppler study now shows reduced diastolic flow in the umbilical artery which was reaching the baseline without any absence or reversal. Suggestive of mild to moderate fetal placental insufficiency, the PI was 1.5. The fetal weight was less than 5 percentile with interval growth lag of 2 weeks. Suggestive of intrauterine growth restriction. After 2 days, this female with IOGR, fetal placental insufficiency, placenta previa with placenta migale and multi cystic lesion presented with heavy bleeding and was admitted for emergency LSEs. The LSEs was done under general anesthesia, female baby was delivered, placenta and membranes delivered completely, placenta was edematous, weighed around 1300 grams and found to have multiple cysts. So these are the gross image of the placenta. The left hand side is the fetal surface and the right hand side is the maternal surface and as we can see there are multiple cysts seen within the placenta. So to summarize from 27 till 31st week, the placental thickness was progressively increasing from 8.9 to 12 centimeter, leica was decreasing from 16 to 10 to 9 and the Doppler findings were initially normal and at 31 week it showed mild to moderate fetal placental insufficiency. Initially there was a satisfactory interval growth lag but then there was a early growth lag with a 2 weeks of growth lag seen till 31st weeks. Fetal weight went down to less than 4 percentile. The placenta was sent for histopathological examination and it revealed no trophoblastic proliferation, scaloping or stromal trophoblastic inclusion and there was a vascular and hydropic villi, fibrin deposition and thrombus, a vascular polyangiometous area therefore suggestive of placental mesenchymal dysplasia. So this is the radiological image of the PMD, the gross image and the histopathological image. So the placental mesenchymal dysplasia is characterized by varying expression of placenta and eurythmally dilated corionic plate vessels, thrombosis of the dilated vessels and large grape like vesicles within the placenta. These appearances may mimic molar pregnancy on ultrasound and on initial gross placental examination following delivery. Placental mesenchymal dysplasia should be considered important differential diagnosis in cases of placenta migale with multi-cystic placental lesions. This is often an under-diagnosed and under-reported case because of the lack of awareness but it has been documented in more in the female fetuses with a ratio of 3.5 is to 1. As we can see in our case also the female fetus was delivered. The outcome of the fetus is variable completely from normal fetus to an increased risk of IOGR which was seen in our case still fetal demise, lack of high velocity signal inside the lesion and a normal k-aryotype favor the diagnosis of PMD. PMD must be differentiated from gestational trophoblastic disease because the management at the outcome before. In contrast to molar pregnancy, the PMD can be associated with normal life-worth as I mentioned associated with fetal growth restriction even macrosomia due to an association with a syndrome called back-with-widman syndrome. Fetal tumors mostly hamatomas, antipartum fetal death and maternal complications especially preecremia. But the definitive diagnosis relies on the histological features including the mesenchymal hyperplasia, edema of the stem cell villi, dilated stem vessels with thickened vasculature and the absence of trophoblastic hyperplasia. Few differential diagnosis of PMD would be partial molar pregnancy, hydropic degeneration of placenta, complete hydriform mole with co-existent fetus, placental infarcts, choreoengeoma, subchoreonic hematoma and spontaneous abortion with hydropic changes. My take-home message would be, bunch of grapes are not always small and placenta is a very vital and important organ of the obstetric examination. We try to focus more on the fetus and the fetus anomaly but a healthy placenta will give a successful pregnancy. These are my few references. Thank you and have a nice day.