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![• Prepregnancy planning and tight
glycemic control (hemoglobin A1c
[HbA1c ] <6.5%) is crucial in
pregestational diabetes in order to
achieve the best outcomes for the
mother and the baby.](https://image.slidesharecdn.com/infantsofdiabeticmothersidm-241211132308-6da9c2bf/75/Infants-of-diabetic-mothers-IDM-pptx-10-2048.jpg)
Infants of diabetic mothers (IDM).pptx
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- 2. Objctives By the endof this lecture the student should • Know the duration of normal pregnancy • Know the definitions of preterm , postterm, low birth weigh,VLBW ,ELBW,SGA,LGA,IUGR • Descibe the pathophysiology of fetal and neonatal morbidities associated with maternal diabetes mellitus • Explain the risk of diabetes on the fetus and neonate
- 3. • Normal pregnancylasts about 280 days (40 weeks) • Premature or preterm :those born before 37 wk from the 1st day of the LMP (born before 37 weeks of pregnancy) • Postterm neonates are those born after 42 completed wk of gestation, as calculated from the mother's LMP.
- 4. 37 0/7 - 38 6/7 weeks Early term 39 0/7 - 40 6/7 weeksFull term 41 0/7 - 41 6/7 weeks Late term
- 5. • Low birthweight (LBW) : infants with a birth weight <2500 g • very low birth weight (VLBW) :infants with a birth weight <1500 g • Extremely low birth weight (ELBW): infants with a birth weight <1000 g
- 6. • Large forgestational age (LGA) : those with birth weight >90th percentile for gestational age • Small for gestational age (SGA) : those with birth weight <10th percentile for gestational age
- 7. • Intrauterine growthrestriction (IUGR) is a prenatal diagnosis to describe a fetus who fails to reach in utero growth potential
- 8. • Amna is25 years old diagnosed as type 1 diabetes mellitus 5 years ago • She is pregnant on 25 weeks • She wants to know about the risk of diabetes mellitus on her baby
- 9. • Complications relatedto diabetes are milder in gestational vs pregestational (preexisting type 1 or type 2) diabetes.
- 10. • Prepregnancy planningand tight glycemic control (hemoglobin A1c [HbA1c ] <6.5%) is crucial in pregestational diabetes in order to achieve the best outcomes for the mother and the baby.
- 11. Pathophysiology • The probablepathogenic sequence is that maternal hyperglycemia causes fetal hyperglycemia , and the fetal pancreatic response leads to fetal hyperinsulinemia , or hyperinsulinism .
- 12. • while maternalglucose crosses the placenta, maternal and exogenous insulin dose not. • Fetal hyperinsulinemia and hyperglycemia cause increased hepatic glucose uptake and glycogen synthesis, accelerated lipogenesis, and augmented protein synthesis
- 13. • Separation ofthe placenta at birth suddenly interrupts glucose infusion into the neonate without a proportional effect on hyperinsulinism, leading to hypoglycemia during the 1st few hr after birth.
- 14. • The riskof rebound hypoglycemia can be diminished by tight blood glucose control during labor and delivery.
- 15. Clinical Manifestations • Hypoglycemia: – Only a small percentage of these infants become symptomatic. – Risk for neonatal hypoglycemia in the 1st hours of life, with an increased risk in both large- and small-for-gestational-age infants. – Infants should initiate feedings within 1 hr after birth.
- 16. • Hypocalcemia and hypomagnesemia: can occur in the 1st 24-72 hr of life due to delayed response of the parathormone system.
- 17. • LGA :IDMtend to be large as a result of increased body fat and enlarged viscera • Normal birth weight if diabetes is well controlled • Low birth weight if they are delivered before term or if their mothers have associated diabetic vascular disease.
- 18. • Puffy, plethoricfacies resembling that of patients who have been receiving corticosteroids. • Birth trauma (brachial plexus injury) :Infants are macrosomic or LGA
- 19. • Birth asphyxia –becauseof their large size @decreased ability to tolerate stress, especially if they have cardiomyopathy and other effects of fetal hyperinsulinemia – Increases the risk of hypoglycemia, hypomagnesemia, and hypocalcemia.
- 20. • Polyhydramnios • Pretermlabor (induced and spontaneous)
- 21. • Fetal mortalityrate is greater in both pregestational and gestational diabetic mothers than in nondiabetic mothers • Fetal loss throughout pregnancy is associated with poorly controlled maternal diabetes, especially diabetic ketoacidosis .
- 22. • The neonatalmortality rate of IDMs is >5 times that of infants of nondiabetic mothers
- 23. • Renal veinthrombosis :should be suspected in the infant with a flank mass, hematuria, and thrombocytopenia.
- 24. • Congenital anomaliesof the central nervous system and cardiovascular system are most common
- 25. • Failure ofneural tube closure (encephalocele, meningomyelocele, and anencephaly) • Congenital heart disease e.g transposition of great vessels,VSD, ASD, Hypoplastic left heart,Aortic stenosis,Coarctation of the aorta • Transient hypertrophic cardiomyopathy (Interventricular septal hypertrophy )
- 26. –Caudal regression syndrome(Less common) –Intestinal atresia (Less common) –Renal agenesis (Less common) –Hydronephrosis (Less common) –Cystic kidneys (Less common)
- 27. Other morbidity inInfants of Diabetic Mothers • Surfactant deficiency-RDS • Transient tachypnea of the newborn • Persistent pulmonary hypertension • Hyperbilirubinemia • Polycythemia • Visceromegaly • Predisposition to later-life obesity, insulin resistance, and diabetes
- 28. Investigations • RBG • CBC(hematocrit for polycythemia) • S.Calcium • ECG and echocardiography if hypertrophic cardiomyopathy or cardiac malformation is suspected
- 29. Summary • Diabetes inpregnancy increases the risk of complications in the mother and the baby. • Prepregnancy planning and tight glycemic control is crucial to achieve the best outcomes • High clinical suspicion ,good prenatal history ,Prenatal ultrasound and a thorough newborn physical examination will identify most of these anomalies.
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- 31. Background • • Hyaline membrane disease(HMD) is the most common cause of respiratory failure in the newborn . • • Occurs almost exclusively in premature infants . • • The incidence and severity of respiratory distress syndrome are related inversely to the gestational age of the newborn infant .
- 32. • • Respiratory distress syndromedevelops in premature infants because of impaired surfactant synthesis and secretion leading to lung atelectasis . • • HMD does not occur in all preterm babies .
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- 34. • Factors decreases therisk of HMD • • Premature rupture of membranes • • Maternal hypertension • • Sub-acute placental rupture • • Maternal use of narcotics
- 35. Clinical presentation • • Tachypnea usually>60 breath cycle per minute . • • Expiratory grunting (from partial closure of glottis) . • • Subcostal and intercostal retractions . • • Cyanosis . • • Nasal flaring . • • Extremely premature neonates may develop apnea and/or hypothermia .
- 36. Diagnosis • • Chest radiographs • − Bilateral, diffuse,reticular granular, or ground glass • appearances • − Air bronchograms (prominent air bronchograms represent aerated bronchioles superimposed on a background of collapsed alveoli) • − Poor lung expansion • • Blood gas • − Hypoxia • − Metabolic acidosis • − Hypercarbia
- 38. Management • • Maintain core temperature . • • Nasalcontinuous positive airway pressure (CPAP) is often used in spontaneously breathing premature infants • immediately after birth . • • Intubation and surfactant therapy as soon as possible . • • Mechanical ventilation if CPAP is not effective
- 39. Management • • 24h in thefirst IV fluids 10% glucose . • • weeks gestation All infant less than 28 receive prophylaxis surfactant therapy . • • Older infant should receive surfactant if they meet the criteria, most neonatologist consider infants who require 50% FiO2 to maintain a PaO2 >50 mmHg as a candidate for surfactant therapy .
- 40. • Prenatal steroids • • Decrease theincidence and severity of HMD . • Usually given to women at 24-34 week with high risk of preterm delivery ,
- 43.