eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Neonatology

Infant of Diabetic Mother: Differential Diagnoses & Workup

Author: Charles F Potter, MD, Consulting Neonatologist, Newborn Care Physicians of Southeastern Wisconsin
Coauthor(s): Stephen D Kicklighter, MD, Clinical Assistant Professor, Department of Pediatrics, Division of Neonatology, University of North Carolina at Raleigh and Wake Medical Center
Contributor Information and Disclosures

Updated: Jun 9, 2009

Differential Diagnoses

Beckwith-Wiedemann Syndrome

Workup

Laboratory Studies

  • CBC count
    • Polycythemia, commonly defined as a central hematocrit level higher than 65% is a potential concern.
    • Maternal-fetal hyperglycemia and fetal hypoxia is a strong stimulus for fetal erythropoietin production and subsequent increase in fetal hemoglobin concentration. Thrombocytopenia may occur because of impaired thrombopoiesis due to "crowding-out" of thrombocytes by the excess of erythroid precursors in the bone marrow.
  • Glucose concentration (serum or whole-blood)
    • Seizures, coma, and long-term brain damage may occur if neonatal hypoglycemia is unrecognized and untreated.
    • Most centers recognize levels lower than 20-40 mg/dL within the first 24 hours after birth as abnormal, but the precise level remains controversial. A policy to screen infants of diabetic mothers (IDMs) for hypoglycemia should be in place in every hospital. A suggestion of operational thresholds was proposed by Cornblath et al.5 Their suggestion in an infant with compromised metabolic adaptation (ie, infant of diabetic mother) should include blood glucose measurements (1) as soon as possible after birth, (2) within 2-3 hours after birth and before feeding, and (3) at any time abnormal clinical signs are observed.
  • Magnesium concentration (serum)
    • Hypomagnesemia is related to younger maternal age, severity of maternal diabetes, and prematurity. Neonatal magnesium levels are also related to maternal serum magnesium, neonatal calcium and phosphorus levels, and neonatal parathyroid function.
    • The clinical significance of low magnesium levels in these infants remains controversial and uncertain.
  • Calcium concentration (serum, ionized or total levels): Low serum calcium levels in infants of diabetic mothers are common. They are speculated to be caused by a functional hypoparathyroidism; however, their clinical relevance remains uncertain and controversial.
  • Bilirubin level (serum, total and unconjugated): Hyperbilirubinemia is notably more common than in the general population of neonates. Causative factors include prematurity, hepatic enzyme immaturity, polycythemia, and reduced RBC half-life.
  • ABG: Assessing oxygenation and ventilation is essential in infants with clinical evidence of respiratory distress. Although noninvasive methods (eg, transcutaneous oxygen and carbon dioxide electrodes, oximeters) have gained wide acceptance at many centers, comparison of results with those from arterial blood is intermittently required.

Imaging Studies

  • Chest radiography
    • Clinical evidence of cardiopulmonary distress requires a detailed evaluation, which should always include a chest radiograph.
    • The chest radiography should be evaluated for adequacy of lung expansion, evidences of focal or diffuse atelectasis, presence of interstitial fluid, signs of free air in pleural or interstitial spaces, and findings of respiratory distress syndrome or pneumonia. The possibility of pulmonary malformations should also be considered. In the infant with macrosomia who has a history of shoulder dystocia, examination of the clavicles should be evaluated on the film as well on physical examination.
    • Cardiac size, shape, and great vessel/outflow tract should be carefully examined.
  • Cardiac echocardiography
    • A thickened myocardium and significant septal hypertrophy may be present in as many as 1 in 3 infants of diabetic mothers. Evidence of a hypercontractile, thickened myocardium, often with septal hypertrophy disproportionate to the size of the ventricular free walls, may be noted on examination. Myocardial contractility should also be evaluated because the myocardium is overstretched and poorly contractile with congenital cardiomyopathies.
    • Evidence of anatomical malformation must be searched for carefully because cardiac malformations are significantly more common in infants with diabetic mothers, including a ventricular septal defect (VSD) and transposition of the great arteries (TGA).
  • Abdominal, pelvic, or lower extremity radiography
    • When caudal dysplasia is present, other orthopedic anomalies should be investigated including fusion of the legs, hypoplastic femur, defects of the tibia and the fibula, flexion contractures of the knee and hip, or clubfoot. Caudal dysplasia or sacral agenesis is the most common orthopedic anomaly in the infant of the diabetic mother.
    • Lower extremity congenital malformations require radiographic evaluation to determine the exact skeletal defect or defects present.
  • Barium enema
    • Infants with feeding intolerance, abdominal distention, nonbilious emesis, or poor passage of meconium may require a barium enema. Congenital anomalies of the GI tract are more common in infants of diabetic mothers. These infants may have "small left colon syndrome," also known as "lazy colon."
    • Clinical features of the small left colon syndrome may mimic those of Hirschsprung disease and distal tapering of the colon is a radiologic feature of both disorders. The 2 disorders can be distinguished using a biopsy because normal ganglionic cells are present in lazy colon and absent in Hirschsprung disease.

Procedures

  • Nasal continuous positive airway pressure (NCPAP) or endotracheal continuous positive airway pressure, endotracheal intubation, and mechanical ventilation
    • NCPAP or endotracheal intubation with intermittent mandatory ventilation (IMV) or synchronized positive pressure ventilation (SIMV) may be used for management of severe respiratory distress.
    • Common criteria for such interventions include inspired oxygen requirements (FiO2) of 60-100% to maintain arterial PO2 of 50-80mm Hg, arterial PCO2 levels higher than 60 mm Hg or rising 10 mm Hg, and apnea. The specific criteria for using these modes of assisted ventilation may vary depending on the underlying respiratory pathology and clinical condition of the infant.
  • Indwelling vascular lines (peripheral, umbilical, or central)
    • Noninvasive blood gas monitoring using transcutaneous electrodes (PaO2 and PaCO2) and oximeters (O2% saturation) has greatly reduced the need for invasive indwelling catheters. However, indwelling lines are often needed early in the course of cardiorespiratory disease. In some instances, the need for continuous arterial blood pressure monitoring may warrant placement of a peripheral or umbilical arterial line.
    • Placement of an umbilical venous or a central venous catheter is often used when the infant requires high concentrations of intravenous dextrose or when peripheral access is limited or exhausted.

Histologic Findings

  • The pancreas has larger and more numerous islets.

    An increase in the number and size of the islets ...

    An increase in the number and size of the islets is commonly seen in the pancreas of infants born to diabetic mothers.

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    An increase in the number and size of the islets ...

    An increase in the number and size of the islets is commonly seen in the pancreas of infants born to diabetic mothers.

  • Sections from neonatal myocardium show cellular hyperplasia and hypertrophy.

More on Infant of Diabetic Mother

Overview: Infant of Diabetic Mother
Differential Diagnoses & Workup: Infant of Diabetic Mother
Treatment & Medication: Infant of Diabetic Mother
Follow-up: Infant of Diabetic Mother
Multimedia: Infant of Diabetic Mother
References
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References

  1. Engelgau MM, Herman WH, Smith PJ, et al. The epidemiology of diabetes and pregnancy in the U.S., 1988. Diabetes Care. 1995;18:1029-33. [Medline].

  2. [Guideline] American Diabetes Association (ADA). Detection and diagnosis of gestational diabetes mellitus (GDM). Standards of medical care in diabetes. Diabetes Care. Jan 2008;31(Suppl 1):S15.

  3. Barnes-Powell LL. Infants of diabetic mothers: the effects of hyperglycemia on the fetus and neonate. Neonatal Netw. Sep-Oct 2007;26(5):283-90. [Medline].

  4. Rosenkrantz TS, Knox I, Zalneraitis EL, et al. Cerebral metabolism and electrocortical activity in the chronically hyperglycemic fetal lamb. Am J Physiol. Dec 1993;265(6 Pt 2):R1262-9. [Medline].

  5. Cornblath M, Hawdon JM, Williams AF, et al. Controversies regarding definition of neonatal hypoglycemia: suggested operational thresholds. Pediatrics. May 2000;105(5):1141-5. [Medline]. [Full Text].

  6. Thompson DM, Dansereau J, Creed M, Ridell L. Tight glucose control results in normal perinatal outcome in 150 patients with gestational diabetes. Obstet Gynecol. 1994;83:362-6. [Medline].

  7. Plagemann A. A matter of insulin: developmental programming of body weight regulation. J Matern Fetal Neonatal Med. Mar 2008;21(3):143-8. [Medline].

  8. DeBoer T, Wewerka S, Bauer PJ, et al. Explicit memory performance in infants of diabetic mothers at 1 year of age. Dev Med Child Neurol. Aug 2005;47(8):525-31. [Medline].

  9. Rizzo T, Metzger BE, Burns WJ, Burns K. Correlations between antepartum maternal metabolism and child intelligence. New Eng J Med. 1991;26:911-6. [Medline].

  10. Rizzo TA, Metzger BE, Dooley SL. Early malnutrition and child neurobehavioral development: insights from the study of children of diabetic mothers. Child Dev. 1997;68:26-38. [Medline].

  11. Ornoy A, Wolf A, Ratzon N, et al. Neurodevelopmental outcome at early school age of children born to mothers with gestational diabetes. Arch Dis Child Fetal Neonatal Ed. 1999;81:F10-F14. [Medline].

  12. Silverman BL, Rizzo T, Green OC, et al. Long-term prospective evaluation of offspring of diabetic mothers. Diabetes. 1991;40:121-5. [Medline].

  13. Boney CM, Verma A, Tucker R, Vohr BR. Metabolic syndrome in childhood: association with birth weight, maternal obesity, and gestational diabetes mellitus. Pediatrics. Mar 2005;115(3):e290-6. [Medline]. [Full Text].

  14. Al-Najashi SS. Control of gestational diabetes. Int J Gynaecol Obstet. 1995;49:131-5. [Medline].

  15. Bromiker R, Rachamim A, Hammerman C, Schimmel M, Kaplan M, Medoff-Cooper B. Immature sucking patterns in infants of mothers with diabetes. J Pediatr. Nov 2006;149(5):640-3. [Medline].

  16. Cordero L, Landon MB. Infant of the diabetic mother. Clin Perinatol. 1993;20:635-48. [Medline].

  17. Cowett RM, Schwartz R. The infant of the diabetic mother. Pediatr Clin North Am. 1982;29:1213-31. [Medline].

  18. Duvanel CB, Fawer CL, Cotting J, et al. Long-term effects of neonatal hypoglycemia on brain growth and psychomotor development in small-for-gestational-age preterm infants. J Pediatr. Apr 1999;134(4):492-8. [Medline].

  19. Georgieff MK. The effect of maternal diabetes during pregnancy on the neurodevelopment of offspring. Minn Med. Mar 2006;89(3):44-7. [Medline].

  20. Greco P, Vimercati A, Scioscia M, et al. Timing of fetal growth acceleration in women with insulin-dependent diabetes. Fetal Diagn Ther. Nov-Dec 2003;18(6):437-41. [Medline].

  21. Hod M, Levy-Shiff R, Lerman M, et al. Developmental outcome of offspring of pregestational diabetic mothers. J Pediatr Endocrinol Metab. 1999;12:867-72. [Medline].

  22. Landon MB, Gabbe SG. Diabetes Mellitus and Pregnancy. Obstetrics and Gynecology Clinics of North America. 1992;19:633-53. [Medline].

  23. McElvy SS, Miodovnik M, Rosenn B, et al. A focused preconceptional and early pregnancy program in women with type 1 diabetes reduces perinatal mortality and malformation rates to general population levels. J Matern Fetal Med. Jan-Feb 2000;9(1):14-20. [Medline].

  24. Nold JL, Georgieff MK. Infants of diabetic mothers. Pediatr Clin North Am. Jun 2004;51(3):619-37, viii. [Medline].

  25. Reece EA, Sivan E, Francis G, Homko CJ. Pregnancy outcomes among women with and without diabetic microvascular disease (White's classes B to FR) versus non-diabetic controls. Am J Perinatol. 1998;15(9):549-55. [Medline].

  26. Rizzo TA, Dooley SL, Metzger BE. Prenatal and perinatal influences on long-term psychomotor development in offspring of diabetic mothers. Am J Obstet Gynecol. 1995;173:1753-8. [Medline].

  27. Rizzo TA, Ogata ES, Dooley SL, et al. Perinatal complications and cognitive development in 2- to 5-year-old children of diabetic mothers. Am J Obsted Gynecol. 1994;171:706-13. [Medline].

  28. Siddiqui F, James D. Fetal monitoring in type 1 diabetic pregnancies. Early Hum Dev. May 2003;72(1):1-13. [Medline].

  29. Stenninger E, Lindqvist A, Aman J, Ostlund I, Schvarcz E. Continuous Subcutaneous Glucose Monitoring System in diabetic mothers during labour and postnatal glucose adaptation of their infants. Diabet Med. Apr 2008;25(4):450-4. [Medline].

  30. Suevo DM. The infant of the diabetic mother. Neonatal Netw. 1997;16:25-33. [Medline].

  31. Tyrala E. The infant of the diabetic mother. Obstetrics and Gynecology Clinics of North America. 1996;23:221-41. [Medline].

  32. Weintrob N, Karp M, Hod M. Short- and long-range complications in offspring of diabetic mothers. J Diabetes Complications. Sep-Oct 1996;10(5):294-301. [Medline].

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Further Reading

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Keywords

infant of diabetic mother, IDM, diabetic mother, glucose intolerance, respiratory distress, macrosomia, polycythemia, hypoglycemia, congenital malformations, hypocalcemia, hypomagnesemia, fetal glucose control, maternal hyperglycemia, gestational diabetes mellitus, diabetes mellitus type 1, diabetes mellitus type 2, large for gestational age, LGA, small for gestational age, SGA, macrosomia, hepatosplenomegaly, cardiomegaly, fetal hyperglycemia, hyperinsulinemia, prematurity, outflow tract obstruction, excessive fetal growth, impaired fetal growth, transient tachypnea of the newborn, pneumonia, necrotizing enterocolitis, renal vein thrombosis, cardiomyopathy, congenital heart defects, ventricular septal defect, VSD, transposition of the great arteries, spina bifida, hydronephrosis, renal agenesis, ureteral duplication, treatment, diagnosis

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Contributor Information and Disclosures

Author

Charles F Potter, MD, Consulting Neonatologist, Newborn Care Physicians of Southeastern Wisconsin
Charles F Potter, MD is a member of the following medical societies: American Academy of Pediatrics and American Medical Association
Disclosure: Nothing to disclose.

Coauthor(s)

Stephen D Kicklighter, MD, Clinical Assistant Professor, Department of Pediatrics, Division of Neonatology, University of North Carolina at Raleigh and Wake Medical Center
Stephen D Kicklighter, MD is a member of the following medical societies: American Academy of Pediatrics and National Perinatal Association
Disclosure: Nothing to disclose.

Medical Editor

George Cassady, MD, Clinical Professor, Department of Pediatrics, Stanford University School of Medicine
George Cassady, MD is a member of the following medical societies: American Academy of Pediatrics, American Pediatric Society, Society for Pediatric Research, and Southern Society for Pediatric Research
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Brian S Carter, MD, FAAP, Professor of Pediatrics (Neonatology), Vanderbilt University School of Medicine; Co-director, Pediatric Advance Comfort Team, Monroe Carell Jr Children's Hospital at Vanderbilt
Brian S Carter, MD, FAAP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Hospice and Palliative Medicine, American Academy of Pediatrics, American Society for Bioethics and Humanities, American Society of Law Medicine and Ethics, National Hospice and Palliative Care Organization, and Southern Society for Pediatric Research
Disclosure: Nothing to disclose.

CME Editor

Carol L Wagner, MD, Professor of Pediatrics, Medical University of South Carolina
Carol L Wagner, MD is a member of the following medical societies: American Academy of Pediatrics, American Chemical Society, American Medical Women's Association, American Public Health Association, American Society for Bone and Mineral Research, American Society for Clinical Nutrition, Massachusetts Medical Society, National Perinatal Association, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Chief Editor

Ted Rosenkrantz, MD, Professor, Departments of Pediatrics and Obstetrics/Gynecology, Division of Neonatal-Perinatal Medicine, University of Connecticut School of Medicine
Ted Rosenkrantz, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Pediatric Society, Connecticut State Medical Society, Eastern Society for Pediatric Research, and Society for Pediatric Research
Disclosure: Nothing to disclose.

 
 
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