Gestational diabetes fetal complications
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]
Overview
Overview
Poor glycemic control and increased insulin level may result in increased metabolic demands in the fetus, which secondarily leads to fetal and neonatal complications. Large for gestational age babies, prematurity, respiratory distress syndrome, hyperbilirubinemia, polycythemia, and congenital anomalies, are the most common complications seen in neonates whose mother had GDM during the pregnancy.
Fetal complications
Fetal complications
- Poor glycemic control during pregnancy may lead to some fetal complications. Congenital malformations are the most common complications seen in baies of mothers with GDM compared to healthy mothers.[1]
- Maternal hyperglycemia leads to hyperinsulinemia in the fetus, which results in fetal macrosomia.
- Fetal macrosomia results in increased metabolic demand, and this can lead to increased mortality, metabolic acidosis, alterations in fetal iron distribution, increased erythropoiesis and polycythemia.[2][3]
- Stillbirth is another complication of GDM and it can be due to the increased catecholamine release, hypertension, and increased cardiac workload.[4] Hypertrophic cardiomyopathy from increased oxidative stress is another cause of stillbirth in hyperglycemic mothers.[5]
Neonatal complications
Neonatal complications
Insulin resistance, hyperinsulinemia, and increased metabolic demands, may result in neonatal co-morbidities such as large for gestational age babies, prematurity, respiratory distress syndrome, hyperbilirubinemia, and polycythemia. The table below shows the observed frequency of these co-morbidities.[6]
| Neonatal complications | Frequency♦ | |
|---|---|---|
| GDM |
|
|
♦ Based on a survey on GDM mothers[6]
† Birth weight greater than the 90th percentile
‡ 14% with gestational age <34 weeks and 22% with GA between 34 and 37 weeks
| Congenital anomalies in GDM | |
|---|---|
| Cardiovascular | Transposition of the great vessels, ventricular septal defect (VSD), coarctation of the aorta, atrial septal defect, single ventricle, hypoplastic left ventricle, pulmonic stenosis, pulmonary valve atresia |
| Gastrointestinal | Duodenal atresia, imperforate anus, anorectal atresia, small left colon syndrome, situs inversus |
| Genitourinary | Ureteral duplication, renal agenesis, hydronephrosis |
| Skeletal | Caudal regression syndrome |
References
References
- ↑ Mitanchez D, Burguet A, Simeoni U (2014). “Infants born to mothers with gestational diabetes mellitus: mild neonatal effects, a long-term threat to global health”. J. Pediatr. 164 (3): 445–50. doi:10.1016/j.jpeds.2013.10.076. PMID 24331686.
- ↑ Nold JL, Georgieff MK (2004). “Infants of diabetic mothers”. Pediatr. Clin. North Am. 51 (3): 619–37, viii. doi:10.1016/j.pcl.2004.01.003. PMID 15157588.
- ↑ Widness JA, Teramo KA, Clemons GK, Voutilainen P, Stenman UH, McKinlay SM, Schwartz R (1990). “Direct relationship of antepartum glucose control and fetal erythropoietin in human type 1 (insulin-dependent) diabetic pregnancy”. Diabetologia. 33 (6): 378–83. PMID 2199280.
- ↑ Kitzmiller JL (1993). “Sweet success with diabetes. The development of insulin therapy and glycemic control for pregnancy”. Diabetes Care. 16 Suppl 3: 107–21. PMID 8299468.
- ↑ Topcuoglu S, Karatekin G, Yavuz T, Arman D, Kaya A, Gursoy T, Ovalı F (2015). “The relationship between the oxidative stress and the cardiac hypertrophy in infants of diabetic mothers”. Diabetes Res. Clin. Pract. 109 (1): 104–9. doi:10.1016/j.diabres.2015.04.022. PMID 25934526.
- ↑ 6.0 6.1 Cordero L, Treuer SH, Landon MB, Gabbe SG (1998). “Management of infants of diabetic mothers”. Arch Pediatr Adolesc Med. 152 (3): 249–54. PMID 9529462.
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