Baby of a Diabetic Mother 2

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Infant of Diabetic Mother

Transcript of Baby of a Diabetic Mother 2

Objectivesy Define y Incidence of IODM y Pathophysiology y Disorders of Growth y Neonatal complications and Congenital Abnormalities y Management and Treatment y In pregnancy y At birth

Case Studyy Mrs. P, 25years, G1P0 is currently in labor and has

been pushing for two hours, the baby is now in fetal distress. y Delivery of the body is delayed secondary to shoulder dystocia. y Initial assessment of the infant includes poor respiratory effort, cyanosis, and HR 80. y A proper history from the mother reveals that the last three prenatal visits before delivery were missed because the mother was in Milan shopping for the baby and was delayed.

Definitiony The infant of a Diabetic Mother (IODM) is an infant

born to a mother with Diabetes GDM

DMI, DMII and

Considerationsy Pregnancy in a Diabetic mother is high risk y Diabetic mothers have a high incidence of polyhydramnios, preeclampsia, pyelonephritis, preterm labor, and chronic hypertension; their fetal mortality rate, which is high at all gestational ages, especially after 32 wk, is greater than that of nondiabetic mothers. Nelson textbook of Pediatrics 18th edition pp 510. y Fetal loss throughout pregnancy is associated with

poorly controlled maternal diabetes (especially ketoacidosis) and congenital anomalies

Difference between GDM and DMIIy Preexisting type 2 DM is associated more with

macrosomia, while microsomia is associated with preexisting type 1y Some studies suggest that Gestational diabetes affects

3-10% of all pregnanciesy The highest incidences occur in Black and Hispanic

populations

Gestational DMy Can occur at any point throughout pregnancy and is any degree of glucose intolerance . This definition acknowledges the possibility that patients may have previously undiagnosed diabetes mellitus. Of course these symptoms can resolve with delivery. y The White classification that assesses the effect of diabetes types on perinatal outcome, is widely used to assess maternal and fetal risk in a DM mother. It distinguishes between gestational diabetes (type A) and diabetes that existed prior to pregnancy (pregestational diabetes). These two groups are further subdivided according to their associated risks and management.

Pathophysiologyy Maternal hyperglycemia causes fetal hyperglycemia, and the fetal

pancreatic response leads to fetal hyperinsulinemia and an increase in islet cells hypertrophic and hyperplasia

y Like we saw with DKA, an imbalance between the catabolic and anabolic hormones that also contribute to insulin resistance , it s the estrogen, human placental lactogen, progesterone and cortisol that counteract insulin leading to hyperglycemia in pregnancy.y Fetal hyperinsulinemia and hyperglycemia lead to an increased

hepatic glucose uptake and glycogen synthesis, accelerated lipogenesis, and protein synthesis

Pathophysiologyy There is an increased weight of the placenta and infant

organs except for the brain, myocardial hypertrophy, increased amount of cytoplasm in liver cells.

y Hyperinsulinemia and hyperglycemia produce fetal

acidosis, which may result in an increased rate of stillbirth.

y At birth when the hyperglycemia from the mother is

removed, hyperinsulinemia leads to hypoglycemia and an abrupt cessation of lipolysis develop during the 1st hr after birth.

Which is the IODM

Presentation Large Baby Cyanosis Hypothermia Weak or high pitched cry Poor feeding Seizures Tachypnea Cardiomegally Hepatomegally

Hypoglycemia y Tremors y Jitteriness y Irritability y Lethargy y Apnea

Perinatal Presentationy Disorders of fetal growth y Intrauterine and perinatal asphyxia y Hypoglycemia y y y y y

Respiratory distress syndrome Hypertrophic Cardiomyopathy Polycythemia Hyperbilirubinemia Hypocalcemia

Disorders of Fetal Growthy Macrosomia- babies born with the body weight of 4kg

(8lbs 19 oz) up to 4.5kgy Term often used synonymously with large for

gestational age where the head circumference, weight or length is above the 90th percentile for gestational age

Macrosomia Pathophysiologyy Insulin and insulin-like growth factorsy Primary growth factors for the fetus y Abnormal adipose deposition y Visceral organ hypertrophy and hyperplasia y Acceleration of skeletal growth

y Increased levels of lipids, ketones, and amino acids

also stimulate insulin secretion

Disorders of Fetal GrowthMacrosomiay Incidence 15 to 45% among IODM y Increased rate of C-section y Birth Traumap shoulder and body dystocia p brachial plexus injury p facial nerve injury p asphyxia p abdominal trauma

Intrauterine Investigations into Macrosomiay USS y Resent studies show that the abdominal circumference in the 3rd week of gestation has been said to be the best indicator for predicting macrosomia y A good history from the mother can t be over stressed y Poor glucose control during pregnancy y History of previous LGA births

Intrauterine Growth Restriction Severe CasesComplicated by vascular disease Polyhydramnios Hypoxia Fetal distress Asphyxia Chronic hypertension, and chronic renal disease result in small fetal size for gestational age, prematurity, and intrauterine death y Neonatal deathy y y y y y

Intrauterine Growth Restrictiony Incidence reported as high as 20 % y Contributing factors: y Maternal vascular disease placental insufficiency y Hypertension y Intrauterine infection y Chromosomal abnormalities

Birth Asphyxiay Incidencey 20 TO 30%

y Primary Risk factors:y Prematurity y Fetal growth disorders y Maternal vascular disease y Peripartum maternal hyperglycemia y Drives catabolism of the oversupply of nutrientsy

depletes fetal O2 stores p episodic fetal hypoxia

Hypoglycemiay Risk Factors y Prematurity y Birth asphyxia y Cesarean section y Disorders of fetal growth y Stimulation of the fetal pancreasy

Pedersen Hypothesis

y Pedersen Hypothesis y Maternal hyperglycemia y Fetal hyperglycemia y Fetal F-cell hyperplasia y Neonatal hyperinsulinemia

Diagnosis-hypoglycemiay Test within 30-60 minutes of admission y Glucose < 40 confirm with serum glucose

Management of Hypoglycemiay Oral Feeding y IV bolus D10 (2cc/kg) over 2 to 5 min. y Continuous infusion D10 at 6 to 8 mg/kg/min y Careful attention to total fluid administrationy

Increase glucose concentration 24 to 48 hrs.

y Resolution of hyperinsulinemiay

Major congenital anomaliesy Congenital heart disease

y CNS malformations account for more than half of

thesey Renal y Gastro Intestinal

Congenital Heart Diseasey Transposition of the great vessels y Patent Ductus Arteriosis y Coarctation with VSD or PDA y Atrial septal defect y Hypertrophic Cardiomyopathy-more common

Congenital Heart Diseasey y y y y

Occurs in IODM and GDM with poor glycemic control Incidence 20 to 30 % Recall generalized organomegally o catecholamines hypertension, cardiac remodeling and hypertrophyy

Variable RV outflow obstruction y LV outflow obstruction y Asymmetric septal hypertrophy y proximity of the anterior leaflet of the MV to the septum y Transient; resolution by 6 to 12 months y Most infants asymptomatic y Heart failure occurs in 5 to 10%

CNS Malformationsy Caudal regression syndromenot considered pathognomonic occurs 600x more frequently among IDDM

y Neural tube defects y Microcephaly

Renaly Hydronephrosis y Renal agenesis y Ureteral duplication

Gastro Intestinaly Duodenal atresia y Anorectal atresia y Small left colon syndrome

Respiratory Distress Syndromey Risk:y 3 to 5 times the risk in the non-diabetic population

y Contributing Factors:y Prematurity y Maternal glycemic control y Increased Cortisol levels

Pathophysiology-Respiratory Distress Syndromey Hyperinsulinemia Decreases or Inhibitsy Number of Type II pneumocytes y Choline uptake in Type II pneumocytes y Steroid-enhanced phospholipid synthesis y Number of lamellar bodies increases y Surfactant Protein A production is decreased

Polycythemiay y y y y y y y y y

Respiratory distress Cardiac failure Decreased renal function Renal vein thrombosis Necrotizing enterocolitis CNS damage Hypoglycemia Hypocalcemia Hypomagnesemia Hyperbilirubinemia

Managing the Diabetic Mothery If previously Diagnosed with DM y Encourage weight loss as an increase or high BMI during pregnancy is the greatest risk factor for macrosomia. y Continue insulin therapy or current drug therapy y In Insulin dependant mothers there may be a 30% increase demand for insulin y glucose control reduces the risk of anomalies and other adverse outcomes y glucose control during labor reduces the incidence of neonatal hypoglycemia. y Women with Type 1 diabetes who have tight glucose control during pregnancy (average daily glucose levels