 Hello everybody, I am Dr. Avni Skandal, lead consultant and head of radiology and equality chief at ASTEMM Scottical. I am also involved in a lot of academic activities and currently the faculty of Indian radiologist. Today I am going to be speaking about gestational trophoplastic disease, primarily the role of ultrasound in identifying, differentiating and prognosticating gestational trophoplastic disease. Gestational trophoplastic disease, I am primarily going to be talking about the ultrasound part of it. It is a pregnancy related disorder due to abnormal trophoblastic proliferation ranging from the benign to the malignant spectrum. The benign end or the pre malignant variety comprises of 80% bulk which is a complete hydratative form mold, the partial hydratative form mold and the lesser known one, the co-existent complete mold with a live fetus. The other end of the spectrum is a gestational trophoblastic newplacia which is the malignant end which has invasive mold and the dreaded coreocarsinoma. The rarer known ones are the placental site trophoblastic tumor and the epithelioid trophoblastic tumor. For these disease we need to utilize a multifactorial approach where we use the clinical features, lab parameters and imaging. It is basically arising due to an error of fertilization. A sperm or the sperms are fertilizing an empty ovum in the case of a complete mold and gives rise to a deployed chromosomal pattern while in partial mold the sperms fertilize a normal ovum giving a triploid chromosomal pattern. In the complete mold there is an absence of the fetus. In partial mold either there is an abnormal fetus or the fetal demise occurs and this most often gets missed and is diagnosed only when the pathology is done. There is a lesser known variety which is a co-existent normal fetus with complete hydratative form mold in which you have a molar gestation in one pregnancy and the other site shows a normal fetus and placenta. So tackling it individually when we come at a complete molar pregnancy we classically see an enlarged uterus which is disproportionate to the size of the expected gestation age and you see uniformly distributed cystic spaces. They give the classical appearance of a snowstorm or bunch of grapes. The most classical finding here is there is an absence of the fetal paths. These lesions can be vascular and when you see a high vascularity there these areas show a high velocity and low impedance flow the resistance being as low as less than 0.5. When we come to the partial molar pregnancy the most important differentiating feature here is you can see a gestation sac or a fetus. When you see a gestation sac it can be an an embryonic pregnancy with no yolk sac or fetal paths. It can be a sac which is empty with just echoes or septations or it can have fetus which is abnormal, growth retarded, dead or a live fetus with hydropic degeneration. Another classical finding that we have to look for is that the placenta is enlarged or the dacetyl reaction that you see will have small cystic areas giving the classical sous-chise pattern but this may often be missed. One finding that has been described in certain studies is that there can be an elongated gestational sac where the ratio of transfers to the antroposterior dimension is greater than 1.5 and we have to keep a lookout for the cystic spaces in the placenta and the dacetyl reaction. These fetus also tend to occur tend to be associated with oligo hydrangeas. This is a spectrum of the various appearances that we can see. In the early pregnancy with a small fetal pole we can see the cystic spaces in the placenta and similar appearance with placenta showing cystic spaces as seen in the rest of the images and the image at the bottom we can see that there is hydropic degeneration of the fetus also seen. Because of the high level of beta Hcg in these cases, these cases most often end up being associated with bilateral thica-lutein cysts which is basically the same principle as ovarian hyperstimulation. The rarer one which we mentioned earlier is a complete molar pregnancy which is coexisting with a normal fetus. This is most often seen with patients who are undergoing infertility treatment and it is very complex and challenging to manage these patients because there is no clear guidance or no clear consensus of how to manage these patients. There is a high propensity for these patients to develop complications in the fetus and in the mother. These fetuses are at a high risk of malformation. So the pregnancy tends to have severe complications like preeclampsia. It is very important to assess the placenta so the severe sampling needs to be done to ascertain that this is not a case of partial moan. Even following the delivery of the child a placental examination to rule out coriocarcinoma needs to be done and the mother needs to be followed up with a beta-HCG follow up following the delivery. Continuation of the pregnancy needs to be done after discussing all the pros and cons with the parents and it should be with respecting the patient's choice. However, the patient needs to be counseled well after telling them all the pros and cons and giving them the choice of continuing the pregnancy ascertaining that they understand the importance of a proper antenatal surveillance and these patients should not be lost to follow. The best way of managing these patients is by us demonstrating a twin peak sign which shows us that this is two discrete pregnancies. There are two discrete amniotic sacs and two discrete corions. So one which is containing a normal pregnancy with a normal placenta and the other one which is having a molar gestation and these patients need to be closely followed up. The differences for these appearances can be varied like placental misincamal dysplasia which is rare. However, there is a lack of the high velocity flow that we see in the molar pregnancy. Also these babies tend to have a normal carotide. Subchlorionic hematoma is something that we come across often but we need to bear in mind that when we are looking at these patients we need to bear in mind if there is any atypical features we need to be considering a molar pregnancy also. Placental coriandrioma is relatively rare. However, we need to bear in mind the similar kind of appearance that can occur and in both all these cases the beta and cg levels will be normal. That is why we have to utilize a multifactorial approach. Next coming to the invasive mole. It is locally invasive so you have to look at the features when you see this heterogeneous cystic areas we have to ascertain that it is not invading the myometrium. We have to look for focal myometrial thinning, look for the margins of the lesions that we are seeing and ascertain that the flow is not invading into the myometrium. Again, there will be a high velocity and low impedance flow seen in these cases also. So, whenever we come across gestational trophoblastic disease we have to look for features of myometrial invasion. Utrein koryocarsenomas is when it is going beyond just the invasive mole where it is going just beyond invading the utrient myometrium. It is going beyond the boundaries of the uterus. This is the most dreaded complication that we see. You can have the gestational and the non-gestational variety. Gestational variety is seen in the childbearing age within one year of an antecedent pregnancy. The non-gestational koryocarsenoma is seen at a later age and it is considered to be rarer and these can occur following complete mole, normal pregnancies, spontaneous abortion or even ectopic pregnancy. The findings can be again it can mimic any of the above mentioned features. It is just basically a heterogeneous hypo-hypercoic mass. Most often it is having a vascular periphery and central tends to be a vascular. On MRI we can demonstrate it to be an infiltrative mass with heterogeneous areas because of necrosis and hemorrhage and the invasion can be demonstrated very well. Chest x-ray and CT thorax needs to be done in these cases to ascertain that there is no pulmonary metastasis which is where the first metastasis is to. Further a whole body CT or MRI or a PET scan can be done to ascertain there are no other metastatic lesions in the liver or elsewhere. Brain MRI or CT also shows us classical cerebral or meningeal metastasis. This is one of those cases where we tend to get hemorrhagic metastasis in the brain. Uterine artery Doppler though many people don't utilize it a lot, it helps us differentiate different types of a gestational trophoblastic disease. There is a lot of studies that have been conducted for this. In a normal pregnancy we tend to have a low velocity high resistance flow in the uterine arteries in the first and the second trimesters. However in gestational trophoblastic disease we see the right reverse pattern. It tends to show a high velocity and a low resistance flow. And the way to differentiate it is in uterine artery RI during the normal pregnancy tends to be the range of 0.6. 0.66 is the average given as per the studies by Zohu Ital. In complete and the partial mold the range of the uterine artery RI tends to be in the range of 0.55, 0.56 while if it is a malignant one the resistance is very low as low as 0.25 to 0.3. So make sure when we see a gestational trophoblastic disease we look at the uterine artery waveform and the values. Then we have the rarer placental site trophoblastic tumor in which the petylcogen tends not to be so high because of lack of syncytropoblastic tissue in that. It tends to have a human placental lactogen level which is high. This again does not have a very classical appearance. It tends to have a heterogeneous endo miameter mass which is a very nonspecific one with a junctional zone which gets disrupted. The variable course of this disease can occur. It can be benign and response to chemotherapy is much less as compared to the rest of the gestational trophoblastic disease. Then we have the other rare variety which is epithelioid trophoblastic tumor. Again this is a very well-defined lesion which has a peripheral vascularity which is considered to be pretty classical for it and serum beta acetylcogen levels are high for this patient. It is very difficult to predict the course. It can be a benign in nature. However, there can be a chance that this can metastasize also. So, commonly what is done is when we follow a molar pregnancy after evacuation, we need to follow it up when we find that we are working it up post molar chose gestational trophoblastic neoplasia needs to be worked up with a pelvic ultrasound or MRI and a chest x-ray because we said that the lung lesions or the lung metastasis is the most common. If you see there is no metastasis to the lung, you need to do no further imaging. But if you see that it is metastasing to the lung, you need a complete workup. So, CT abdomen with arterial phase is important because arterial phase is where these lesions enhance and brain MRI needs to be done. The same workup needs to be done for the non molar gestational trophoblastic neoplasia also. So, basically in this cumbersome slide what we need to know for sure is when we are looking at the pelvic ultrasound of the gestational trophoblastic neoplasia, what we need to mention is the location of the mass, whether it is endometrial, miometrial, invading or not, size of the lesion and command on the uterine artery, resistive index and the pulsatality index. You can have a rare presentation of an ectopic molar pregnancy. There is no way we can differentiate it by imaging. On MRI, you might be able to see numerous signal voids, but there is no way you can tell it. There is a high propensity for these lesions to rupture and it is going to be managed just as a normal gestational trophoblastic neoplasia. There is also an important role that uterine artery PI plays to predict a methotrexate resistance. PI of the uterine artery as per many studies has been found to be an indirect measure of the functional vasculature of the tumor and it is considered as an independent predictor of the resistance to chemotherapy. Even if you use Figo scoring of resistance to chemotherapy, even then despite using that scoring, this is considered as an independent predictor and a uterine artery PI of less than or equal to 1 suggests that there is an increased risk of methotrexate resistance. So, we have to make a note of uterine artery RI and PI also. The other things that we need to look for when we are looking for the in these patients is development of a uterine artery uterine arteriovenous malformation. Normally, these patients only undergo a beta HCG surveillance. Imaging is not routinely needed unless we are expecting some complications and when we are doing an imaging follow-up, what do we look for? An echogenic lesion tends to become anechoic, the size tends to reduce, vascularity reduces, the endometrial thickness comes down less than 10 millimeters. The similar changes can also be seen in MRI and the zonal anatomy comes back to normal. So, to conclude, it is a complex spectrum of disorders. It does not have any classical imaging finding unless you see the snowstorm appearance or those kind of very classical cystic changes. It is not having a very classical appearance in any of the other spectrums. So, we have to keep our eyes and mind open for it. Ultrasonic is the initial evaluation for the gestational trophoblastic disease and it is also used to assess residual or recurrent disease. CT is used for staging. MRI is good for local extent and also for the cerebral metastasis. Embalization is done to manage complications such as formation of AVMs. If we are aware of things, we will be able to tackle it better. So, keep your mind open for the spectrum of the appearances that can occur and we would be able to pick this up at a much earlier stage and do better to the patient. Thank you.