OGSSI Hyperglycemia in pregnancy

Añadido: 2026-05-27

[00:00:00]No first kashri first.

[00:00:03]>> Oh fine. Okay, >> we are live now. Please go ahead.

[00:00:07]>> Good evening and a warm welcome to one and all. A million thanks to our oxy presidents for giving me this opportunity to be the chairperson along with our my dear friend Dr. K Pradeshi as a part of the medical education committee of Oxy. It gives me immense pleasure to host this webinar every year year after year and this time we have a every time the president comes with a new new ideas of how to conduct this medical education programs and it's uh very thoughtful of madam to involve the lot of young members consultants who are actually the stalwarts and who have dug deep into the topic. So this time uh the topic here is hypoglycemia and pregnancy. We all know that uncontrolled blood sugar during conception acts as a terogen. That is one important thing we should never forget. The glycemic control at the time of conception is so so important. So this topic has been chosen as the first topic because of the magnitude of it carries in clinical practice.

[00:01:09]Thank you Dana madam and the entire oxy team for giving me this opportunity and I thank all the faculty and delegates who have logged in. So without much ado we'll go ahead with the uh session.

[00:01:21]Saiti. Yeah. Now I uh request uh our very close friend Dr. Priyashni who is also an easy member of Oxy and as associate professor at Institute of Social Obstetrics KGH to give the Oxy prayer.

[00:01:36]>> Good afternoon one and all. I take a great privilege to be a part of this medical education committee. I thank Dr. Dhanasham, Madame President Oxy and all the dignitaries for giving me this opportunity to start the first program and I welcome all the postgraduates and the faculties and the eminent persons who are going to give light to the young bingians.

[00:02:02]It's really uh amazing uh to teach the youngsters and uh see them bing and growing and becoming great persons and being a part of this program and take immense pleasure to first present the oxy prayer. Uh we move on to the oxy prayer. Thank you God. In humility we gather in gratitude we pray for all the good things you have given us. Shower us with your blessings. To pass on the healing touch, to celebrate the arrival of each new life and a warm reborn, the courage to deal with it all. And when things are not perfect, and to remember that we are but messengers to keep our woman safe and free from sorrow, we bow before your kindness and the magnanimity of your endless love.

[00:02:54]Thank you.

[00:02:57]Thank you Pradeshi. Now uh this topic hypoglycemia and pregnancy I sincerely welcome our coordinator Dr. Vidya Jashri who is a very good friend of mine to carry on the session and host the session and go ahead. Welcome Vidya Jri.

[00:03:14]Vidya Jashri is the Vidya Jashi Sahiti.

[00:03:21]Yeah. Yeah. Vidya Jri is a very good friend and she's assent professor Institute of Obstics and Gynecology.

[00:03:27]She's a coordinator for the session and she'll carry on the session. Take the session forward. Over to you Vidya Jes.

[00:03:33]>> Thank you Karpakamal for your kind uh introduction. Uh thank you Dana ma'am for giving me this opportunity. Uh there's a small change in the program. First we will be having a talk on the basic and advances in hypoglycemia followed by the case discussion. I'm here to u introduce Dr. Krypas Chantri who's currently working as a senior resident at SRM medical college. She did our MBBS and MSG at MMC and she's a member of the Royal College of Oxy. Welcome Krypa Chankri. And uh next I welcome Dr. Deepati Rajan ma'am.

[00:04:18]Yeah, she's a consultant obstitrician and gynecologist with specialization in her city. She's the director of the SAI welcome women's clinic Chennai. She's a visiting consultant at the motherhood cloud9 hospitals. Uh over to you for the talk ma'am. First Krypa Dr. Krypa Shankri will be talking on the basics of hypoglycemia and pregnancy.

[00:04:41]>> Thank you ma'am. Thank you for the kind introduction and before starting I would like to thank Dana ma'am and all the esteemed faculty here for giving me this wonderful opportunity for budding doctors like me. This means more than we all think. So I will now talk about carbohydrate metabolism in pregnancy.

[00:04:57]Am I clearly audible mom?

[00:05:01]>> Yes kupa you're audible.

[00:05:03]>> Yes you can share your screen. Yeah >> yes ma'am.

[00:05:08]>> Are my slides visible ma'am? Yes.

[00:05:13]Screen.

[00:05:14]>> Yes ma'am.

[00:05:15]>> I will now talk about carbohydrate metabolism in pregnancy.

[00:05:19]So when we talk about carbohydrate metabolism in pregnancy, these are the three phrases that we have to remember because ultimately whatever we are going to speak upon is going to land up in this one fasting hypoglycemia, two postprandial hypoglycemia and three is hyperinsulinemia. But before going into what happens in pregnancy, I will initially talk about how glucose molecules cause insulin release and a few points about the glucose transporters and also how insulin will cause increased uptake of glucose. First look into this slide. The blue molecules that are labeled as glucose are going to enter the beta cells of pancreas. That is when we are in a well-fed state, the glucose molecules will enter the beta cells of pancreas via the glut one or the glut 2 receptors. In beta cells of pancreas glut 2 receptors are in maximum amount but a minor amount of glut one is also present. This glucose once it enters the beta cell it is going to get converted to glucose 6 phosphate and it will undergo glycolysis. The end product that we get that is the pyroate which is the end product will enter the crep cycle and as a result of all these pathways we are going to get so much of ATP molecules being produced. When there is increased intracellular concentration of ATP molecules, this will close the potassium channels that is present in the cell membrane because these potassium channels are sensitive to the increasing amount of ATP inside. Once potassium channels close, the plasma membrane depolarizes. In response to this deolarization, the calcium channels will open. Because the calcium channels open, there will be influx of so much of calcium ions and this will cause release of insulin. As we all know when calcium is moving into the cell it will try to push something out of the cell. In this case it is insulin because this is happening in the beta cells of pancreas.

[00:07:08]Insulin will already be synthesized as preproinsulin and then it will be cleared by proteasis resulting in the release of pro-inssulin which is nothing but the A chain of insulin and the B chain of insulin joined together by the ceptide. Once the C peptide is cleaved off the pro-insulin becomes insulin ready to act.

[00:07:28]And the same thing depicted in words here. Glucose mediated insulin release.

[00:07:32]Glucose entering the beta cells become glucose 6 phosphate under goes glycolysis and oxidative phosphorilation. There will be an elevated ATP count. This will close the potassium channels depolarizing the plasma membrane of the beta cell causing calcium channels to open thereby releasing insulin.

[00:07:51]Now a few points about blood transporters. These are nothing about the transporters which are going to transport the glucose from the blood circulation into the respected cell. We have various kinds but of of the various kinds what is of clinical significance to us is glut one to glut 7. Out of these glut 6 is a pseudo gene and glut 2 is that receptor which is present in beta cells of pancreas and glut 4 is that glucose transporter which is sensitive to insulin. These receptors are present only in the muscles and the adiposytes. These sort of clinical significance because we have questions in the end.

[00:08:30]Uh now a few basic points about insulin.

[00:08:33]As we all know it is a polyeptide hormone containing two chains an A chain and a B chain. The A chain will have 21 amino acids and the B chain will have 30 amino acids joined together by the dulfide bonds. Now looking through this picture, we're all able to see a cell membrane. And I'm hopeful that we are also able to see a floral receptor that is spanning the cell membrane. The blue color part of this floral receptor that is lying outside the cell membrane is the alpha subunit to which insulin actually binds. And that part, the lavender part that is traversing through the cell membrane and also lying intracellular is the beta subunit. So this insulin that is secreted is going to attach to the alpha subunit thereby causing activation of the beta subunit.

[00:09:19]In other words, the tyros and kynise inside the beta subunit gets phosphorolated. When this happens, the second messenger pathways get activated thereby transllocating the glut transporters to the cell membrane. So the main function of insulin that we are worried about is uptake of glucose into the muscles and the adiposytes because blood for transporters are the only transporters that is sensitive to insulin. So how does insulin bring about this action? Basically by transllocating more and more of blood for transporters to the plasma membrane.

[00:09:54]Now we will see what happens in pregnancy. One thing we have to remember is glucose and amino acids are the main fuel for the fetus. It is not going to take up anything and everything that lies there. Maternal glucose is being constantly used by the ftopplasal unit which results in fasting hypoglycemia.

[00:10:13]So the fetus just doesn't care. It doesn't care whether the maternal glucose is 200s, 300s or even just 50.

[00:10:19]It just keeps taking more and more of insulin, more and more of glucose into its circulation. and that is attributed to glut one transporters in the placenta. Insulin sensitivity is increased in the first trimester but it decreases progressively in the second and third trimester.

[00:10:36]Hence there is fasting hypoglycemia and postprandial hypoglycemia. So we'll go back to the first slide where I said these are the three phrases that we have to remember. We already have answers for two. One is fasting hypoglycemia because irrespective of the maternal plus uh maternal plasma glucose concentration the fetus is just going to take up more and more of glucose. So when the woman fasts when the pregnant woman fasts it will still keep taking up more of glucose resulting in fasting hypoglycemia. This will be a problem when uh especially Muslim women come to us in the month of Ramsan asking whether we can fast. The main thing that we tell in medical nutrition therapy for the treatment of gestational diabetes melatus is that uh avoid fasting or feasting because if she's going to fast then she will end up in fasting hypoglycemia and if she's going to go in for a feast she will go in for postprandial hypoglycemia and why is this postprandial hypoglycemia happening? Obviously because of the hormones that is secreted by the placenta. The insulin resistance is because of the hormones like human placenta lactogen, cortisol, progesterone and the inflammatory markers. But when you look into it, there is actually something more interesting because the body is naturally trying to keep more and more of glucose available in the circulation for the fetus to take up more. It is trying to help the fetus. It is it is the magical normaly of the nature that has uh kept uh all the biochemical processes in a check and it has transformed it to a fetus favorable biochemical process. So there is postprandial hypoglycemia once the woman takes in glucose or any form of food that is because of all these hormones which is going to cause resistance to the insulin hormone that is secreted. In response to increasing insulin resistance, the number and size of beta cells of pancreas increase causing increased secretion of insulin resulting in hyperinsulinemia. And this is the third point that we were talking about in the first slide. Because the insulin is not exerting its action because there is resistance to the secreted insulin.

[00:12:41]What the body thinks is there is not enough insulin and that's the reason there are there is a negative feedback happening and the beta cells are thinking that there is not enough insulin and I should do my job better.

[00:12:53]So it is undergoing hyperplacia and it will start secretreting more and more of insulin but in vain. This will result in hyperinsulinemia. As a result glucose is also high in the circulation. Insulin is also high in the circulation but the glucose is not being able to taken up by the muscles and the adipost tissue.

[00:13:12]Hence pregnancy is a triad of fasting hypoglycemia, postprandial hypoglycemia and hyperinsulinemia.

[00:13:20]And what is accelerated starvation?

[00:13:22]Normally in prolonged fasting by normally I mean in a non-pregant man or a woman sorry a non-pregant woman of course glycogen depletes after 12 to 24 hours. Then gluconneioenesis begins from amino acids and glycerol. After 2 to three days is when the ketones will come into the picture. But in pregnancy there is an exaggerated fasting response where ketosis and hypoglycemia will develop within just 8 to 12 hours of fasting.

[00:13:50]That is uh you don't have to wait for 2 to 3 days as in a non-pregant state for ketosis to begin. It will happen just within 8 to 12 hours which is very rapid. And why does this happen? It is again because of the pregnancy hormones which causes insulin resistance by causing lipolyis. See there are various hormones but there is only one hormone that acts like insulin in the body and that is insulin. Every other hormone that is secreted you name one I can tell it is definitely going to be against insulin. For example, human pleasant progesterone cortisol maybe the modes they act can be different but the ultimate pathway they land up in they're going to act against insulin in one or more pathways. Human placental laptogen is going to enhance the lipolyis that is breakdown of fats and thereby causing fat mobilization earlier.

[00:14:38]>> So this will cause accelerated starvation just within 8 to 12 hours.

[00:14:42]Again this is going to be uh risky for the mother. That's why we are telling her not to fast.

[00:14:48]>> Now dawn versus somogi phenomenon.

[00:14:51]The the point in common here that we have to note is both present with fasting hyperglycemia.

[00:14:58]Say for example, we start a woman on insulin and she's coming back with her self-moniitored blood glucose levels and the fasting levels are higher for two women but you don't know what the reason is. You don't know if it's because of dawn or somogi. So what do you do? You have to go back to a 3:00 a.m. sugars.

[00:15:14]What are the ways to monitor sugar levels? There are two kinds. One is a 7point profile and a fourpoint profile.

[00:15:20]A sevenpoint profile is where you do premeal and postmeal thrice and a 3:00 a.m. sample. For a four-point profile, you just do the fasting that is pre-re and postmeal for every for the breakfast, lunch and dinner. So, you get a four-point profile where you cannot look into the 3:00 a.m. sample. But 3:00 a.m. sample is very important for this very reason because when a woman has higher fasting samples, you need to know what the problem is because without knowing the problem, you cannot you will not be able to come to a conclusion whether you have to increase or decrease the bedtime dose of insulin. I will explain why. Dawn phenomenon is where there is a natural early morning rise and blood glucose due to surge of anti-insulinogenic hormones. Uh when you follow the circadian rhythm in the early morning, every hormone is going to most of the hormones are going to spike at around 4:00 a.m. or 5:00 a.m. or or around 3:00 a.m. And most of the hormones as I already told are going to act against insulin. So because of these hormones the blood sugar is going to be transiently high in that period and that will be taken over till the fasting. So if you're going to differentiate between dawn and somogi you will have to check the 3:00 a.m. blood sugars. But in somogi it is because of the reborn nocturnal hypoglycemia due to the excessive dose of night insulin. Because the woman has already received so much of bedtime insulin at the night, there is responsive hypoglycemia and because of this there is a rebound hypoglycemia in her fasting. So the treatment for dawn's phenomenon is going to be increasing the basal insulin because that has to counteract the anti-insulinogenic hormones that is going to surge at around 3:00 a.m. But the but the treatment for somogi phenomenon is just the opposite. you will have to reduce the basal dose of insulin because somogi is happening in response to the raise bedtime dose. This is very important to differentiate because fasting hypoglycemia can occur in both these conditions.

[00:17:14]So now I got a couple of questions. One, pregnancy is a state of insulin resistance.

[00:17:21]But how does giving insulin help in GDM when there is resistant to it? Can anyone try the PGs who are presenting?

[00:17:35]Am I still in the meeting or am I I'm away?

[00:17:41]>> Meeting. You are in the meeting, Ka?

[00:17:44]>> Yes, ma'am. But the PGs who are presenting, are they are they in the meeting, ma'am?

[00:17:48]>> Yes. Yes. Yes, they are all in the meeting.

[00:17:51]>> So, the PGs, can you try can you try answering this question? We are all talking about insulin resistance that is happening in pregnancy. But we are again giving insulin. Is that really going to help?

[00:18:05]>> Yes.

[00:18:05]>> I'm not able to huh I'm not able to hear you nor am I able to go back.

[00:18:13]>> Hello ma'am. Is it audible ma'am?

[00:18:15]>> Yes you're audible. It's enough if you're audible. Just tell me if it's going to help by giving insulin.

[00:18:22]Um uh um giving insulin is helpful because the resistance is not like absolute resistance >> relative resistance. Giving insulin in GD is helping you.

[00:18:38]>> Yes. So that's one way to put it. See as you rightly said it's not an absolute resistance. It is a relative resistance.

[00:18:44]But one another way to see it is that uh for example you're trying to open a box.

[00:18:49]You're trying to lift something heavy and you're not able to do it alone. what do you do? You call for help, right? You need more force to do that. So, this is one such condition where it can be both qualitative and quantitative. It is just that uh the the receptors are not able to respond properly to insulin that can be because of reduced number of receptors or it can be reduced phosphorilation of the beta subunit or there can be multiple other reasons. So, the body is actually producing insulin in fact supraphysiological doses of insulin because of the beta cell hyper hyperplasia. But for some reason this resistance is not not being overcome.

[00:19:25]For that reason we are giving that extra boosting dose of insulin from outside the exogenous dose which is going to break the threshold for resistance and now the the receptors will be activated.

[00:19:36]So as I already told there is no hormone that acts like insulin but insulin. All right? So there is no way you have to give insulin but in a higher dose. It is not that once you give insulin the body will stop producing insulin. No, you're just giving that extra dose so that that resistance is being broken. And the second question, how does walking improve blood sugars when there is insulin resistance?

[00:20:01]We are telling the women to walk. That is the main part of medical nutrition therapy, right? Not just three major meals, three minor meals. We also ask her to walk around walk for about 15 20 minutes after each meal. Do we say that or not?

[00:20:16]By walking uh the skeletal muscle will be uh skeletal muscle uptake of glucose will be more. So >> how will that happen? How the skeletal muscles take up more glucose >> using sensitive insulin right? There is insulin resistance.

[00:20:36]>> The insulin sensitivity gets getting into >> it increases the sensitivity.

[00:20:41]>> Yes, that is also partly right. By doing some exercise, by causing muscle contraction, some something it can be an walking or any exercise that causes muscle contraction, the insulin sensitivity, the the sensitivity of the receptor to insulin increases. And one another way is glut 4 receptors are getting transllocated to the plasma membrane by insulin. Right? There is not just the only way for the blood for transporters to be transllocated. There is an insulin mediated translocation of blood flow receptors and there is a contraction mediated transllocation of blood flow receptors. So even if this is not going to work the contraction mediated is going to work thereby causing more transllocation of blood for receptors to the plasma membrane thereby inc uh improving uh insulin sensitivity or glucose uptake. All right.

[00:21:33]All right. That's my session. Thank you ma'am. Thank you all for the opportunity.

[00:21:39]Thank you Krypa for the elaborate explanation on the metabolism of insulin. Now over to Dr. Deepa ma'am for the talk on recent advances in hypoglycemia and pregnancy.

[00:21:50]>> Uh before that hi I'm Dr. Vija and uh am I audible?

[00:21:57]>> Yes madam >> you're audible madam.

[00:22:00]>> I would like to congratulate Kria. She's my postgraduate and I am really aruck by the way she took the basics of uh insulin and glucose metabolism and very good ka. I just wanted to share my happiness when my student excels beyond the teacher.

[00:22:19]Thank you ma'am. I just unmuted myself.

[00:22:23]Thank you ma'am. Thank you KP Ma'am.

[00:22:25]Vidya Jri Ma Vijay ma'am it's it was a pleasure seeing you all again ma'am.

[00:22:28]Thank you ma'am.

[00:22:30]>> Thank you Ka. Thank you.

[00:22:31]>> We welcome Dr. Vijay madam to this session on hypoglycemia and pregnancy. Thank you madam for joining amidst your bus schedule.

[00:22:41]>> Yes.

[00:22:46]>> Vidya.

[00:22:47]>> Yes ma'am.

[00:22:49]>> Can I uh present?

[00:22:52]>> Yes ma'am.

[00:22:55]>> So that was an excellent talk by Dr. with Krypa Shankri which sort of set the um stage and it's a very difficult concept to understand and she made it really easy to understand the subsequent talks and uh that was very nice of Dr. Vijaya to you know um give all the kudos to her student and thank you very much oxy medical education team um committee to make me a part of the committee and also giving me this opportunity.

[00:23:26]I'll just share my screen now.

[00:23:38]>> You see this?

[00:23:40]>> Yes, ma'am.

[00:23:52]Yes. So, the topic given to me is very good. It's uh an update in glucose monitoring and insulin delivery and the main reference is paper which has come out very recently in diabetes care in 2026 on the management of diabetes and pregnancy standards of care in diabetes 2026.

[00:24:14]So diabetes you all know management is a team- based care. You can either do it in a single specialized center or there can be multiple centers with lot of team members in different centers who can collaborate and I will not go into the details for management you need nutrition counseling lifestyle behavior change which 70 to 85% of GDM can be managed with this teley health and in-person visits can help especially with GDM and insulin a few words about insulin insulin you already heard can be used for type 1 diabetes. It is also a preferred agent in the management of GDM and type 2 diabetics in pregnancy.

[00:25:00]Metformin and glyoride individually or in combination should not be used as firstline agents because they both cross the placenta to the fetus and may not be sufficient to achieve the glycemic goals. just to remember this point and what are the glycemic goals in pregnancy. So you all know that you have to maintain your sugar levels and a little bit about insulin physiology pregnancy in people with normal glucose metabolism who are not diabetic. People who have normal glucose metabolism the fasting sugars are lower. This is insulin independent and it is a glucose uptake by the fetus and the placenta.

[00:25:44]Then after a meal there will be a little bit of hyperglycemia and carbohydrate intolerance and this is due to the placenta initiated diabettogenic placental factors. And in early pregnancy there is a lower glucose level due to enhanced insulin sensitivity.

[00:26:08]But later in pregnancy in the second and the third trimester there is a progressive insulin resistance which you already heard. And in women with normal pancreatic function insulin production is sufficient to meet the challenge of this insulin resistance and you will maintain normal glucose levels. But in women with diabetes hyperglycemia occurs and if treatment is not adjusted properly. So this is the reason why we need to monitor the sugar levels. So how are you going to monitor their levels?

[00:26:44]You do a fasting a prerandial as well as a postrandial monitoring. The aim is to achieve optimal glucose levels. And what are these glucose levels? We want to achieve fasting less than 95, 1 hour postprandial less than 140 mg and a 2hour postprandial less than 120 mg.

[00:27:08]and goals for pregnant women according to the uh American Diabetic Association.

[00:27:15]Fasting between 70 to 95 for a type 1 or type 2 diabetes with a GDM treated with insulin again 70 to 95 and a GDM not treated with insulin less than 95. 1 hour between 110 to 140 for type 1 or type 2 diabetic and a GDM treated with insulin. and GDM not treated with insulin less than 140 and 2-hour postprandial 100 to 120 for type 1 diabetic and GDM treated with insulin and less than 120 for GDM not treated with insulin.

[00:27:50]Hypoglycemia threshold level. Current recommendation is if it is less than 70 mgs per deciliter, it is called as hypoglycemia.

[00:28:00]And this kind of less than 70. And if you're using a sensor less than 63 is considered as hypoglycemia.

[00:28:08]With type 1 diabetics, it is very difficult to achieve proper levels and you will get significant hypoglycemia.

[00:28:18]then you aim for a less stringent goal and individuals with JDM you definitely use these levels which is less than 70 hyperglycemia in women with less than over diabetes on early pregnancy. What they mean by this is if you do a O GTT and if it is just in the impaired glucose range then should you treat these people the benefits were uncertain. So there was a trial called the Tobogum trial which is treatment of booking gestational diabetes melatus which was a large multic-enter randomized control trial which looked at early screening for GDM. They randomized women into early treatment versus repeat Ott 28 weeks and they saw that in onethird of the group who were in the observation side observation arm there was a regression of GDM when they were retested. These are these women are unlikely to benefit from treatment in early gestation. So you don't have to treat everyone who is impaired glucose tolerance >> and O GTT results in the lower glycemic range when treated can increase the risk of SGAA infants. Hence we need to identify those women in whom the hypoglycemia will persist and treat only these women. And how do you know that?

[00:29:40]If the fasting is persistently more than 110 then the treatment will benefit. For this you do a fasting glucose three to four times per week. If the fasting levels is persistently more than 110 prior to 15 weeks of gestation then start testing them daily and intensify the treatment.

[00:30:01]>> Do we use HBA1C? Can you hear me? Sorry.

[00:30:04]Are you trying to tell me something?

[00:30:08]>> Can I go on? Yes ma'am. Yes ma'am.

[00:30:11]>> HB1C in pregnancy. Is this useful? HB1C in pregnancy is slightly lower in people with and without diabetes due to an increased red blood cell turnover. So ideal HBAC in pregnancy should be less than 6% and this should be achieved without any hypoglycemia.

[00:30:32]You can relax it to 7% to prevent hypoglycemia. If the woman is getting persistent hypoglycemia, it has been seen that in women without any diabetes, pre-existing diabetes, if her A1C levels are increasing within the normal range, then this can be associated with adverse outcomes in the baby. So there was a study called hapo study hyperglycemia and adverse pregnancy outcome study which showed increasing levels of glycemia was associated with worsening outcome in the baby.

[00:31:11]In women with pre-existing diabetes, you definitely want their HB1C to be between 6 to 6.5 very early in gestation because only then you will have lowest rates of adverse fetal outcomes. The disadvantage of HBAC is it gives you a value over 3 months and it will not fully capture the postrandial hypoglycemia which you get and this postrandial hypoglycemia is the one which causes macrosomia. So A1C may be useful only as a secondary measure of glycemia and pregnancy and glucose monitoring should be the primary measure and HB1C in second and third trimester again less than 6% will show you the lowest risk of LGA infants pre-term delivery and preeacclampsia and there's no point in measuring A1C once in 3 months you have to do it monthly.

[00:32:09]So when you look at glucose monitoring, blood glucose monitoring, fasting and postprandial mainly to achieve glycemic goals in the pregnant people with diabetes, pre-brandial testing especially in women using insulin pumps or basalbus therapy and to adjust your pre-meal rapid acting insulin dose and postrandial you monitor to get better glycemic outcomes and to lower the risk of preeacclampsia. This is the basis for why we do all this fasting preprandial and postprandial testing.

[00:32:47]Home glucose monitoring is the best way of doing it. You check your blood sugar level. You keep a record and you send it to your doctor or the diabetist.

[00:32:57]Continuous glucose monitoring. Whom do we use this continuous glucose monitoring? Especially for pregnant women with type 1 diabetes where you have a metronic instinct sensor.

[00:33:08]to suspend or increase the insulin as the glucose levels shift. There was a trial called a concept trial which looked at continuous glucose monitoring in the pregnant women with type 1 diabetes where you had two arms. One arm where they got the standard care and the other arm where there was a realtime continuous glucose monitoring along with standard care. So what they saw was there was a mild improvement in A1C when you use the continuous glucose monitoring. There was a significant improvement in the maternal glucose time in range and time above range without an increase in hypoglycemia and also there was a reduction in large for gestational age infants length of the days the baby spent in NICU and length of u and the severe neonatal hypoglycemia.

[00:34:02]So the CGM also showed what is called as the time in range assessment of glycemic outcomes in people with type 1 diabetes was very very useful with the CGM. Is it cost effective? When you look at the maternal and the neonatal outcome which is include along with this definitely on the long run it becomes cost effective.

[00:34:24]Can it be used in type 2 diabetes or GDM? There's still insufficient data to support the use in all women. you have to individualize the use in type 2 diabetes or GDM and CGM in DG uh in GDM there is a randomized control trial which looked at CGM with BGM versus blood glucose monitoring alone and they showed that the 24-hour mean glucose was much lower with CGM use and again when you use a sensor what is the range of glucose you use the time below range that is hypoglycemia is when it goes below 63. The level two hypoglycemia is when it goes below 54 and the time above range is u more than 140 and the above range should be less than 25% of the times.

[00:35:20]So this will help you continuous glucose monitoring will help you to achieve the glycemic goals the time in range the time above range HPC goals and especially in type 1 diabetes and may be beneficial in other types of diabetes in pregnancy who should be recommended again type 1 diabetics and let us look at the insulin delivery devices.

[00:35:45]So insulin little bit about the physiology of pregnancy in early pregnancy with type 1 diabetes the insulin requirements is lower and there is an increased risk of hypoglycemia in type 1 diabetics in the early pregnancy.

[00:36:02]At around 16 weeks the insulin resistance begins to increase and the total daily dose increases. The daily dose of insulin requirement increases by about 5% per week and it will go keep on increasing up to 36 weeks and there is almost a doubling of the pre-reg dose of insulin which you were taking.

[00:36:25]There is also an increase in the basal insulin requirement and the bolus dose of insulin requirement and by the end of third trimester the insulin requirement will just level off.

[00:36:37]If there is a rapid reduction of the insulin requirement, it may mean that a placental insufficiency is setting in.

[00:36:46]Important point to note is insulin do not cross the placenta and the changing requirement needs which you see during pregnancy requires frequent titration of the insulin dose and this requires daily and frequent glucose monitoring. That's the reason why we do frequent glucose monitoring. Insulin options in pregnancy. The basal insulin you use a long acting insulin like the insulin glyen or the intermediate acting the NPH insulin or the ultra long acting which is the insulin dloc insulin dlodec which you which we don't use because it is ultra long acting and 42 hours and if you need to change the dose you have to do it only once in 3 to 4 days. Rapid actic insulin options are the insulin aspart, insulin lisp probe and insulin faster aspart.

[00:37:36]The insulin delivery devices where do we inject the insulin? We inject it into the subcutaneous tissue into the fat and these are the areas where you can you all know insulin syringes which we were using where we would load the insulin into a syringe and inject it into the skin. There are a lot of advantages like it costs less. It will allow you to mix different types of insulin and it's available in a variety of lens and gauges. But the disadvantage is more complicated, less comfortable, less compact and the risk of needle bending when you're trying to drop the medication because the needle is very, very thin. Insulin pens. These are modern. They look like writing pen. At one end you have the needle which is attached and you have either a pre-filled pen or you have cartridges which are refillable and you inject the medicine subcutaneously.

[00:38:30]The advantages are easier to use, more compact, may cost less than the pumps and usually covered by insurance.

[00:38:36]Disadvantage is it may cost more than the vials and syringes and require more injections each day than the pumps. Then you have something called as smart insulin pens. What do you mean by smart insulin pens?

[00:38:50]They are recommended if you require a bless meal time insulin and you don't use an insulin pump. What is smart about it? It connects wirelessly to a smartphone app and a continuous glucose monitoring and it simplifies the management of insulin delivery. So you can track the insulin dosing, you can calculate the insulin doses, you can get downloadable data, it will also send you missed dose reminder and you can transmit the data to your healthcare team.

[00:39:25]Then you have smart connected pen cap.

[00:39:28]On top of a pen, you can have a special cap which has got a sensor and you can see that this sensor is linked to your smartphone. So what happens is uh the smart pen cap the CGM system will record your realtime blood glucose um monitoring and then those levels will be transmitted to this pen cap sensor and that will tell you how much insulin you have to inject which is very very convenient.

[00:40:00]And then you have something called as a traditional insulin pump where you put this insulin cartridge into this u pump and the pump is called as a reservoir.

[00:40:11]Then you have a tube which travels into your body and it inserts via a needle which is called as a canula into the skin and this is held in place by an adhesive sticker.

[00:40:27]Now traditional insulin pump delivers insulin in two ways. A low and constant flow to maintain blood sugar levels overnight that is called as basil dosing. And an additional burst of insulin at meal time. This is known as the bolus dosing. And this pump has got a digital display. It will let you program the amount and the frequency of insulin deliveries.

[00:40:52]Many of them can be connected to smartphones.

[00:40:55]Now advantage is you don't have to inject the insulin. It will deliver the insulin in very small dose and with high precision. It will deliver the meal time insulin with ease. It reduces major swings in your blood sugar. It reduces your episodes of hypoglycemia or low blood sugar. It may improve your A1C and it allows for flexibility in dosing to fit your lifestyle needs. That is whenever you're on a diet or exercise and improves the quality of life. The disadvantage is it's more expensive.

[00:41:27]It's bulky and every 2 to 7 days you have to change where you inject it. You require close monitoring and you should have the right supplies. You it may cause skin irritation or infection and it requires training.

[00:41:43]Then there is something called as a patch pump. This is very sleek.

[00:41:47]Everything is inside this patch. It has got a sensor. It has got an insulin delivery. everything inside the patch and that is connected to a device either a handheld device or a smartphone app.

[00:42:01]Again, patch pumps improve your quality of life. It reduces diabetes related distress. It is preferred by patients.

[00:42:08]Disadvantage, you have to change the patch every two to three days and you have to switch the site each time to improve the absorption.

[00:42:16]Then you have what is called as automated insulin delivery. Insulin pump can be paired with a CGM system to create an automated insulin delivery system. This is recommended for people with type 1 diabetes or people with type 2 diabetes that require a meal time insulin to reach their glucose targets.

[00:42:36]So lot of FDA approved automated insulin delivery systems are available. You have a pump as well as a CGM.

[00:42:47]Now how does it work? The CGM will sense your blood sugar and it will send a message to either the pump or uh from your smartphone and then that will give how much insulin has to go into the skin. This is how the aid system works and the important thing about this is before eating you must manually enter how much carbohydrate you are eating.

[00:43:12]This will allow the system to calculate and deliver the appropriate insulin dose.

[00:43:18]The advantages are you can use it with type one and type two to keep the glucose levels with target. It will allow the health care professional to receive information. Parents and guardians can monitor a child's blood sugar levels remotely.

[00:43:33]It will prevent hyperglycemia and hypoglycemia. And some AD systems include features that help simplify the complexity of meal time gl uh insulin administration. The disadvantages you have to input information to determine the bolus meal time doses. But with any insulin pump it is very important to keep insulin pen or vial or syringes available in case the pump stops working.

[00:44:02]There was a trial called the IDA trial which looked at automated insulin delivery among pregnant women with type 1 diabetes. So they saw that whoever used this automated insulin delivery, they had a higher time in range, lower time above range, lower A1C, more enjoyment of pregnancy, better sleep and less worry. So in future they're trying to bring in fully closed loop system where you can automatically calculate and deliver the meal time dose also without the need to enter the carbohydrate or any announced meals. And also under development is a dual hormone insulin and glucagon closed loop system.

[00:44:44]There is also something called as inhaled insulin where you inhale some insulin with an inhaler device before each meal in a powdered form. And this powder will quickly pass into your lungs and then into your blood. For your basil long-lasting doses, you will still need to use a pump. This is only for a meal time bolus dose. Inhaled insulin advantage no need for injection acts quickly but disadvantage is expensive.

[00:45:16]Patient can start coughing less precise insulin dosing. Injection of pump is still needed for your basil insulin and not suitable for patients with ama or other respiratory problem. And ketones.

[00:45:31]If your sugar goes high, you can check for ketones every 4 to 6 hours either in your urine or in your blood. And this is a ketone strip where you can easily see how much ketones. And when you have to measure the ketones, it will only tell you whether it is small, moderate or large amounts.

[00:45:51]There are also something called a cell replacement therapies which is you transplant eyelet cells from a donor into a recipient. But this therapy is only for people experiencing significant hypoglycemia and requires lifelong imunosuppressent therapy. You can see you take the eyelid cells from the donor, you inject it into the portal vein of the recipient and that will start releasing the insulin.

[00:46:20]If you want to change to a different device each year, you have to discuss your diabetes technology and reconsider what you want to shift to and you have to see whether all your devices are working in proper order.

[00:46:38]And long-term use of devices, you have to keep a lot of things in mind or follow all the instructions for cleaning and work with your diabetes team. Remove the sensor gently to avoid harming your skin. Rotate the placement of sensors on needle stick every one week or three to four days to avoid scarring and always keep up with the latest app updates and integrations.

[00:47:01]So the key term is time in range where the blood sugar should be in range between 70 to 180 and then time below range where if it goes below 70, time above range when it goes more than 180.

[00:47:20]And when you compare time in range versus A1C, the emergence of continuous glucose monitoring by checking the time in range offered a much more accurate measure of your blood sugar control on a dayto-day basis.

[00:47:36]So you can share your data with your smartphone, your family members and your health care professionals and you have to maintain your diabetes technology.

[00:47:46]So thank you very much for your patient listening. It was a very interesting topic and it did make me read a lot and I will be happy to answer your questions.

[00:47:58]>> Any questions ma'am?

[00:48:01]>> Yeah postgraduates.

[00:48:03]>> Thank you Deepa. It was really a good session with lot of new points especially the 2026 this one latest ADA I was also going through but this postgraduates make us to read. uh that is one of the advantage of being a teacher all the time and almost all the continuous glucose pump and automated delivery system the patch and everything you have taken I'm sure that time in and time above range and time below range all those things are we are not following in GDM monitoring as such maybe in future we will maybe Karthik also would like to throw some light on it and I think we can take the questions on the chat box if there is anything >> yeah yeah yeah >> go with the case discussion Yes. Yes madam.

[00:48:48]>> Yeah, even Deepa can join in for a case discussion if she >> Hi Katika.

[00:48:55]>> Hi ma'am.

[00:48:56]>> Good evening ma'am.

[00:48:57]>> We'll go on to the case discussion. I'm very happy and delighted to introduce Dr. Vijaya ma'am. She was my teacher.

[00:49:04]She's at present working in ESI Medical College Hospital. She was a former director of the IOG Madras Medical College and the former president of the Oxy. Welcome ma'am. I welcome Dr. Kartika Prahu ma'am who is a professor of the SRM medical college Kartangalur and uh over to you ma'am uh the PGs Dr. Harsha Dr. Uh the three PGs from SRNC will be presenting.

[00:49:35]>> Together the same laptop they are there.

[00:49:38]>> They together they together.

[00:49:42]>> Okay.

[00:49:42]>> Yes.

[00:49:43]>> Can I share my uh >> Yes.

[00:49:45]>> Yes my >> yes yes ma'am. Start Ashita >> before you start presenting I don't want the regular A and history presentation whatever the important points you would like to tell us regarding this case you just so that the time will be saved and the discussion will be good for you. Yes ma'am.

[00:50:13]Ma'am regarding this case uh she's a uh a primig gravida with 30 year old 30-y old primig gravida with gestational age of 32 weeks and uh where uh oct according to dipsy criteria was done around 28 weeks and uh it was found to be pos like it was 151 and uh by after that two weeks of Mnt was advised medical nutritional therapy was advised and her sugars were found to be elevated. So uh she has been started on metformin and uh for uh the further checkup she has come and sugars were raised. So we've admitted for glycemic profiling and control now.

[00:50:55]>> Okay. What about her early screening?

[00:50:58]>> Early screening in the first trimester was done which was normal.

[00:51:02]>> What is the usual guidelines now according to who?

[00:51:06]>> According to WH we will be screening.

[00:51:09]Let me finish the question. Should we do three times at 14 weeks, 24, 28 weeks, 30 to 34 weeks or we are going to do two times?

[00:51:18]>> Ma'am, we should be doing in the uh three times ma'am in the first uh booking visit and uh during the 24 to 28 weeks and 32 to 34 weeks.

[00:51:28]>> That is gi says it's better you do only early pregnancy 14 and again at 24.

[00:51:38]Okay. Okay.

[00:51:41]any who are all the I mean it is a universal screening as per DIY and as per government of India guidelines but is there any risk uh stratification where the high-risk uh pres yeah who are all those people age more than 30 years and then the previous history of GVM and family history of type 2DM and previous history of LGM >> macrosomia >> previous history HD >> and what is >> obesity is also included ma'am >> BMI then >> BMI more than 30 >> previous history of still birth and HB of more than or equal to 5.7 to less than 6.4 is also under high risk.

[00:52:26]>> What about PCOS?

[00:52:28]>> PCOS is also cardiovascular.

[00:52:35]>> What what are the one you missed?

[00:52:42]Abnormal lipid profile. No, anyone with a hypertrigademia, they are more prone for and also on psychotropic drugs.

[00:52:49]These are the two three things that has added recently. The usual things it is there in the book time in and out. Okay.

[00:52:56]So it is okay you start metforming in the third trimester. What is what no what what do you know about metforming?

[00:53:05]Is it acceptable in pregnancy? Metformin and glyoride and which are all the conditions you will uh start metforming or which are the condition start directly insulin. Ma'am met Metformin is a category V drug and uh for like for directly starting insulin when uh patient is less than 20 weeks and the patient is more than 30 weeks and if there is macrosomia in the scan uh we can directly start uh insulin and uh >> when does macrosomia start?

[00:53:39]Um if uh in the uh in a scan if 75th percentile if the AC abdominal circumstance is more than gestational age is especially noted from early growth scan. So insulin is especially started whenever the patient is having uncontrolled profile GDM patients with uncontrolled glycemic profile with M& as well as OBDM patients with uncontrolled sugar spell start and according to AC there are other two indications when AC is more than 75th percentile and estimated more than 90% I'll be directly starting insulin for those patients >> okay actually GDM the macrosome occurs only in the third trimester okay at that time if you start metforming whether it'll difficult to control the blood sugar level. So what about the people already taking metformin and getting conceived?

[00:54:31]Do you want to continue the metformin?

[00:54:33]>> No ma'am. According to >> we have to insulin mom.

[00:54:37]>> So according to ADA guidelines the metformin which has been taken for history of PCOD and ovulation has to be stopped >> start at 14 weeks. Okay. At the end of the first trimester you have to stop and then you have to start them on. Okay.

[00:54:51]That is the one point I want to stress on it. Okay. Then >> fasting blood sugar is high whether you will start insulin or metformin.

[00:55:00]>> If the fasting was more than one or five we should directly start on insulin now more than 126 and the random blood sugar is more than 200 A1C is more than 6.5 start insulin only. Okay. Even though the recent trials have said that metformin and glyoride can be given during pregnancy, it has its own advantage and disadvantage. Okay.

[00:55:25]Metformin has a long-term effect on the infants. So that we have to take care of that also. Okay. Why do you think uh GDM is common? Why pregnancy is a thing for diabetic? Now why is it? Because there is an significant insulin resistance is especially noted during pregnancy from 24 to 28 weeks of gestation.

[00:55:46]>> I am not asking why why pregnancy is diabetic. I'm not asking that. Why we are discovering pregnant hyperglycemia and pregnancy? What happens actually?

[00:56:00]>> Because of insulin resistance and hormones responsible for the insulin resistance >> because there is a demand. No, there's a demand by the fetus. It exposes the glucose intolerance. That is in pregnancy most of the diagnosis of GDM occurs because of the metabolic demand by the fetus which exposes the occult glucose intolerance. Okay. Okay.

[00:56:23]Then next >> m and the patient was admitted for uh sugar control. Mom.

[00:56:34]>> Okay. Because it is at 28 weeks you have diagnosed. Suppose has come early. What do you think about HBA1C? Madam has also talked about it but still what is the role of HBA1C?

[00:56:50]>> Why it is not very popular in GDM? Even though it is very very good for type one and type two in GDM we don't do HBAC right? Why? Yes ma'am. In uh G in GDM generally HBO and C uh is on the lower side will decrease.

[00:57:11]Mom >> why?

[00:57:13]>> Because of the increased red blood cell turnover.

[00:57:16]>> Okay. So in pregnancy there's increased red blood cell turnover. Second second there is a physiological hemo dilution.

[00:57:26]No. So the value will not be that much correctly reflect and moreover it reflects the previous 3 months control >> last 3 months. Yes.

[00:57:35]>> But every month you want to know whether it is it is doesn't and doesn't show us whether it is a postprandial hypoglycemia or fasting hyper it just generally says the average blood sugar level but what we want to make sure is we want to adjust the insulin dose whether it is a pandal pre or post that is why we don't rely on hpawc that much.

[00:57:56]only in type one and type two diabetes it is very very important because more than 6 what is the thing more than >> 6.5 >> what is the percentage of anomalies >> ma'am if it is less than seven it is uh not at risk ma'am if it is 7 to 7 to 8.5 it is 5% risk ma'am if it is more than 10 it is 22% risk >> so what do you say if they come with the 10 what is the advice you will give >> uh we will ask uh like we will if they've come with HPM and C10 we will ask for lifestyle modification and we'll start them on insulin or >> will what how will you counel the patient >> I'll explain all the possible >> counel and then >> what I am asking is would you adise MTP >> yes ma'am >> yes ma'am >> MTP will be advised and you adise or you will counsel for MTP ma'am but it is There may be chances of anomaly. So it's a patient and you cannot 100% say no no no you have to go for MTP. You cannot for it is only counseling the patient with the hemoglobin A1C is very high.

[00:59:08]Okay.

[00:59:09]>> Yes ma'am.

[00:59:10]>> What do you we'll go randomly here and there based on the thing. What do you can you define Mnt?

[00:59:20]M is a medical therapy which comprises of diet modification with a moderate exercise >> exercise should be done at least 30 minutes per day in 5 days a week and uh >> and there should be a brisk walking >> brisk walking post meeting no no combine mk and exercise I am asking you to define medical nutritional therapy diet >> so it is mainly of diet modification itself Total calories has to be calculated.

[00:59:51]>> No, no, we should maintain normal glycemia which should have optimal maternal weight gain and without any ketosis. So she should diagn that. Okay.

[01:00:05]It is a carbohydrate. It is a food modification where they'll have optimal glycemia with an optimal weight gain for the mother without any ketosis. So that is called medical nutrition therapy. As you said it has a carbohydrate, fat and protein content and then along with the exercise. So exercise should be always >> should be moderate >> when exercise >> after the male at least 10 to 13 minutes post meal >> and if they are going into the third treas it is better to restrict to the upper body >> because they might go in for a pre-term labor. Okay.

[01:00:49]Then then what are the other things?

[01:00:55]When will you do the you you think anomalies are common in GDM?

[01:00:59]>> Yes ma'am. Early anomaly scans would be done when it occurs diabetes it is common.

[01:01:08]>> Uh why >> is mainly because hypoglycemia is ftoxic. It produce free radicals. So it produces periodical injuries to the fetus resulting in congenitalations for the >> okay but why it is not common in GDM >> because the period of orogenesis is already over in the gestation.

[01:01:28]By the time >> after 24 weeks of >> it is common in GDM.

[01:01:37]>> UTI vaginal infections are common ma'am and >> macros is common is more common and anomalies are more common in type one and type.

[01:01:47]>> Okay. Okay. Why the why abortion is common? Can you tell us the complications? Maternal fetal everyone knows it is in the book but you should know why it occurs. Why abortion is more common in diabetes?

[01:02:06]You thought they will answer immediately. I was just waiting. Why abortions are more common? What happens?

[01:02:13]>> Placental damage might happen because of >> there is a yolk suck yolk suck injury.

[01:02:20]Okay. That is because all because of hypoglycemia only. If it is not controlled at the time of embryogenesis, there will be toxic to the yolk sack and the nutritional transfer to the embryo is prevented. That is why it is very very common to control the sugar levels in the at the conception. Whereas in anomalies are mainly due to as you said there may be free radicals all are because of hypoglycemia.

[01:02:48]Hypoglygasm and also there is >> effective argonic acid metabolism and a lot of inhibitors all you have to write in the theory paper. No, you have to write the anomaly the causes also you should write free oxygen radicals and inhibitors all those things. Okay. Is preeacclampsia common?

[01:03:08]>> Yes.

[01:03:09]>> Yes. 15% of preeacclampsia is there in a gestation.

[01:03:17]>> Okay. So you when will you start insulin if it is not controlled with the mnt >> after two weeks of giving medical that is in early gestation. Suppose as you said in the third trimester she has come and her OGCT is positive then you have to start uh after one week >> I in the second trimester you will start within two weeks ma'am and the third trimester we will ask for M& for one week and then uh if it is not controlled we'll start on insulin >> so then you will stop Mnt is it >> no ma'am along with along with Mnt also continue the thing what is four point profile and what is sevenpoint profile Four point profile includes seeing uh FBS fasting blood sugars as well as sugars blood sugars post meal all three times breakfast lunch as well as post dinner has to be seen >> in seven point profile all the uh preood and post of breakfast lunch and dinner along with it 3:00 a.m. CBG should be done now.

[01:04:19]>> 3A. Okay. When will you do seven point profile?

[01:04:22]>> Seven point profile is done for uh type 2DM patients on insulin mom and also GM under insulin who are taking higher doses of insulin.

[01:04:32]>> Yes. Especially of insulin is uncontrolled sugars and if you need to keep on changing the dose take such time you have to do a seven.

[01:04:44]sugars is well controlled and the insulin doses become static. How will you monitor the blood sugar? Karthik if you want to interrupt you can interrupt.

[01:04:53]No ma'am I'll be asking so I'll be asking them to do FBS as well as three PBVS which is scattered over a week now and then >> okay or anyone scattered every month you can do fasting and postprandial that is enough that thing it can be either after lunch or after breakfast or anything of that sort okay suppose if they're asking you to tell about the medical nutrition therapy and what are the foods she should avoid High GI index foods we should be avoiding and low GI foods like oats, bajra, millets all should be to be taken >> and complex carbohydrates should be taken and should avoid sugary substances >> like ice creams and ready sugars. No biscuits.

[01:05:44]>> What about fruits? What are the fruits they can take?

[01:05:47]>> Ma'am, they can take Goa.

[01:05:50]Goa, apple. They can be taken and should avoid the mango.

[01:05:56]>> And when tell goa apple goa apple banana also can be advised >> banana very rarely once a week one or like that. What what other fruit she can take?

[01:06:16]>> Orange then berries.

[01:06:19]>> Berries they can take strawberry, blueberry all which are not available in India know that they can take. So goa is important that they can take not an issue. What about vegetarian source of proteins?

[01:06:33]Soy >> I'm saying they can be taking uh paneer and soy products ma'am so >> soy know soya products they can take that is very important okay then what is gium plate >> so the size of >> gium plate has a size plate size of 23 cm and it has to be the 50% of the plate should contain an high fiber diet and then the other 25% should contain carbolex carbohydrates and the other 25% should contain proteins.

[01:07:09]>> You have controlled the blood sugar with insulin and suddenly a nearing term know that insulin requirement reduces.

[01:07:17]>> Yes.

[01:07:18]>> What uh why >> ma'am? Uh this is because placental insufficiency would happen and uh generally insulin resistance decreases in the third trimester. Mom, >> why? That's what I'm asking >> not because the placental in I'm not telling that why during labor there will be >> the growth of the placenta plateaus no all the thing it's coming to an end so even the lus start reducing so the contrainsulin hormone secretion the placental growth plateaus and moreover the fetus will have the beta cell hyperplasia it will handle the sugar levels more because that that fetal pancreas will start secretreting insulin so sugar level will be handled. So usually the insulin level for the mother requirement reduces as they are nearing the term pregnancy. Another one is a sudden drop in insulin also you should think of ud sudden intrain fetal death also can happen. So you should not be very happy.

[01:08:25]Oh thank god the 100 units has become 20 units like that we cannot be very happy you should also anticipate intraidentical death also at the same time. Okay. Why there is macrosomia?

[01:08:40]Mainly because of hypothesis. So whenever there is maternal hypoglycemia there will be hypoglycemia and hyperinsulinemia and insulin is in growth factor resulting in macrosia.

[01:08:51]>> Why there is shoulder dystocia?

[01:08:56]fat around the shoulder.

[01:09:02]>> Why there is increased shoulder deposition?

[01:09:05]>> Because it inhibits the lipolyis resulting in fat accumulation your shoulder and the abdomen >> other area it won't be >> more more around the shoulder area.

[01:09:14]>> That is why I'm asking why more insulin growth receptors are there in the intapular areas. Okay. So that is why more fats in is getting deposited in that area. Adipicoytes are deposited because of the insulin growth factor receptors are very high in the shoulder regions. Okay. Okay. And why there is polyhydramas?

[01:09:40]>> Same because of hypoglycemia and resulting in polyry of the baby also resulting in polyas.

[01:09:45]>> Okay. Hypoglycemia hypoglycemia resulting in polyure of the only one amniotic fluid glucose is >> it the amniotic membrane okay it is start secretreting more fluid okay and also sometime associated anomalies like open neural tube defects maybe DJ.

[01:10:16]>> Okay. What about u uh anomalies?

[01:10:23]>> More common is ventricular septile defect.

[01:10:26]>> Serious.

[01:10:27]>> No, no, no. TGV TGV is more common.

[01:10:34]>> TGV, VSG, ESG then >> senis cordal regression.

[01:10:42]>> Cordal regression syndrome. So most specific anomaly is >> most common anomaly is TGV >> TGV.

[01:10:52]>> So these are all very common only in type one and type two diabetes. Correct.

[01:10:57]Okay. If the pregnant mother is known diabetic becoming pregnant will you do any other special investigation? You start preconception start from preconception counseling.

[01:11:09]>> Yes ma'am. uh so in the preconceptional period the first thing I'll be doing is optimizing her via my mom and then I'll be advising all the diet plans for the patient plus I'll be advising the physical exercises and then I'll be checking her FBS PBS HB and I'll be checking her good whether it is under good glycemic control folic acid advice folic acid supplementation and uh check for diabetic retinopathy fun examination should be done along with it cardiac intervention And for nephropathy urine al like urine alumin should be checked and uh >> if she's taking any drugs for hypertension like AC and ARB it has to be stopped and it has to be interchanged to uh the other drugs ma >> and also other oral hypogly insulin. Okay. And what about statins?

[01:12:03]>> Statins also.

[01:12:05]>> Yeah. Start recent guideline you should not take statins when you are conceiving. Okay. Suppose if she has come to you uh suddenly without any preconceptual counseling she has conceived and she has come to you and if she has taken her retinal examination just two months back. Would you like to repeat again or you want to give a allowance?

[01:12:27]>> Ma'am we should be repeated again ma'am.

[01:12:31]uh it should be repeated again and most probably if it uh preconceptionally and around 20 >> she has conceived she has conceived and come and she has said I have just done everything two months back but suddenly I've conceived so would you like to repeat the retinal and renal profile see what the guidelines say is within 3 to 6 months if they have done it there is no need to repeat it can you do a laser photo coagulation for ninopathy during pregnancy.

[01:13:01]>> Yes ma'am.

[01:13:03]>> Earlier they said it is contraindicated.

[01:13:04]Now it's not contraindicated. What about delivery? Is is it a contraindication for a normal vaginal delivery?

[01:13:12]>> Proliferative retinopathy is a contra indication. Ma'am in proliferative active proliferative retinopathy is a contra indication. Otherwise known retinopathy patient normal labor is not a contra indication. Okay. Then what about uh so uh mother everything you have said the complication abortions anomalies then they're more prone for pre-term labor prem because of polyram what is theolytic of choice >> or you should avoid betaist diabetic patient you should avoid betaist and the preterm suppose if you are giving steroids so what care you should take >> doing monitoring for the patient even the patient is on steroids now so I'll >> frequently you might have to adjust the dose of the in accordingly to the CPG >> okay so what about uh baby baby is only after birth more complications no so during birth when will you deliver >> ma'am if the sugars are under well control we will deliver from 39 to 40 plus 6 weeks 6 months.

[01:14:25]>> Wait, wait. Okay. On M& and controlled with insulin you can deliver on date. No.

[01:14:34]>> Yes.

[01:14:37]>> So even with insulin they say on date but at least by 38 to 39 weeks. But if they are on high dose of insulin or associated with other complication you should admit them >> 37 completed weeks or by 38 weeks is macrosomia as an indication for severe >> if it is more than 4 kg >> 4.5 kg in patient then it can be an indication >> what about this IAPS criteria we know about dip criteria right that 75 g you know very well about dipsy criteria And what about IADPSG criteria?

[01:15:17]>> According to IADSG, 75 grams of uh glucose has to be taken uh uh with fasting and uh fasting sample should be taken and it should be less than 92 and 1 hour value should be less than 180 and 2 value should be less than 140. 153 any one value abnormal now we taking either two or more like now it is one is we are taking them as diabetes okay >> and uh what about monitoring during labor >> ma'am if we are inducing the labor induction of labor should be done in early morning hours ma'am previous night dose of insulin should be given the patient. Morning dose of insulin should be withheld. Uh when patient is on mechanical uh induction uh she can continue her diet and her dosing of insulin once she enters into active phase of labor. Preferably CBG should be checked every uh one hourly mom and uh because labor is a very uh strenous exercise activity. uh her CBG should be monitored and accordingly insulin should be started from >> should ideal to maintain around 100 no around 100 >> average glucose should be mean glucose should be 100 >> around 100 there is no unless there is an obsetic indication there is no indication for what about the c clamping tell me about c clamping M normal uh delay cord clamping >> early clamping or delayed cord clamping.

[01:17:07]What is this? Delay cord clamping.

[01:17:12]>> So usually we do early cord clamping. No but why? Because there is a theory that says the troponine will cause myioardial eskeemia to the baby. Okay. The troponin levels in the card blood will be very high. So they may cause migra that is why they prefer early C clamping only in diabetic pregnancies. Okay. Then anything else?

[01:17:37]Uh carta >> postpartum followup >> postpartum follow. will be doing and sugaring on day three of delivery month followed by in 4 to 12 weeks around 6 weeks of postpartum I'll be doing 75 gram of OGTT followed by and after one year I'll be asking them to repeat 75 g of OGT and then annual follow with FPS issue >> when will you check the blood sugar for the baby >> so delivery I'll be checking the baby's blood it has to be checked So, 24 hours you have to check till three stable sugar levels are obtained.

[01:18:27]So, three times four ideally mother and baby should be checked blood before feeding before she gets the breastfeed. No. So, what is the advantage of breastfeeding?

[01:18:41]In diabetic mother chances of neonal hypoglycemia will reduce >> reduce and mother sugar levels also will get because of breastfeeding. So decreases incidence of that in the motheration.

[01:19:02]>> Okay. What about contraception?

[01:19:06]>> Barrier methods are preferable.

[01:19:09]uh in uh if uh and PPI like copper can also be used if there is no infection in the mother and progesterones can progesterone can related only pills can also be given >> okay can be given no >> can be given except for this property there should be a precaution of infection >> nothing I want to tell them >> can we backm We have to rule out macrosia and before that we have to assess the pelvis also.

[01:19:43]So if we can follow the patients for >> um what is the pregnancy related risk the baby will go in for long term long-term effect for the fetuses they may go in for obesity diabetes and they will also go in for lot of autism.

[01:20:07]Autism, attention specific disorder. So many problems with the baby that is why we're worried about GDM right what are the pregnancy related risk factor that will conver transfer to the baby in pregnancy there is a >> m birth injuries can happen >> no no in the sugar level I'm asking if the mother is on a high dose of insulin even if it is a GDM if it's a high dose of insulin and a shorter duration of breastfeeding and recurrent GDM uh they are hypoglycemic in the first trimester itself those are all the risk factors that will reflect on the long-term outcome to the infant so these are all the things we should be very very careful when we about um anything else about the nephro you said no uh eGFR usually you do in renal diseases that is not very valid in pregnancy because the GFR itself will be increased. So you have to go with the spot protein creatinine ratio and also the >> microalaminora and other things. Okay.

[01:21:19]Okay. Anything else we missed?

[01:21:24]>> We have covered mostly everything ma'am.

[01:21:26]We have covered everything.

[01:21:28]>> Anything we missed something abortion and all you told no policy everything you told. Okay. I think we have it. Any other big topic to be covered?

[01:21:41]>> And also you should do 24 weeks if you have seen the fourth chamber and the outflow tract and all you can see at 20 weeks. But still we have to do the thing.

[01:21:56]>> So that that real time monitoring continuous glucose monitoring. What about insulin? Now we are using lispro and aspart right? They're all insulin analogs and also long acting insulin dete can be used. It has come recently delute earlier they said there you cannot use it but recent trials have come and madam has already told about the m trial and the concept trial all those trials you have to read for insulin okay diabetes edm otherwise I think we are done with the thing yeah >> thank you thank you so much uh the faculty and the students and the two uh speakers Dr. Shankar and Dr. Dr. Deepatiagar Rajamorti and the excellent coordination done by Dr. Vidya. I'm very happy that she has collected everything so beautifully and sorry I couldn't join at the beginning to welcome you all but I take this opportunity to thank Dr. Karpagal Sairam and Dr. K Priyadni who has put up this first webinar for this uh tenure through their medical education committee. Both of them did excellent work as committee chairpersons and the credit that goes to them. It is them who chose the topic should be on basics and on advanc so that it matches it kind of beginning and end of a case discussion. You need to know basics so that when it comes to discussion the advances in the recent advances would help them get a overall picture. So they suggest that uh template and we went ahead with that and uh with the same tempo we will be meeting all of you all on uh in the next uh discussion on an important topic a complex topic on amoria and over to Dr. Kpagal and Dr. Bria and to Vidya uh to wind up the session and say thanks to everyone who has contributed to this wonderful session.

[01:24:06]Uh thank you so much uh madam I mean it's something like you know every thing about GDM was and diabetes was discussed here. Thank you so much. It's you know it's a learning and you know sometimes you have to unlearn and relearn. So that is what is the most important thing in terms of medical practice because uh we keep things keep getting evolved and innovations keep coming. Thank you so much Vija madam kartika prahu and kpashank Dr. Deepa and all the post-graduates you really answered very well wishing you all the best and uh thank you so much everyone for joining it's nice to be a part of the medical education committee and keep learning and now I request our vesi to give the word of thanks yes first of all I would like to thank our president Dr. Dan Lakshmi madam who is a voracious academician uh to say that madam is thirst of knowledge like every time at any time she'll be thinking of only uh the committee meetings webinars and everything madam hats off to you madam really you are a big academician and we are so much inspired by your thirst for knowledge and also I thank the treasurer uh Dr. Sumati preman madam and also the secretary Dr. Malaraj madam and uh I thank Dr. Vidya Jri for wonderfully coordinating this session. It was a wonderful uh session and you did it very well Dr. Vidya Jri and the carbohydrate metabolism in pregnancy was superbly dealt by my student postgraduate Dr. Kpa Shankri I take this moment to be proud of you Dr. with Dr. Krypa thank you so much and I thank Dr. Deepa madam for giving us elaborate updates in glucose monitoring and insulin delivery and it was very new to us madam that smart pen cap sensor system patch pumps and that inhaled insulin uh therapy also it was very good madam and the pgs will had a good time learning about new things thank you Dr. Deepa madam and finally thank you so much Vijaya madam and I know about Vijaya madam uh even in her busy schedule in IOG when she was the director of IOG uh when she has a class or a lecture or a case discussion she will definitely take some time to prepare that and then come and discuss.

[01:26:29]She will say she will set off everything and then sit and read and come for the session. Just like that she will not enter into that case discussion or lecture. Until now you are doing the same. Madam you have elaborately covered each and every u thing whichever a post-graduate has to know about GDM and diabetes during pregnancy. Thank you Dr. Vijaya madam it was an excellent session and Dr. Kartika I thank you so much uh for bringing your postgraduates. They did the excellent job. Thank you Dr. Harsha and your team for presenting the case and answering all the questions. Thank you and all the best to all the postgraduates. Please do join in all our webinars from the medical education committee and thanks everyone. Thank you so much.

[01:27:20]>> Thank you ma'am.

[01:27:21]>> We have video on please. We'll just take a photo.

[01:27:24]>> Yeah, we'll just take a picture.

[01:27:24]>> Anita and go video. Yeah, thank you. And >> yeah, I'm taking a screenshot madam.

[01:27:33]>> Yes, ma'am. I have also taken few things.

[01:27:36]>> Please welcome to our oxy clinical meeting tomorrow and thank you Sahiti.

[01:27:40]You've been really tremendous in giving us a platform very >> again important topic to be discussed induction of labor by Dr. Pyapin is going to be very important and our next topic webinar is Minor on 26th of June.

[01:27:52]So please do join us and there are number of web webinars going on nine webinars per month. Please do join from the comfort of your house.