 A very good afternoon to all the viewers. I Doctor Brigadier Ashok Saxena, HOD Neonatology Manipal Hospital, welcome you to this webinar on RH isomanized baby. It was a very interesting case and very remarkable for a couple of things. One, that it happened. It happened in a multi-gravity. It happened in a book and supervised pregnancy. And surprisingly and sadly, the place where the baby was born did not have the basic pediatric facilities. Now, without much ado, I would straight away go to the presentation part. The other presentation would be the case presentation by Dr. Gyanam, who's our specialist in pediatrics, followed by the endonatal management of an RH isomanized baby by Dr. Gitanjali Bahel, who's our fetal medicine specialist. And finally, I would speak about the neonatal management, conclude and take all the questions if there are any. So over to Dr. Gyanam Bhushra. A very good afternoon, everyone. I'm Dr. Gyanam Bhushra, a specialist in pediatrics, working in Manipal Hospital. So I was a newborn who presented to our ER on IPPR with bag and tube ventilation at 10 hours of life. The baby was a boy who was born on 15th of April, 2020 at 8.23 a.m. at 38 weeks of gestation by normal vaginal delivery in a private nursing home at Churchill. The Lycorvus meconium stain, the baby cried at birth and the birth weight was 3.37 kg. The baby was vaccinated and injection vitamin K was given at birth. The baby was then referred to another center because of non-availability of pediatrician in that center as the baby was a high risk and had RH isomanization. The total serum bilirupin at five hours of life was seven milligram per deciliter. In the second center, he was intubated in view of poor breathing efforts and was referred to our hospital. The mother was a 35-year-old multigravida. The couple was married for 13 years. She was gravita six para-three and had two abortions. Her first issue was MTP at five and a half months of gestation for congenital anomaly which was a neural tube defect. Her second issue was a spontaneous abortion at two and a half months of gestation. Her third issue is an eight-year-old girl child who was born by normal vaginal delivery. There was no history of any jaundice in neonatal period and her blood group was depositive. Her fourth issue was a six-year-old boy who was born by normal vaginal delivery. This boy had jaundice after birth. Exchange transfusion was done on day four and day five of life at a medical college in Rohtak. This baby developed connectorous and later on developed dystonic cerebral palsy. Now this child is undergoing treatment at all in the Institute of Medical Sciences. His blood group was also depositive. Her fifth issue was a two-and-a-half-year-old girl who was born by a normal vaginal delivery. There was no jaundice in the neonatal period and her blood group was B-negative. And the sixth issue was our patient. The LMP was on 22nd of July 2019. Her EDD was 27th of April 2020. She was booked at a private hospital in Sonipur. She took folic acid in first trimester, was given dipnestoxide, and iron and folic acid tablets and calcium was started from second trimester onwards. Utter sound was done at 14 weeks and 19 weeks and were normal. Her quadruple macobus negative. In her investigations, hemoglobin was 10.6. RBS and TSH were normal. Her blood group was B-negative. Viral markers were normal. Indirect foams tests were positive. In torch panel, IgM was negative, and IgG was positive for CMV and Rubella. In examination of our baby, in general examination, the heart rate was 110. CRT was less than three seconds. BP was 65 by 40, mean BP 50. Respiratory rate was 40 per minute on ventilator. Temperature was 36.4, Ecterus was present, and Cibiopella was present. In systemic examination, in chest bilateral entry was equal. In cardiovascular system, normal heart sounds with a hypodynamic precordia, and there were no more. In abdominal examination, abdomen was soft. Liver was five centimeter below the right cluster margin, and spleen was also five centimeter below the cluster margin. In CNS examination, the baby was lethargic and hypotonic. At admission, the RBS was 46 milligrams per deciliter, and other irreinvestigations were sent after two hours of intensive phototherapy and stabilization of the baby. The total lymphocyte count was 1 lakh. Neutrophils were 9.8%. Lymphocyte was 78.3%. Hemoglobin was 6.4%, and platelet was 1 lakh 20,000. CRP was negative. In venous blood gas, PH was 7.34%. PCO2 was 34.7%. TO2 was 41%. Bicarbonate was 18.6%. Mother's blood group was B negative. Mother's indirect wounds test was positive. Baby's blood group was B positive, and direct wounds test was also positive. The total serum will rubin was 9.6 at around 11 hours of birth. Direct billy rubin was 3.3%. So our diagnosis was a 10-hour-old term boy appropriate for gestational age with severe anemia, jaundice, and cephalopathy, hepatosplenomegaly due to RH ISO immunization. Initial treatment was started with mechanical ventilation with initial settings of SIMV mode, FiO2 of 100%, respiratory rate of 40, PIP of 20, and PPO5. 10% dextrose was given in view of hypoglycemia. Intensive phototropy was started. Packed RBC transfusion was started in view of severe anemia. IVIG first dose was given. Injection phenobarbitone was started as the baby had subtle seizures. IV antibiotics, injection calcium, gluconate, and IV fluids were also started. In subsequent investigations, the total serum will rubin levels at 11 hours of life at the time of admission was 9.6, which gradually increased to 14.6 by 34 hours of life and then gradually decreased to 6.8 by day 7 of life after management. The hemoglobin at the time of admission was 6.4 after which a packed RBC was given which the hemoglobin transiently increased to 11 but again dropped down to 9.1 when again a packed RBC was given. The baby was discharged with a hemoglobin of 10.6 on day 8 of life. Initial total leukocyte count was 1 lakh which was most probably because of the nucleated RBCs which gradually decreased down to 7.230 by the time of discharge. The baby also had thrombocytopenia. Initial leukocyte count was 1 lakh 20,000 which was decreased to around 85,000 by the time of discharge. So plotting the total serum bilirupin levels on the butanese chart, the bilirupin levels fall above 95th percentile suggesting that this baby was at increased risk. The bilirupin levels were also plotted on the graph for guidelines of phototherapy in hospitalised impents. Our reference line was the middle line because this infant was at medium risk 38 weeks of gestation which with RH incompatibility. So definitely the bilirupin levels were above the reference line suggesting this baby required phototherapy. We also plotted the bilirupin levels of the baby chart for guidelines of exchange transfusion in hospitalised impents. The bilirupin levels, our reference line was again the middle line which is for medium risk more than 38 weeks and risk factors but the bilirupin levels in our case did not reach the middle line. Other investigations that we did were a peripheral smear in which RBCs were normal cytoknomal criming, WBCs were within normal range, platelets were less than 18. Blood culture showed no growth. Urine RM was also within normal limits. In LFT, STOT was 107, STPT was 38, alkaline phosphatase was 198 and albumin was 3.4, TSH was 12.2. The chest X-ray was also within normal limits. During the course of stay, the sensorium of the baby improved by 30 hours of life and there were no further seizures. We were able to wean off the baby from mechanical ventilator by 60 hours of life. Intensive phototherapy was given for 5 days. During intensive phototherapy, the baby had high colour urine which the colour turned out to be normal after discontinuing phototherapy after 24 hours. Packed RBC transfusion was given at 16 hours of life and then again at 42 hours of life. We gave two doses of IVIG, one at admission and one at 38 hours of life. Phenobarbitone was given for a total of 7 days. IV antibiotics were given for 7 days. Injection calcium gluconate for 72 hours and tube feeding was initiated on D3 of life and gradually increased to full speeds. The baby was finally discharged on exclusive breastfeeding. This is the picture of the phototherapy, the baby who is getting phototherapy, intensive phototherapy. The baby came for follow-up at 2 months of age. The baby was on exclusive breastfeeding and was vaccinated at one and a half months of age. The urine and stool colour were normal. In anthropometry, weight was 4.45 kg and all length and head circumference were within normal limits. Also on examination, the spleen and liver had also regressed in size. In neurodevelopmental examination, according to the mother, the baby turns the head towards down and has developed social smile. The baby had a normal amulticin with normal passive tone, normal head control and there was no obligate 80 an hour. The hemoglobin was 9.5, total serum bilirubin was 0.4, OE was normal and various plant at 3 months of age. Currently, the baby is on exclusive breastfeeding, vitamin B3, D3 and iron drops. So here is the picture of our little patient with this mother. Thank you. Now, I would request Dr. Gitanjali, a fetal medicine expert, to give her presentation on antinatal management, which we think is absolutely important to ensure that such cases are firstly prevented. That means the solution lies in prevention of arish isomanization. Secondly, to diagnose early and if possible to treat while in utero to plan delivery. There are many aspects to it. I think she would be the best person to talk about it. So to over to Dr. Gitanjali. So when the arish negative mother carries arish positive fetals, so due to fetal methanol hamperage, few of the fetal RBC, they can cross the placenta and they reach into the methanol circulation and they can stimulate the immune system of the mother. So immune system will start forming antibodies. These antibodies they can cross the placenta and enter into the fetal circulation. They will cover the fetal RBCs and these antibody rotator RBCs then they will remove by the fetal reticulitis system by the process of semolysis. So this is actually the natural course of disease of arish isomanization. So because of this semolysis there will be fetal anemia and hypoxia. So compensatory mechanism will start working. There will be extra medullary retropoiesis. So it will lead to the pregnancy of regalia and hypoxia dysfunction, hypoproteinemia. There will be collection of fluid in the different body cavities like ural effusion, pericardial effusion, acytase and hydrox. And if it will not get correct then there are chances of interurban fetal demise like in our case. So this is actually I want to share optical history of this mother. She is actually in para-4, life-4, A2 and according to her she has received injection entity in all her pregnancies. So the first one was termination of pregnancy and 5 and a half month of gestation due to neurodiphex. Second one again it was coordination abortion and because she received injection entity it is a good policy. We should prescribe injection entity after abortion and proper pregnancy or any other antenatal invasive procedure. So liberal use of injection entity is the reason for declining trend of RHI so immunization nowadays. Third one was normal pregnancy. The fourth one actually now this is very important in fourth pregnancy the baby was showing the features of hemolytic disease and received injection entity to also develop connectress and later distorted CP. So that means it is actually a isomanized pregnancy develop complications. So Kishan may raise although she has received injection entity in previous pregnancy but now again this pregnancy is affected pregnancy. The reason could be a large pitot methanol handish which may not get neutralized by the standard rules of injection entity. The next one again it is actually an unaffected pregnancy so reason behind this is actually the gyrosity of the father whether the father is homogenous or retrogynous because in homogenous father all the children will be RHI positive while in the retrogynous father few of the children may be RHI negative. So it is true for our case the female we have actually noted that the blood group of this female was RHI negative so that was the reason of his pregnancy. Now since the pregnancy the case which we are discussing here again showing the features of hemolytic disease so now actually is very sad patient is already having a history of unaffected baby again she was not managed well in her any later period. So all these complications were preventable but because of lack of that obstetrical care she developed all these things so actually now how to manage RHI negative pregnancy. So whenever a patient come to us in her first RHI negative mother in her first time it will visit only we should advise her in direct group test in respect of her pregnancy whether she is pregnant or a multi who has received injection entity. So we should advise activity if it is negative and husband is positive in that case we should follow the pregnancy at 28 weeks we should administer injection entity and after delivery we should check the blood group of the baby and direct home test should be done. If the baby blood group is RHI positive and DCD is negative we should advise injection entity. So this is the management of RHI negative non immunized pregnancy but if we are getting indirect home test positive so if the indirect home test is positive always see the title again. So title if it is actually sometimes what happened in the title if we are getting in the low title in that case always conform again whether it is truly positive or not. If it is ICD positive that means it is an iso immunized pregnancy and we have to manage it accordingly. So what is the aim of management in an RHI immunized pregnancy? The aim is we have to detect fetal anemia as soon as possible and if there is fetal anemia we have to treat that. So this is a basic aim for treatment of RHI immunized pregnancy. So these are the actually absolute method of monitoring nowadays we are not using that. The first one is actually ICD tighter estimation especially in the first immunized pregnancy we were doing that but nowadays this is not in use. The second one is ladies method is central photometric analysis of it is an invasive test and now totally opposite because we have so nowadays test of choice for monitoring RHI immunized pregnancy is middle cerebral artery doctor. So why so? Because it is a noninvasive method and ultrasound is easily accessible but why middle cerebral artery doctor? So for this we should understand the physiological response of fetal anemia. So whenever there is fetal anemia there will be always there will be decrease in the blood viscosity and there will be increase in the stroke volume it will lead to increase in the cardiac output ultimately there will be increase in the blood flow and blood velocity in all the blood vessels of the body. So then why we are choosing only middle cerebral artery not any other vessel. So the answer is because it is vessel of choice because we could be sample at zero intonation angle. So what is actually it is ultrasound physics whenever we want to estimate the blood velocity of any blood vessel the ultrasound being should be parallel to the blood flow. If it will be on any other angle or perpendicular we could not get the velocity exact measurement we could not get. So here we can see this is actually ultrasound being but this is actually flow direction there is circle of middle cerebral artery right and left middle cerebral artery. So here we can see the blood flow direction is actually parallel to the ultrasound and we can see here the angle of intonation is the intonation is zero. So this is the perfect position and we will get the correct measurement of velocity because the further estimation is totally depends on the velocity value. So for example if I want to measure this vessel velocity so it will not be possible because now ultrasound blood is flowing in this vessel also but the ultrasound being parallel is actually in this way and blood is flowing perpendicular to this intonation. So this is actually 90 degree intonation we will get the velocity is zero if we will monitor in this stage. So this is the reason. Other reason is actually MCA vessel is sensitive to effect of hypoxia and we can detect fetal anemia in condition other than RHM memorization there the hemorrhage is a cause for fetal anemia but like in Parvo virus B19 infection for cal sensitization where bone marrow suppression is a cause so it will cause fetal anemia. So definitely it will increase the velocity but if we want to do estimation according to Lili's method so that is actually analyzing the amniotic fluid movement which will only be raised in condition where hemorrhage will be there. So this is the reason why this is test of choice. So MCA doctor normally we usually integrate in the multiple of medium so multiple of medium means the test results how much there is deviation from the medium. So when the value of MCA is 1 by 5 or more than that equivalent to 1 by 5 mom or more than that it is suggestive of model to see the fetal anemia. So this is a graph plotted taken from the and it is a graph where MCA velocity is actually this graph plotted against the gestational agent means and we are able to see here there are four zones A means B and B. So A what is the meaning of A zone? A zone means MCA PSP value is equivalent to 1.5 mom or more than that. So that means it is a dangerous zone and intervention is required whether it is informed in order or delivered. The second is B zone. B zone means it is a zone of which is showing mild anemia. Mild anemia means MCA doctor MCA PSP value is in between 1.29 to 1.5 mom. So whenever we are getting higher value of MCA PSP then always there should be a practice to see other ultrasound features of fetal anemia that I will discuss later. So whenever we are getting our MCA PSP in this zone we should be very careful and monitoring can be done in 5 to 7 days. But additionally if we are getting any other ultrasound features of fetal anemia we can increase the frequency accordingly. C and A zone is comparatively safer zone we can monitor it by 2 to 4 weekly. So this is the main protocol. Now this is actually a reference chart which is showing MCA PSP value according to gestational. So on rough as we mentioned what is the point we can see that if the MCA PSP is more than twice the period of gestation in weeks then it is the gestive of severe anemia. So then we can take a rough idea about that. For example here 18 weeks gestation the value is 36 that is almost double and 20 weeks the value is around 39.5. So we can get the idea that the baby is having severe anemia. So we have to do, we have to intervene. One more special thing here actually MCA when to start the MCA PSP surveillance in a case of Irish isomerised pregnancy. So usually we start it by 80 weeks only. So what is the reason? Reason is actually the fetal reticulitis reticulitis system usually can be sure by getting to 20 weeks only and that is the before then this fetus will not show the fetal anemia will not develop before this gestation. So this is the reason why we usually start surveillance only after in only 18 weeks onward. So I will just want to talk about the other under some features which are such as which can be such as the development of fetal anemia. So always see always have some practice if we are getting MCA doctor on the higher side because sometimes what happens if we are applying more progression or if we are taking MCA doctor in the fetal activity phase we can get higher value of the MCPSP. Whether it is actually exact to value or it is just because of some other reason we should see any other features of anemia is present or not. For example here we can see this is the screen we can measure the planning size and labor size and we can compare it with the reference chart available for this situation. This is the area actually it is prenatal thickness if it is more than 5 millimeter that is actually suggestive of subcutaneous edema we should see whether there is any cardiomegaly or pericardial infusion like tricuspid regurgitation is present or not because it is a sensitive indicator for development of cytosine hydrox. So here we can see cardiomegaly along with the pericardial infusion this is actually a cytosine this is a picture showing gross cytosine. So all these are features of fetal anemia in ultrasound additionally we should see the placental thickness and amount of glycol because we can see the endomials and placental megari they are another features of fetal anemia ultrasound features of fetal anemia. So these are the methods of surveillance. Now what if we are getting mcpsc more than 1.5 hour and it is actually modded to severe anemia there is a requirement of intervention. Intervention could be in term of interloperate blood transducer or delivery. So how to decide? So major deciding factor is the gestational age for example if I am getting this finding at 34-35 weeks in that case I would like to go with the delivery I will give the steroid cover and I will deliver the baby and I will transuse the blood in the neonatal period but similarly if I am getting this finding in at 28 weeks only then I would like to go in favor of intrauterine blood transducer because baby is extremely mature I cannot impose hydrogenic prematurity and related complications additional to the fetal anemia. Second when there are certain rules for intrauterine blood transducer for example if the fetal anemia developed in between 80 to 26 weeks the hematocrit we will transuse the blood when the hematocrit will be less than 25 while more than 26 weeks the criteria is if the hematocrit value is less than 30 weeks and there should be a habit of correction of anemia completely ideally post-translucent hematocrit should be between 45 to 50 because under correction will require more frequent transducer and related risk and actually this is whenever we want the fetal transducer at an earlier gestation age usually it will carry more prognosis that means the fetus drolla very severe disease in very early gestation age. So these are the features and there are various rules for intrauterine transducer I will not go much in debate and this was actually antinatal monitoring and management for cases of RSI immunization. So I will thank you and I will thank you I think very very simple that it is caused by transplanted passage of maternal antibodies against paternal RSI antigen of the fetus or fetal RDCs we all know that. And how does it happen? It happens because of fetal maternal hemorrhages 90% of these RH isomerized cases are caused by the D antigen the rest having been caused by the C and the E antigen I always wonder as to what is the incidence of RH negative blood group in our country it is about 5 to 6% in Japan you rarely find an RH negative person while in America it is about 14% so I think we need to know the epidemiology and as because we told all of us that some of the fathers are heterozygous and then the baby can be RH negative as was one of the babies in our case. So these babies obviously would escape affection despite the mother being RH isomerized so what we estimate is that the chances of RH incompatibility setting being discovered in a normal risk antinatal OPD should be around 3 to 4% so 3 to 4% of your patients of obstetricians in a normal antinatal OPD would have an RH negative mother with a RH positive husband and for reasons that you would perhaps delineate subsequently only 5% of the at risk mothers have neonates with significant hemolytic disease now pathogenesis a little bit about it now the fetal metal hemorrhages they occur throughout the pregnancy we must understand that is 3% in first trimester 12% in second trimester and 46% in third trimester so that's why we recommend NTT to be given after abortion or after CVS, Coriocorionic Valise sampling or amniocentesis or after 28 weeks and so that's why we recommend the NTT administration in between as well but yes the chances keep on increasing as the pregnancy advances now the initial antibody is IgM to begin with which does not cross present time and the IgG antibody which crosses the present takes 6 months to be synthesized that's how the first baby escapes from getting affected now sensitization can be as I said can be caused by abortion, by ectopic pregnancy, by abdominal trauma Corionic Valise sampling, amniocentesis version which are so very rare and certain things which make fitometrial hemorrhages more likely at the time of delivery so what affects the severity of these hemorrhages volume of fitometrial hemorrhages as a drama unfolded in our case despite administration of NTT as Gitanjdi told you in every after every abortion or MTP or delivery we still had RH isomerization and the baby was affected so whenever the volume is high you may have to give a higher dosage of NTT so that may prevent the RH sensitization of the mother there are other factors which affect immunogenicity of antigens for example D antigen is more immunogenic metal response to RH antigen varies some mothers somehow form antibodies more readily and more vigorously the type of antibodies I just spoke about that is the IgG antibodies which cross and not the IgM antibody that's how the first pregnancy usually escapes from RH sensitization the immune compatibility is somehow protected against RH isomerization because the moment the cells cross over to the maternal circulation they are quickly destroyed and there is little time for RH sensitization the gravity status the smaller the family size the less the chances of sensitization so our mother obviously was 6th gravity so that was another factor that perhaps affected the increase the chances of the baby getting affected the clinical features the severity may be mild with baby just needing conventional phototherapy but the classical RH isomerization is what when it is moderate where babies require intensive phototherapy with possible exchange transfusion this is the typical profile that we all are familiar with but the most dreaded and most dire complication of RH isomerization is this hydrophospitalis needed resuscitation abdominal paracentrosis bilateral pylulotap with IPPR and DR itself and sometimes the laryngeal edema is so severe that you have to negotiate a very small size and rotate it to you and in fact told us why what is the pathogenesis of all the clinical features the hemolysis causes anemia which may be immediate may be in fact may be in utero may develop after soon after birth or may be delayed it may take place after several weeks after the baby is born elevated bilrubin of course this is what concerns most of us because is the bilrubin that is neurotoxic and if you remember the sibling of the baby is had coniferous anus handicap he can't even walk so this is the problem and if you ask me hydrophospitalis is not so common but elevated bilrubin causing conic truss is something that all the pediatricians and unitologists dread the most X-ray medullary hematopoiesis which causes hepatitis planomagyl it also results in pressure of the intrahepatic arteries which result in hepatocellular dysfunction cardiac failure which perhaps our baby had to begin with hepatocellular dysfunction which I just spoke about because of the X-ray medullary hematopoiesis the cardiac failure and may be chronic hypoxia hydrophospitalis Gitanji just told us about the initial assessment of the early features of hydrophospitalis may be placenta thickening a double ball a double sign in the ultrasound and the hepatocellular medullary of course once the baby has severe hydrophospitalis you would have the pneumocytitis the pleurofusions the pericardial fusions etc thrombocytopenia no this is poorly understood as to why the baby has thrombocytopenia is it because of decreased production is it antibody mediated or is it because of hyper splenism we do not know much about it fetal happiness is well known and results in hypoglycemia and delayed lung maturity so we should know that's why Gitanji talked about the delivery so before you deliver at 35 weeks in a severely affected baby I would rather have the baby being given intratrain transfusion and antinatal corticosteroids and then you would have the baby delivered but the most complicated is bilirubin now we all know that the risk of bilirubin in addition to the bilirubin levels is aggravated by low albumin which decreases the bilirubin binding and the unconjugated bilirubin crosses the blood-brain barrier more readily prematurely and any kind of sickness I won't go into details investigations are very simple companies that count what they did blood probe, DCT, peripheral blood smear somehow I think the a few things are missed in the peripheral blood smear this happens in clinical practice you never get a copy book picture in your you know when you are practicing if you get it you are very very lucky serum bilirubin I would talk about the fact that there are positive bilirubin later now management now this is the scenario that all of us are most should I say would likely to happen a new net requiring delivery room resuscitation as the baby has hydroxytalis such babies as I said require not only intubation they require abdominal paracentesis thoracosynthesis and may require sort of a car subsequently fluid management very very careful fluid management so those cases are very very difficult to manage of course a very severe anemia where the SBE has dropped to 2 to 4 grams may require partial exchange transfusion with that RDC so one of the indications for exchange or partial exchange is the very very severe anemia because they are perhaps giving back RDCs may precipitate congestive cardiac failure so so this is one of the indications for partial exchange transfusion yes now this is what our talk is all about if you go back to initial bilirubin levels were very very high and perhaps if we had not given intensive phototherapy the baby would have in fact 40.6 was if I can see was just two milligrams below the exchange line and it was still rising and we know that piece around 48 hours or so and we could avoid that and we could bring the bilirubin down is because of intensive phototherapy so what it is I talk about in some detail so intensive phototherapy if I may say so has changed the complete management of isomanization I still recall when I read 1986 got in every edition so it was called bilirubin of 5 milligrams called SBE of 10 grams per deciliter reticulocyte 15 percent and blah blah blah this has all changed now there is only one indication for exchange transfusion and that is the bilirubin approach the levels at which exchange transfusion is indicated first you decide as to which this graph does the baby belong to as Dr. Ghanan just showed you so very very well and once you see that you do exchange or you perform exchange only if you think that the levels are reaching where an exchange transfusion may be indicated as per the those AP graphs but so how we manage this arch-estimulized frequency we manage join this with intensive phototherapy and we manage an even a bit that's a transmission it is said once the bilirubin is within 2 to 3 milligrams of exchange you get ID ID the dose is 0.5 to 1 gram some people say one dose is enough some people say you get two dosages we give two dosages to our baby and lastly double volume exchange transfusion not this may be a very very rare event it is estimated in US the incidence of DVT is about 3 per lakh pregnancies is that rare so that means if you manage your baby's well they should not require double volume exchange transfusion this is a graph that Ghanan showed you and now this is the how to make this is something very close to my heart this is what I do normally we start immediately we do not wait I go there myself start phototherapy immediately it's called the crash card approach we start all special do we are very clear about it we don't use because you got to bring down the bilirubin and especially is there a saturation point there may be some saturation point that is the combination of the configurational isomers like 4 Z 15 but there is no saturation point for the structural isomer that is new room in so the more those you get the more women is found and the more rapidly it falls so we use classically we use to under surface for the therapy with the baby blankets we put six LEDs on the top and we cover the baby with the reflecting surface we also at times remove the diaper for some time and that is gone absolutely done so you ensure maximum area coverage by using double surface for the therapy make the natty as small as possible and remove it for some time if it is approaching dangerous levels we of course as I said we use six from top and two from below decrease the distance as much as you can. There is no light should be perpendicular to the incubator was and we do not interrupt for the therapy if the woman is very, very high and as I said the line the best in it with reflecting material a few things I think if you want to make your hospital for the therapy effective see that the check it with flux meter they are maintenance staff comes and checks it at periodic interval clean the plastic glass she and the tube lights does accumulates and somehow decrease the reflectance or the transmission of the flux. How much can you break it down handsome reported about 10 to 11 milligrams fall in two to three hours and we've had fall of 10 milligrams in four hours and the saying is the higher the bill room and the higher the dose of phototherapy the more rapid the decline so you can hope to bring down very, very dramatically other agents now this baby had as Dr. Gannon brought out had certain seizures most likely the bill room never were even close distance to 20 it was more very, very in fact that when the baby came babies levels for seven milligrams so most likely it was the hypoxia that the baby had which exerted it but one thing good it did was that the barbiton must have led to rapid conjugation and one thing about you know barbiton is it is not useful at all in first 48 hours so it cannot bring down a bill room which is high but once you're given for the therapy it may after a couple of days may prevent subsequent resurgence of bill room and the he oxygen is inhibitors like 10 protocol firing have been spoken about since 1988 but never used because maybe because of the advent of intensive phototherapy close vibrate and poorly sat which prevent the absorption and dbt as I said if the phototherapy fails these are the levels so if you see at 34 hours 40.6 was when was it 14.6 34 hours now if it was 34 hours at 40 at 34 hours would be somewhere here and and the the line for exchange would have been around 16.5 or 70 so we were just two milligrams short of it and we did not allow it to rise and the urine was very dark yellow and the moment we stopped phototherapy within 24 hours of it it came down the the urine color became normal now I was been had that positive why was it that positive also it is elicitable and the levels went up the causes could be many one could be cardiac failure with bad incantation which results in hepatocellular dysfunction which I spoke about the extraordinary hematopoiesis which might have compressed the hepatic arteries and led to hepatocellular dysfunction but to my mind I'm very clear that it was a measurement of photo isomers the limirubin the 4 z 15 which were measured measured as direct driven because after stopping phototherapy the direct positive the urine color declined it became almost normal and as the follow-up revealed that the baby has no evidence of conjugated hyper bilirubinemia prevention Dr. Gitanjee spoke about we give NTD 300 microgram to the RS negative mother within 72 hours after delivery of RS positive neonate we also give it after every abortion after every abdomen trauma, apoptic pregnancy amniocentesis larger than 10 mfutometer hemorrhages require high dose so when do you expect larger phetometrial hemorrhages anti-partum hemorrhage especially if the neonate is anemic where there has been maternal removal of placenta there you may have to give higher dose another dose at 28 to 32 weeks is also recommended and it avoids the or it kind of brings down the incidence of malnutrition even further awarding version memory separation placenta and small family size are other measures which can prevent or decrease the incidence of this issue or this problem thank you very much so now if any questions I'll take all the questions if you want to ask anything concerning the antinatal management she's there to answer those questions and Dr. Ghanam of cost would answer anything regarding the presentation part blood transfusion on day 1 okay now firstly we did get Pat cell transfusion on day 1 itself so that is not that we did not give blood transfusion IVIG is something that you are absolutely right and guidelines I don't think I would follow an NF guidelines at my level we follow the standard text so you don't have to give there was no indication if you met blood transfusion we gave blood transfusion on within let's say 6 hours of arrival so we did give blood transfusion that's the transmission in fact we did give 1 we give 2 we did give so and IVIG of course is something which is indicated by most of the standard text so we gave it so we had a very interesting case which was as I said is remarkable because it happened in today's scenario it happened in a book that supervised pregnancy it happened in a multi-gravity and it was a little ironic that despite having been supervised in a in a by a good obstetrician she ended up the she had to deliver the baby in a center with ever hard in pediatrics. Thank you very much for your your share. Thank you.