Hyperglycemia in the1st trimester linked to perinatal death

By Glenn Sims,2014-04-16 21:42
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Hyperglycemia in the1st trimester linked to perinatal death

    Infants of Mothers with Diabetes

    The rate of diabetes during pregnancy in the U.S. is on the rise. In 2002, 32.8 per 1,000 births complicated by diabetes, 41% of women had cesareans. This represents a 40% increase in the rate of diabetes in pregnancy between 1989 and 2002. These rates of diabetes in pregnancy are expected to rise in the U.S.

The Pedersen Hypothesis

    The current theory of describing how diabetes during pregnancy leads to fetal complications the Pedersen hypothesis which states:

Maternal hyperglycemia ; Fetal hyperglycemia ; Fetal hyperinsulinemia

    Almost all of the complications associated with diabetes in pregnancy are linked to maternal hyperglycemia. Glucose can readily cross the placenta, while maternal insulin doe not cross the placenta. Pregnancy is considered a diabetogenic state. The hormones that promote fetal growth partially do so by altering the mother’s sensitivity to insulin and metabolism. During pregnancy, fetal blood glucose is 80% of maternal value. Prior to 20 weeks the fetus does not produce its own insulin and therefore cannot avoid exposure to hyperglycemia. Early fetal exposure to hyperglycemia is more likely in women who have undiagnosed diabetes or preexisting diabetes.

    After 20 weeks the fetal pancreas produces insulin and can control fetal glucose levels. Thus, maternal hyperglycemia causes fetal hyperglycemia and the fetus produces large amounts of insulin to avoid prolonged hyperglycemic state. This can lead to fetal pancreatic hypertrophy.

    Within the Pedersen hypothesis, controlling maternal hyperglycemia is the key to preventing neonatal hyperglycemia and associated neonatal complications.

Hyperglycemia Impact on the Fetus

Neonatal growth and development

     Wide swings in maternal blood glucose cause swings in fetal glucose. The hyperinsulinemic

    fetus can become hypoglycemic if the mother experiences hypoglycemia. Maternal

    hypoglycemia and wide swings in maternal blood sugar are associated with miscarriage and

    fetal mortality.

     Impaired growth or macrosomia

    o Before 20 weeks hyperglycemia slows fetal growth

    o After 20 weeks hyperinsulinemia and hyperglycemia create a perfect storm for

    excessive fetal fat deposition. Most of fetal weight in diabetic mothers is laid

    down after 32 weeks.

     Altered organ development and maturation

    o Hyperglycemia contributes to hepatomegaly, splenomegaly, cardiomegaly.

    o Small left colon syndrome: occurs in the second half of pregnancy, so infants of

    GDMs are at risk. Linked to severe maternal glucose swings. Signs/symptoms-

    intestinal obstruction, feeding intolerance, vomiting, abdominal distention By ?问候语? 1 of 9

    o Continued hyperinsulinemia through the third trimester is thought to impair fetal

    cortisol surge that trigger fetal lung and organ maturation prior to birth.

    o Hyperglycemia is also thought to contribute to decreased neonatal intestinal

    motility resulting in poor feeding.

Increased Fetal Oxygen Needs

     Fetal hyperglycemia and hyperinsulinemia increases O needs by as much as 30%. However 2

    the placenta cannot increase O transport to meet demand. This leads to: 2

    o Fetal hypoxemia

    o Polycythemia and tissue iron deficiency

    ; Erythropoiesis In order to increase O carrrying capacity, RBC 2

    production is increased. However, iron transport cannot meet the need

    because glycosalated hemoglobin carries less transferring. The fetus

    redistributes iron to RBC production and organs become iron deficient.

    ; Iron redistribution occurs after birth as the fetal RBCs are broken down

Preexisting Maternal Diabetes

    Pre and peri - conception glycemic control is key. Poor glucose control prior to conception and at and early in pregnancy is correlated with poor outcomes.

Maternal hyperglycemia early in pregnancy linked to:

     Spontaneous abortion

     Congenital Anomalies: Fetal ultrasound assessment may identify many of the congenital

    anomalies in-utero. However, assessment at birth remains key to identifying undiagnosed


    Common Anomalies

    Nervous System neural tube defects - meningomyelocele, encephalocele, anencephaly

    Cardiovascular transposition of great vessles, ventricular & atrial septal defects, left-sided

    obstructions: hypoplastic left heart, aortic stenosis, coarctation of the aorta

    Renal renal agenesis, hydronephrosis, cystic kidneys

    Gastrointestinal duodenun and rectal atresia, small left colon syndrome

     Mothers with preexisting vasculopathy are at risk for developing placental vasculopathies

    compromising the transfer of nutrients to the fetus. This intern can cause small for gestation

    age infants, which are more common in pregestational diabetic mother than GDM

HgbA and congenital anomalies 1c

    In mothers with preexisiting diabetes, the glycosalated hemoglobin is correlated to the risk of congenital anomalies and fetal/neonatal compromise.

    HgbA at 14 weeks Risk of anomalies 1c

    <7% No increased risk compared to non-diabetic

    7-8.5% 5%

    >10% 22%

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Gestational Diabetes

    Women with gestational diabetes (GDM) generally do not have hyperglycemia in early pregnancy. The glucose tolerance test for GDM is usually administered between 24 and 28 weeks gestation. GDM may be controlled with diet, insulin, or oral hypoglycemics. Diet controlled GDM mothers do not have an elevated risk of fetal demise or malformations as pregestionally diabetic women. Women who utilize insulin do have similar increases in risk for demise and congenital anomalies as pregestational diabetics.

Key points about GDM:

     Treatment goal is to achieve best glycemic control possible

     HgbA not impacted and therefore not a predictor of neonatel complications, because 1c

    measure previous 5 months of glycemic control, which should be normal in GDMs. ALL GDM pregnancies still at risk for

    o Macrosomia- excessive diabetes related fetal growth occurs in the third trimester.

    Despite increased monitoring and glycemic control GDMs are still at risk for

    having a macrosomic infant and cesarean delivery.

    o Altered organ development and maturation

    ; Fetal hyperinsulinemia still inhibits fetal lung and other organ maturation.

    ; Studies also show that septal hypertrophy can also occur. Glycogen is laid

    down in 34-40 weeks - so neonates of GDM are at risk.

    Common Complications in Infants of Diabetic Mothers (IDM)


    Definition: neonate > 90% percentile by weight.

    Although less than <10% of macrosomic neonates have diabetic mothers, 20-35% of neonates of diabetic mothers (IDMs) are macrosomic. If macrosomia is suspected prior to birth in a diabetic mother, the infant will often be delivered via cesarean.

Why is macrosomia in diabetic mothers different?

    Macrosomic IDMs have altered weight distribution. Infant head size is generally normal, but there is increased fat deposition in the shoulders and chest. This increases the risk of shoulder dystocia and cephalopelvic disproportion.

Risks associated with macrosomia


    o Birth trauma: increased the risk of broken clavicles, hypoxia, asphyxia

    o Shoulder dystocia

    o cephalopelvic disproportion (CPD)


    o Macrosomia is correlated with neonatal: hypoglycemia, hypocalcemia, respiratory

    distress, cardiac septal hypertrophy, and polycythemia.

By ?问候语? 3 of 9

     Perinatal asphyxia

    o Increased risk with macrosomia related to CPD and shoulder dystocia. Risk also

    increased secondary to likelihood of neonatal hypoxia, cardiomyopathy, and

    tissue iron deficiency.

    o Signs/Symptoms: hypotonia, flaccidity followed by increased tone, jitteriness,

    meconium, seizure risk peaks in first 24 hrs

    o Care: resuscitation - entubation, IV access, vassopressors, anticonvulsants

     Clavicle fracture

    o Signs/Symptoms: shoulder crepitus, decreased movement in affected arm, pain

    on palpation, visible altered bone or hematoma

    o Care: immobilize arm and x-ray

     Brachial plexus injuries

    o Brachial plexus injuries can be transient

    or permanent. They may resolve in 1-2

    weeks and achieve full function after a

    couple months.

    o Care: immobilize when found on

    assessment and notify care provider

    o Erb’s palsy th Stretch injury of 5-6 cervical roots from downward force on shoulder and

    lateral flexion of the neck - more common in neonates >4500g

     Signs/Symptoms: Effected arm is tightly adducted with extension at the

    elbow and internal rotation at the shoulder. Moro reflex absent or weak on

    effected side. Paralysis of upper arm muscle and absent DTR, but intact

    palmar grasp. If diaphragm involved, there is asymmetrical chest

    expansion, tachypnea, cyanosis, and dyspnea.

    o Klumpke’s paralysis

     Rare C8 to T1 nerve roots injured

     Signs/Symptoms: Wrist and hand involved - absent grasp reflex, hand

    limply flexed, and is not able to make voluntary hand movements. Often

    seen with Horner’s syndrome - unilaternal miosis, lid droop variation in

    temp of affected area

    Shoulder Dystocia

    Shoulder dystocia occurs in 3-8% of diabetes complicated pregnancies. Majority of

    shoulder dystocia occurs in neonates >4000g

    Signs of shoulder dystocia

     Prolonged time between delivery of body after delivery of head

    o >60 seconds for body to delivery after the head (normal average is 24.2


    By ?问候语? 4 of 9

    In addition to the birth trauma associated with macosomia. Shoulder dystocia

    also places the neonate at risk for facial nerve damage from pressure on facial

    nerves or forceps. The baby may have difficulty feeding.

     Facial Nerve damage

    o Signs/Symptoms: affected eye will not completely close

    with crying, forehead will not wrinkle, side of face will in

    wrinkle, mouth droops

Action during Shoulder Dystocia

    Primary action is to assist with maneuvers to promote delivery of neonate and to alert the

    neonatal resuscitation team. NEVER PROVIDE FUNDAL PRESSURE.

    Acceptable nurse assisted interventions for shoulder dystocia

     mother in supine squat to increase

     pelvic outlet

    McRoberts maneuver

     downward pressure over the right or left

     suprapubic area

Suprapubic pressure

     mother moved to onto fours - hands

     and knees position

    Gaskin maneuver

Respiratory Distress

    IDMs are at risk for both respiratory distress syndrome and transient tachypnea.

     Transient Tachypnea

    o caused by retained lung fluid or failure to clear lung fluid

    o present first hour of life and resolves within 96 hours

    o Signs/Symptoms: resp. rate 60-140 breaths per min, grunting, mild

    retractions, nasal flaring, possible mild cyanosis, no rales

    o Actions: maintain hydration and feeding, oxygen as needed to keep ABGs

    within normal limits

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     Respiratory Distress Syndrome

    o RDS from hyperinsulinemia induced delayed maturation of type II

    alveolar cells, which produce surfactant. Insufficient surfactant results.

    maybe complicated by persistent pulmonary hypertension

    o Ideally, delivery occurs when lungs are mature, as evidence by

    lecithin/sphingomyelin ratio greater than 2:1 or phosphatidylglycerol >3%

    o Signs/Symptoms: Grunting, nasal flaring, retracting, tachypnea >60

    breaths/min, decreased or unequal breaths sounds on auscultation, skin is

    pale, dusky, or cyanotic.

    o Actions: Decrease stress and stimuli, prevent cold stress. Initially may

    give blow by oxygen, but the neonate may need resuscitation and

    intubation. Exogenous surfactant may be administered. Maintain hydration

    and follow ABGs.

Cardiac Anomalies

    Cardiac anomalies are present in 30% of IDMs and 10% of these IDMs have heart failure.

     Intraventricular septal hypertrophy

    o Related to glycogen deposition in the septum. Directly correlates to the

    degree of maternal hyperglycemia. Although, women with diet controlled

    GDM can have infants with this anomaly.

    o Often will spontaneous resolve over time. Can result in hypertophic

    subaortic stenosis, in which case cardiomyopahty may result


    o Secondary to septal hypertrophy or anemia

     Signs/Symptoms: May be asymptomatic or left ventricular outflow obstruction signs

     diminished pulses, poor peripheral perfusion, poor capillary refill, cold extremities,

    respiratory difficulties, poor feeding


    o Often resolves without treatment

    o Maintain hydration

    o If severe, maybe treated with beta-blockers other medication


    Hypoglycemia is common in macrosomic or growth-restricted IDMs. The neonatal glycemic nadir occurs 1 to 3 hours after birth. There is disagreement on the point at which an infant should be considered hypoglycemic by blood glucose measure. At the Johnson Center <36 mg/dL requires continued monitoring and increased feeds, and <25 mg/dL at any time requires immediate action with IV therapy.

Causes of hypoglycemia in IDMs

     Growth restricted neonate: hypoglycemia is secondary to inadequate glycogen stores

     Macrosomic neonate: hypoglycemia is caused by hyperinsulinemia with sudden

    cessation of access to maternal glucose supply.

     Stress during birth contributes to hypoglycemia. However, stress related

    hypoglycemia in the IDM is exaggerated when compared to non-IDM neonate who

    was equally stressed. Hypoglycemia may persist up to 72 hours or longer. By ?问候语? 6 of 9


    Hypoglycemia appear similar to hypocalcemia. However, hypoglycemia usually occurs in the first 24-48 hours of life while hypocalcemia occurs later

     Lethary, jittery, tachypnea or apnea, seizure, agitation, respiratory distress

Hypoglycemia Care & Treatment

    Some research is showing that hypoglycemic events may have lasting effects on the brain function. So treatment must be partially based on symptoms to avoid not treating a relative hypoglycemia or false reading

Abbreviated Johnson Center Hypoglycemia Protocol

     see full protocol for complete explanation of policy and procedures

     Initiate hypoglycemia protocol at birth for IDMs

     Initiate feeding in first 30-60 minutes of life

    o Check blood glucose 30 minutes after feed

    ; If <36 mg/dL additional feeds of breastmilk or 15 ml of formula and

    recheck blood glucose 30 minutes after feed

    ; If >36 mg/dL check blood glucose before next feed

    ; If >36 mg/dL before 3 consecutive feeds discontinued glucose checks Notify physician for blood glucose

     <20 mg/dL at 30-90 minutes of life o

    o <25 mg/dL at any other time

    o <36 mg/dL at three consecutive feeds


    Hypocalcemia is neonatal serum calcium < 7mg/dL and occurs in up to 50% of neonates in insulin dependent mothers. It is caused by a delayed parathyroid response. Calcium does cross the placenta, so fetal parathyroid relatively inactive. In normal transition in fetal to neonate life, the parathyroid is usually active at the end of first 72 hours. However, parathyroid activity is delayed in neonates of diabetic mothers. Hypomagnesia also thought to be related to delayed parathyroid response. Neonates with respiratory distress of asphyxia at higher risk.

     Onset: usually days 1-4 of life

     Signs/symptoms: jittery, tachypnea, irritability, seizures, prolonged Q-T

     Treatment: only symptomatic neonates are treated

    o Hypocalcemia: Slow admin of 10% calcium gluconate

    o Hypomagnesia: 5% magnesium sulfate 0.5-2.5 mL/kg of 5% magnesium

    sulfate over 1 hr with continuous heart monitoring due to risk of heart

    block, bradycardia, and hypotension


    Polycythemia is defined as: Hgb > 20g/dL or Hct > 65%. Occurs in 20-30% of IDMs. Hemoglobin (Hgb) and hematocrit (Hct) may increase in first three days of life, falling Hgb/Hct may indicate bleed. Erroneous polycythemia may result from hemoconcentration for heel sticks.

Erythropoiesis ; Polycythemia ; Hyperviscosity

    By ?问候语? 7 of 9

    Erythropoiesis occurs in response to the increased fetal oxygen need secondary to hyperglycemia. It may also occur secondary to heart anomaly, which also impacts oxygen capacity in the fetus. Polycythemia is associated with complications resulting from increased blood viscosity and blockage in macro or micro-vasculature of the brain such as: stroke, seizure, necrotizing enterocolitis, renal vein thrombosis

Signs/symptoms of Polycythemia

    General Plethoric (blood vessel congestion, seen as redness of the skin), sluggish, lethargic

    CNS Irritable, jittery, high-pitched cry

    Resp Pulmonary hypertension

    Renal Hematuria, flank masses, thrombocytopenia, hypertension

    GI Feeding intolerance or necrotizing enterocolitis

Actions for Polycythemia

     Initial Hgb & Hct at birth and follow for 3 days

     Watch for symptoms

     If asymptomatic - hydrate neonate. Asymptomatic with hct 65-70% - hydrate 100 ml/kg/day

     If symptomatic or hct >70% - partial transfusion


    The fetal need for oxygen stimulate excess RBC production in diabetic pregnancies. The RBCs are larger than usual and increase the amount of bilirubin that must be excreted when they are degraded by 30%. Also, any birth injury such as hematoma will increase risk of hyperbilirubinemia. In addition, as in most newborns, the IDMs liver is inefficient at conjugating bilirubin - with the addition of excess large RBCs increases the likelihood of hyperbilirubinemia. The nurse should watch for jaundice in the first day of life and take appropriate measures such as encouraging feeding, maintaining hydration, assisting with bilirubin monitoring and therapy.

By ?问候语? 8 of 9


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