Medical notes | LY ® Document Style @ Upload © Tag * GDM Al — refers to the cases where glycemic control is 1 achieved without medical intervention * GDM A2 — refers to the cases where glycemic control is 2 achieved with medical intervention * pathophysiology ¢ defining features of GDM Vv * increased insulin resistance * what are the hormones that are responsible to increasing insulin resistance > human placental lactogen, prolactin, cortisol and estrogen * what is the primary aim of secretion of these hormones by the fetal placenta? + the primary aim of increasing insulin resistance is to allow for increased glucose concentration to allow for the survival of the fetus * beta-cell dysfunction — loss of the ability to adequately sense blood glucose concentration or to release sufficient insulin in response * impaired regulation of hepatic glucose production * Etiology + Risk factor for gestational DM + 1 * diabetes ina first degree relative * maternal weight >85Kg * BMI >30 ([weight in Kg]/[height in meters]2)* previous baby >4.5kg * previous unexplained perinatal deaths, still births or repeated abortions * previous congenital abnormality * two or more episodes of glycosuria on routine testing * Complications of DM in pregnancy Fetal complications J * fetal macrosomia * fetal macrosomia is define as weight in the 90th ¥ percentile or birth weight of >4Kg »_ in term infants * pathophysiology + fetal hyperglycemia secondary to uncontrolled maternal hyperglycemia leads to increased production of IGF-1 (aim — cause hyperplasia of the pancreatic beta cells to increase insulin production to achieve glycemic hemostasis) and |GFBP-3 (aim — to increase bioavailability of IGF). IGF leads to stimulation of growth which can cause fetal macrosomia * impaired fetal growth * pathophysiology > maternal hyperglycemia can lead to vascular damage, hypoxia and cellular dysfunction * pulmonary complications * pulmonary complications such as Y ~ 1. RDS * pathophysiology > hyperinsulinemia interferes with the timing of glucocorticoid-induced biosynthesis of surfactant leading to RDS by inducing reduced production of fibroblasts pneumonia TTN 2° to fetal macrosomia Pen persistent pulmonary hypertension* pathophysiology > PPH can be caused by several factors such as impaired lung development and pulmonary vascular remodeling * Gastrointestinal problems * suchas 4 1. feeding intolerance 2. duodenal atresia 3. anorectal atresia 4, smali-left colon syndrome 5. Hirschsprung disease * Renal complications * complications such as + 1. hydronephrosis 2. renal agenesis 3. urethral duplication * metabolic and electrolyte abnormalities * suchas 4 ~ 1. hypoglycemia * pathophysiology > maternal hyperglycemia directly translates to fetal hyperglycemia, this in turn leads to increased fetal insulin production. at this time too, the liver is not well equipped to store glucose. When the baby is delivered and the cord is clamped, there is a sudden loss of glucose supply, coupled with the increased insulin production and lack of glycogen stores (and sufficient glucagon production) the baby becomes hypoglycemic * consequences + fetal hyperglycemia can lead to brain damage, RDS and affect the heart rhythm and function 2. perinatal stress 3. hypocalcemia4. hypomagnesemia * hematologic complications * suchas 4 1. polycythemia 2. thrombocytopenia 3. hyperbilirubinemia * Cardiovascular abnormalities * suchas 4 1. cardiomyopathy 2. CHD * Birth trauma * suchas J © 1. shoulder dystocia * common complications of shoulder dystocia are > brachial plexus injury and fractured clavicle 2. visceral hemorrhage 3. Birth asphyxia * CNS malformations * suchas 4 * anecephaly * spina bifida * caudal dysplasia * neurologic immaturit ¢ Maternal complications + * Diabetic Ketoacidosis * hypoglycemia * vasculopathy * neuropathy hypertensive disorders infection or sepsis* obstetric complications + © difficult labor — obstructed labor, shoulder dystocia due to fetal macrosomnia * diminished uteroplacental blood flow — vasculopathy potentially inducing vasculopathy * Diagnostic formulation + Investigations ¢ Labs v * oral glucose tolerant test (not performed in lab) * indication > if one or more risk factors are present (Risk factor for gestational DM) * One-step approach * how it is performed v * the patient is required to fast for 8 hours * fasting blood glucose is noted * the patient is given a solution containing 75g glucose then reading are taken 1 hour and 2 hours post ingestion of the solution * readings that are positive for GDM? > FBG >5.lmmol/L, 1 hour >10mmol/L and 2 hour >8.5 mmol/L * how is the diagnosis made? + the diagnosis is made when =1 plasma glucose value is at or above the threshold * Scenario: what if the FBG >7.0 mmol/L or 2 hour reading >11.1 mmol/L, what is the diagnosis? > pregestational diabetes * Two step approach * how is it done? J © the patient is not required to fast* first step: give the patient 50g of glucose solution, administered without regard for the time of day * serum glucose is measured after 1 hour. Only if the serum glucose reading >7.8mmol/L then the patient is allowed to proceed with the second step * the patient will then fast and a fasting blood glucose is taken then they will be given 100g glucose solution * serum glucose is then recorded 1 hour post intake then 2 hours post intake and finally 3 hours post intake * How is the diagnosis made? > a positive test is generally defined as =2 glucose values at or above threshold * readings positive for GDM ? > fasting >5.3mmol/L, 1 hour >10mmol/L, 2 hour >8.6mmol/L. and 3 hour >7.8mmol/L. * glycosylated hemoglobin © what is the normal HbAIC? > 6.5% ¢ Imaging + © Ultrasound scan * what to evaluate during ultrasound + fetal welfare, growth monitoring and the exclusion of congenital malformations + Management * Preconception * Particular emphasis on normalizing glucose levels before conception * what is the advantages of this? it reduces the risk of birth defects, they tend to occur 3 to 6 weeks after conception * during pregnancy* Screening in the first trimester * If the FBG is >7.0mmol/L (126mg/dl) or RBG is >11.1mmol/L (200mg/dl) and the patient is exhibiting symptoms or the HbA\c reading is greater than 6.5% then the diagnosis is pregestational diabetes (Overt diabetes) * Prenatal care Y * individualized diet intake to prevent weight gain of more than about 6.8 - 11.3 kg * moderate exercises (at least 30 min light walking) * women should undergo screening at 24-28 weeks especially for those considered high risk patients * ANC testing together with the following from 32 weeks to delivery; NST(weekly), BPP (weekly), fetal kick chart and AFI * insulin therapy to be started for unsuccessful glucose control via diet and GDM A2, Patients should be admitted for close follow up * insulin dosage > 0.7units/Kg - 1.0units/kg * Timing of delivery * timing of delivery for mothers with GDM A2 > 39+0 to 39+6 weeks * timing of delivery for mothers with GDM Al > 39 weeks too 40 + 6 weeks * timing of delivery for mother with poorly controlled diabetes > 37 weeks to 38+6 weeks * Question: in which conditions would there be a need to deliver the baby for a mother with GDM with <37 weeks GA? > when aggressive efforts to control blood sugar such as hospitalization have failed * Pre-requisite for scheduled cesarian delivery for women with GDM > fetal weight <4500g * Corticosteroid use in GDM motherswhat is the effects of corticosteroids in pregnant mothers with GDM? > it caused transient hyperglycemia * pathophysiology? ~ corticosteroids counteract the effect of insulin * what are the corrections that have to be made of the insulin regiments in GDM mothers receiving corticosteroids? 4 * Day 1— 25% increase of the total insulin dose * Day 2— 40% increase of the total insulin dose * Day 3 — 40% increase of the total insulin dose * Day 4 — 20% increase of the total insulin dose * Day 5— 10% to 20% increase of the total insulin dose * Day 6 — revert back to insulin dose before the administration of corticosteroids © Labor and deliver * sought after method of delivery for women with GDM? > vaginal delivery * what are the indications for C/section for pregnant mothers with GDM? > same obstetric complications * Insulin management during labor and delivery 4 * usual dose of intermediate acting insulin is given at bed time the night before and insulin is withheld the morning after * start the patient in normal saline * when the patient starts active labor or when blood glucose drops to <3.8 mmol/L (70mg/dL), switch the NS for 5% DNS at 100-150mis/hour * glucose levels should be checked every hour allowing for adjustment in the insulin or glucose infusion rate * regular short-acting insulin is administered by infusion at 1.25unit/hour if glucose level exceeds 5.5mmol/L (100mg/dL) * monitor fHR carefullyhalve the insulin dose immediately after delivery for the next 24 hours, then start the patient on the insulin dose during pre-pregnancy period * what is the rationale in halving the insulin dose? > immediately after the delivery of the placenta, there is a drop in the diabetogenic hormones that were responsible for insulin resistance, hence insulin sensitivity is increased and hence there is a big risk of the patient having hypoglycemia if the dose is not halved * this continues until the patient starts taking meals * Post natal follow up: * when should you screen mothers with hx of GDM post partum for DM or Pre-DM? > between 4-12 weeks together with 1-2 yearly follow up * The blood glucose level should be checked after 24 hours following delivery; if elevated it should be treated with insulin » and not OHA's ~ if the mother has begun breastfeeding. * The baby * Macrosomia common but can be reduced with good control. * Fetal islets hyperplasia is common and neonates must be observed for signs of hypoglycemia. * The baby usually are given hypertonic solution of glucose immediately after delivery. * Therefore blood sugar level should be checked regularly in the neonates. * Mother can breastfeed, and this is encouraged to keep the blood sugars in control. * post delivery contraception* what is the best method of contraception in women with GDM > puerperal sterilization is the best. Progestin only or parenteral contraceptive may be considered because of their effect on carbohydrate metabolism. COC’s are not recommended because they increase the risk of thrombovascular accident and IUCD’s increase the risk of infection + Lactation * why are metformin, glyburide and insulin contraindicated during lactation? > all these drugs have the capacity to be transferred during lactation and hence risk severe hypoglycemia * measures taken to correct this Y * reduce the basal insulin dosage * carbohydrate intake prior to breastfeeding * why type of diabetic patients are at risk for this? > women with TIDM * what could be a substitute for breast milk? > Soy based milk