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Preexisting DM in pregnancy

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PROF ABOUBAKR ELNASHAR

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Preexisting DM in pregnancy

  1. 1. DIABETES IN PREGNANCY Prof. Aboubakr Elnashar Benha ubiversity Hospital, Egypt elnashar53@hotmail.com PHYSIOLOGICAL CHANGES 1. Insulin resistance & relative glucose intolerance. ▪ Increasing after the first trimester ▪ Due to diabetogenic(anti-insulin)hormones secreted by placenta ▪ human placental lactogen ▪ Cortisol ▪ Glucagon ▪ oestrogen ▪ progesterone ▪ Insulin requirements increase throughout, maximal at term.
  2. 2. 2. The renal tubular threshold for glucose falls: ▪ Glycosuria ▪ Glycosuria is not a reliable diagnostic tool for impaired glucose tolerance or diabetes in pregnancy. 3. Starvation results in early breakdown of triglyceride: liberation of fatty acids&ketone bodies: increased risk of ketoacidosis. ▪ This is most marked in the third trimester.
  3. 3. PRE-EXISTING DIABETES MELLITUS 1. PREVALENCE ▪ 1–2% of pregnancies. ▪ In the UK, ▪ type 1 is about 0.5% ▪ type 2 about 3%–4% (lower in women of childbearing age, but higher in Afro- Caribbean and 10% in Asian ethnicities). ▪ pre-existing diabetes in pregnancy 0.4% (0.27% type 1 and 0.1% type 2). 2. DIAGNOSIS OF DM (IN NON-PREGNANT WOMEN) ▪ One of the following criteria must be confirmed by repeated testing on a subsequent day unless the patient is symptomatic (i.e., polyuria, polydipsia, unexplained weight loss) in which case a single abnormal value suffices: ▪ R venous plasma glucose ≥11.1 mmol/L (200mg/dl) ▪ F plasma glucose ≥7.0 mmol/L (126mg/dl) (whole blood ≥6.1 mmol/L) (110mg/dl) ▪ 2-hour plasma glucose ≥11.1 mmol/L (200mg/dl). 2 hours after 75 g OGTT ▪ Type 2 diabetes diagnosed using HbA1C threshold of 48 mmol/L (6.5%). ▪ Diagnosis requires a second value above 48 mmol/L. ▪ 42–47 mmol/L (6.0%–6.4%) are deemed at high risk of diabetes&should have lifestyle advice&annual monitoring.
  4. 4. Diagnosis of impaired glucose tolerance ▪ IGT is a stage of impaired glucose regulation ▪ F plasma glucose <7.0 mmol/L (126mg/dl) and ▪ OGTT 2-hour value ≥7.8 mmol/L (140mg/dl) but <11.1 mmol/L.(200mg/dl) Impaired fasting glucose ▪ F glucose ≥6.1 mmol/L(110mg/dl) but <7.0 mmol/L.(126mg/dl) 3. EFFECT OF PREGNANCY ON DIABETES 1. Insulin requirements ▪ {normal pregnancy is associated with an increase in insulin production & insulin resistance} ▪ Type 1 diabetes require increasing doses of insulin as pregnancy progresses. ▪ Maximum requirements at term usually reach at least 2 fold pre-pregnancy doses. ▪ Type 2 diabetes often need the addition of insulin to their therapy or increasing doses of insulin. ▪ Rapid increases in insulin requirements between 28& 32 w, when the fetus is growing rapidly.
  5. 5. 2. Hypoglycaemia ▪ More common in pregnancy {intensified diabetic control ‘hypoglycaemia unawareness}’. ▪ Many maternal deaths caused by diabetes are due to hypoglycaemia. ▪ For every 1% fall in HbA1C, there is a 33% increase in hypoglycaemic attacks. 3. Ketoacidosis: ▪Rare ▪may be associated with ▪Hyperemesis ▪Infection ▪Tocolysis ( β sympathomimetics), or ▪Steroid therapy.
  6. 6. 4. Retinopathy: ▪Two-fold increased risk of development or progression of existing disease. ▪Rapid improvement in glycaemic control: increased retinal blood flow, which can cause retinopathy. ▪All diabetic women should have assessment for retinopathy in pregnancy, and proliferative retinopathy requires treatment. ▪Early changes usually revert after delivery. 5. Nephropathy: ▪5–10%. ▪Renal function & proteinuria may worsen during pregnancy. ▪usually temporary. ▪increased risk of ▪pre-eclampsia ▪IUGR ▪ increased surveillance is required.
  7. 7. 6. Ischaemic heart disease: ▪{Pregnancy increases cardiac workload}. ▪Women with symptoms should be assessed by a cardiologist before conception. 7. Women with autonomic neuropathy and gastric paresis often experience deterioration of their symptoms in pregnancy. 4. EFFECT OF DIABETES ON PREGNANCY I. Maternal hyperglycaemia: fetal hyperglycaemia. II. Fetal hyperglycaemia: hyperinsulinaemia (through β –cell hyperplasia in fetal pancreatic cells). Insulin acts as a growth promoter: • macrosomia • organomegaly • increase erythropoiesis • fetal polyuria (polyhydramnios).
  8. 8. III. Neonatal hypoglycaemia: {removal of maternal glucose supply at birth from a hyperinsulinaemic fetus}. Respiratory distress syndrome: ▪more common {surfactant deficiency occurring through reduced production of pulmonary phospholipids}.
  9. 9. 5. COMPLICATIONS OF DIABETES IN PREGNANCY I. Maternal •Infections: UTI., recurrent vulvovaginal candidiasis, respiratory, endometrial, wound infections • Pregnancy-induced hypertension/pre-eclampsia. • Retinopathy (15%). • Nephropathy. • Cardiac disease. ▪Obstructed labour. • Operative deliveries: CS & assisted vaginal deliveries. II. Fetal • Miscarriage* • Congenital abnormalities: In diabetics with poor control ▪ The specific: sacral agenesis, but this is very rare ▪ More common: congenital heart defects, skeletal abnormalities, NTD. • Preterm labour. • Polyhydramnios (25%). • Macrosomia (25–40%). • IUGR. • Unexplained IUD.
  10. 10. ▪ Congenital abnormalities. ▪ Incidence: 4% (double background) ▪ 3fold increase of NTD and congenital heart disease. ▪ Risk: directly related to ▪ glycaemic control around the time of conception ▪ HbA1C. ▪ <8%: risk of 5% ▪ >10%: risk is as high as 25%. ▪ Normal: risk is eliminated ▪ Recommendation at the time of conception. ▪ HbA1C should be <7% (USA) <6.1%in (UK) ▪ Macrosomia ▪ B wt>4.5 kg or >90th percentile for g age. ▪ Insulin is an anabolic, growth-promoting hormon ▪ baby is fat and plethoric, with all organs enlarged particularly the liver ▪ More common with poor diabetic control, but may also occur in cases of excellent control. ▪ incidence increases significantly when mean maternal blood glucose >7.2 mmol/L(130mg/dl) ▪ incidence of b wt >4 kg was 21% ▪ incidence of shoulder dystocia was 8%. ▪ Often associated with polyhydramnios {fetal polyuria}: preterm PROM and cord prolapse. ▪ increases the risk of traumatic delivery, particularly shoulder dystocia.
  11. 11. ▪ Sudden unexplained IUD ▪ inversely related to the degree of diabetic control ▪ highest after 36w. ▪ Chronic hypoxia (more common in macrosomic babies in the presence of hyperglycaemia & lactic acidosis. ▪ Not predicted from CTG, Doppler velocimetry or FBP. ▪ Maternal hyperglycaemia, and particularly ketoacidosis ▪ detrimental to the fetus, high (10%–25%) fetal mortality ▪ In contrast, maternal hypoglycaemia is well tolerated by fetus. III. Neonatal • Polycythaemia. • Jaundice. • Hypoglycaemia. • Hypocalcaemia. • Hypomagnesaemia. • Hypothermia. • Cardiomegaly. • Birth trauma: shoulder dystocia, fractures, Erb’s palsy, asphyxia. • Respiratory distress syndrome.
  12. 12. ▪ Fetal hyperinsulinaemia ▪ may lead to chronic fetal hypoxia: stimulates extramedullary haemopoiesis, fetal polycythaemia and neonatal jaundice. ▪ In the presence of fetal hyperinsulinaemia, when the cord is clamped, the neonate is ‘cut off’ from its supply of glucose from the mother and is at risk of neonatal hypoglycaemia. ▪ Perinatal and neonatal mortality rates ▪ can be increased five- to tenfold in babies ▪ relate to HbA1C at conception and in early pregnancy. ▪ perinatal mortality rate for both type 1 and type 2 diabetes was about 3%.
  13. 13. 7. MANAGEMENT I. Prepregnancy care ▪ This is one of the most important aspects 1. Achievement of optimal control: ▪ FBS: between 63-106mg/dl ▪ 1h post-prandial <140 mg/dl (increased risk of miscarriage and congenital abnormalities with poor control). 2 . Assessment of severity of diabetes: check for ▪Hypertension ▪Nephropathy ▪U&E ▪Urinalysis ▪urinary protein: creatinine ratio ▪24h urine for protein. Proteinuria should be documented and quantified prior to pregnancy with an ACR or PCR. ▪Creatinine clearance {PET is increased in the presence of microalbuminuria (30– 300 mg/day) although to a lesser degree than in those with frank nephropathy (>300 mg/day).
  14. 14. ▪Retinopathy ▪fundoscopy, ophthalmology assessment. ▪If necessary, proliferative retinopathy may be treated with photocoagulation prior to conception ▪Neuropathy ▪clinical assessment ▪Cardiac disease. 3. Education ▪Good control: ▪Decreased F congenital abnormalities& preeclampsia ▪improved pregnancy outcome ▪Effects of hyperglycaemia on fetus ▪Need for tight control ▪To inform doctor as soon as pregnancy confirmed ▪Some drugs may need stopping (ACEIs). 4. General health: ▪stop smoking ▪optimize weight (aim for a normal BMI),
  15. 15. 6. Medications ▪ Folic acid: {Increased risk of NTD}: 1mg folic acid. ▪ Rubella status: offer vaccination if not rubella immune. ▪ Contraception: until good control achieved ▪ Unplanned pregnancy is a risk factor for LFGA ▪ Contraindications to pregnancy ▪ ischaemic heart disease ▪ untreated proliferative retinopathy, ▪ severe gastroparesis ▪ severe renal impairment (CKD 4/5; creatinine >250 μmol/L). II. Antenatal care ▪Multidisciplinary team with a diabetologist. 1. Medical management 1. Control of DM ▪ Diet: ▪ Strict adherence to a low-sugar, low-fat, high-fibre diet ▪ low glycaemic index. ▪ Starvation and severe calorie restriction should be avoided because of the risk of ketoacidosis ▪ HbA1c every month: ▪ reflects control over the preceding 2mths. .
  16. 16. ▪ Home blood glucose monitoring (HBGM) ▪ using ▪ glucose oxidase strips and glucose meters or ▪ ideally a continuous glucose monitoring sensor (CGMS) (such as the Freestyle Libre®). ▪ spend more time within target glucose levels. ▪ lower rate of LGA babies, and improved neonatal outcome ▪Test blood glucose levels at least 4 times/d ▪usually before meals but post-meal glucose may give tighter control ▪before going to bed at night. ▪ Target capillary blood glucose ▪ Fasting: 3.5–5.3 mmol/L (63-95mg/dl) ▪ 1 H PP: <7.8 mmol/L (140mg/dl) (the same for types 1, 2 and gestational diabetes). ▪ Outcomes such as b wt & neonatal hypoglycaemia correlate better with postprandial than with preprandial glucose levels. ▪ Using postprandial targets also leads to better improvements in maternal HbA1C levels.
  17. 17. ▪ Management of type 1 diabetes ▪ Increasing doses of insulin throughout pregnancy, although insulin requirements may fall or be variable in 1 st trimester. ▪ The inevitable result of tighter control is an increased risk of hypoglycaemic attacks. ▪ Women should be warned about risks of hypoglycaemia& unawareness of hypoglycaemia particularly in 1st trimester. ▪ usually require a ‘snack’ mid-morning, mid-afternoon, and before retiring at night. ▪ Women should be provided with concentrated glucose solution for use in the event of hypoglycaemia. ▪ Relatives or partners may be taught how to administer IM glucagon injections to avert profound hypoglycaemia in situations where the woman is unable or unwilling to eat or drink. The woman should be advised that glucagon provides only temporary relief from hypoglycaemia and should always be followed by oral ▪ Most women are managed with basal bolus regimens using fast-acting insulin analogues (Humalog® insulin lispro, Novorapid® insulin aspart) taken with meals. ▪ The long-acting insulin analogues detemir and glargine are the long-acting insulins of choice in pregnancy. ▪ Glargine dose is often divided into a BD regime from ws 16 to 20 in order to achieve good preprandial control. ▪ In some countries NPG (isophane) insulin is still used in pregnancy and this is also often used as a BD regime. ▪ Insulin often need to be increased in the presence of infection, use of corticosteroids ▪ Women should be offered blood ketone testing strips and a meter and advised to test for ketonaemia if they become hyperglycaemic or unwell.
  18. 18. ▪ Management of type 2 diabetes ▪ Most women require tt with insulin during pregnancy. ▪ Metformin ▪ biguanide can be used as an adjunct or alternative to insulin (NICE). ▪ Thiazolidinediones ▪ e.g., rosiglitazone, pioglitazone ▪ reduce peripheral insulin resistance. ▪ Out with pregnancy they are used as 2 nd line therapy added to either metformin or sulphonylureas ▪ Their use is avoided in pregnancy. ▪ Sitagliptin ▪ dipeptidyl peptidase-4 (DPP-4) inhibitor increasing the production of insulin and decreasing the production of glucagon by the pancreas. ▪ It is also avoided in pregnancy. ▪ Glucagon-like peptide-1 (GLP-1) receptor agonists and SGLT2 inhibitors are also avoided in pregnancy. 2. Prevention of Diabetic complications ▪ Retinopathy: ▪ ophthalmological examination with digital imaging of the retina with mydriasis using tropicamide pre-pregnancy and in early pregnancy if their annual assessment occurred more than 3 months previously and at 28 weeks. If diabetic retinopathy is present, the next assessment should be at 16–20 weeks. Laser photocoagulation can be used either to treat or prevent proliferative retinopathy in pregnancy. ▪ Diabetic retinopathy is not a contraindication to rapid optimization of glycaemic control nor to vaginal delivery. ▪ Women with pre-proliferative diabetic retinopathy should have ophthalmological follow up for at least 6 months postpartum.
  19. 19. ▪ Nephropathy: ▪ Referral to a nephrologist pre-pregnancy or in early pregnancy if the serum creatinine is ≥120 μmol/L or the protein leak is >0.5 g/day or albumin creatinine ratio [ACR] > 30 mg/mmol. ▪ Women with diabetic nephropathy: ▪ regular monitoring of renal function ▪ quantification of proteinuria (protein creatinine ratio [PCR] or albumin creatinine ratio ▪ Hypertension ▪ 30% of women with diabetic nephropathy ▪ 75% will develop hypertension by the end of pregnancy. ▪ Strict control of hypertension in pregnancy is important to prevent ongoing renal damage. ▪ Therefore in hypertensive or nephropathic women with diabetes, a low threshold for antihypertensive therapy (e.g., 135/85) is used.
  20. 20. 2. Obstetrical management Antenatal 1. Regular BP and urinalysis checks to detect PET 2. US: 1. Dating & viability scan: early 2. NT scan: at 11–13 w 3. Anomaly scan at 18–20 w’, including 4-chambered assessment of f heart. 4. Regular scans for f growth and liquor volume in the third trimester (e.g. 28, 32, and 36 w) to detect macrosomia and polyhydramnios 3. Low-dose aspirin to all women with diabetes {increased risk of PET}. 4. Corticosteroids ▪ to induce fetal lung maturation ▪ additional insulin prescribed ▪ close monitoring to avoid severe hyperglycaemia and DKA.
  21. 21. II. Intrapartum ❑ Timing and mode of delivery ▪should be individualized, based on ▪EFW ▪obstetric factors ▪previous mode of delivery ▪Gestation ▪glycaemic control ▪antenatal complications ▪Balance the risks of ▪PTL and its associated complications ▪late IUD and macrosomia with its complications. ❑Timing of delivery (NICE) ▪ induction of labour or elective CS if indicated between 37 and 38 + 6 w for women with ▪ no maternal or fetal complications ▪ good glycaemic control. ▪ Delivery should be expedited if complications occur.
  22. 22. ❑Mode of delivery ▪Vaginal delivery is preferred. ▪Continuous electronic fetal monitoring ▪Shoulder dystocia ▪more common at all birth weights than in the non-diabetic population. ▪ CS: (both elective and emergency) are increased ▪ Overall: 67% ▪ Emergency: 38%. ▪ {high rate of macrosomia (21% of babies weighed more than 4 kg; 6% >4.5 kg), this high rate may be unavoidable. ▪Elective CS if ▪EFW is >4.5kg. ▪EFW is 4–4.5kg use obstetric factors to influence decision. ▪Antibiotic and thromboprophylaxis
  23. 23. ❑ Glycaemic control ▪ type 2 diabetes An insulin infusion is not usually required ▪ type 1 diabetes ▪ sliding scale/variable rate insulin infusion. ▪ IV infusions of short-acting insulin and dextrose are administered throughout active labour and delivery via separate giving sets, to allow acceleration of glucose infusion and cessation of insulin in the event of hypoglycaemia. ▪ women using insulin pumps: continue these in labour but to discontinue for CS. ▪ The capillary blood glucose should be estimated hourly, and the insulin infusion rate altered according to a sliding scale determined by the individual daily insulin requirements. ▪ The usual dose range is 2–6 U/hr. ▪ The target glucose level during labour and delivery is 4–7 mmol/L (72-126mg/dl), the aim being to avoid hypoglycaemia. ▪ The dextrose infusion (5% or 10%) should provide 500 mL of fluid every 8 hours. ▪ Insulin drives extracellular potassium into the cells. It is important, therefore, to include potassium replacement with the i.v. dextrose to avoid hypokalaemia which may otherwise result especially if glucose levels are high.
  24. 24. III. Post-partum care ▪Baby ▪early feeding ▪glucose monitoring. ▪Breast-feeding ▪Encourage ▪Avoid oral hypoglycaemic drugs if breastfeeding ▪metformin and insulin are safe. ▪ Type 1 diabetes ▪ Following delivery of the placenta, the rate of infusion of insulin is halved ▪ Postpartum, insulin requirements return rapidly to pre-pregnancy levels. ▪ Once women are eating normally, SC insulin at either the pre-pregnancy dose or at a 25%–40% lower dose if the women intends to breastfeed, which is associated with increased energy expenditure. ▪ type 2 diabetes ▪ who are breastfeeding can resume or continue taking metformin or glibenclamide (glyburide). ▪ Other oral hypoglycaemic drugs are avoided in breast feeding.
  25. 25. ▪Contraception • Avoid the COCP if ▪breast-feeding or ▪vascular complications. ▪Progesterone-based contraception Safe ▪No contraindications to an IUCD. ▪should be fitted from 6w post-partum onwards. ▪Sterilization or vasectomy ▪should be considered if the family is complete.
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