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OB28 Obstetrics
Medical Complications of Pregnancy
Toronto Notes 2019
Table 14. Complications of DM in Pregnancy
Maternal
Obstetric
HTN/preeclampsia (especially if pre-existing nephropathy/ proteinuria): insulin resistance is implicated in etiology of HTN Polyhydramnios: maternal hyperglycemia leads to fetal hyperglycemia, which leads to fetal polyuria (a major source of amniotic fluid)
Diabetic Emergencies
Hypoglycemia Ketoacidosis Diabetic coma
End-Organ Involvement or Deterioration
(occur in type 1 DM and type 2 DM, not in GDM) Retinopathy
Nephropathy
Other
Pyelonephritis/UTI: glucosuria provides a culture medium for E. coli and other bacteria
Increased incidence of spontaneous abortion (in type 1 DM and type 2 DM, not in GDM): related to pre-conception glycemic control
Long-Term Maternal Complications
Fetal
Growth Abnormalities
Macrosomia: maternal hyperglycemia leads to fetal hyperinsulinism resulting in accelerated anabolism IUGR: due to placental vascular insufficiency
Delayed Organ Maturity
Fetal lung immaturity: hyperglycemia interferes with surfactant synthesis (respiratory distress syndrome)
Congenital Anomalies (occur in type 1 DM and type 2 DM, not in GDM)
2-7x increased risk of cardiac (ventricular septal defect), NTD, GU (cystic kidneys), GI (anal atresia), and MSK (sacral agenesis) anomalies due to hyperglycemia
Note: Pregnancies complicated by GDM do not manifest an increased risk of congenital anomalies because GDM develops after the critical period of organogenesis (in T1)
Labour and Delivery
Preterm labour/prematurity: most commonly in patients with HTN/preeclampsia
Preterm labour is associated with poor glycemic control but the exact mechanism is unknown
Increased incidence of stillbirth
Birth trauma: due to macrosomia, can lead to difficult vaginal delivery and shoulder dystocia
Neonatal
Hypoglycemia: due to pancreatic hyperplasia and excess insulin secretion in the neonate
Hyperbilirubinemia and jaundice: due to prematurity and polycythemia
Hypocalcemia: exact pathophysiology not understood, may be related to functional hypoparathyroidism
Polycythemia: hyperglycemia stimulates fetal erythropoietin production
Indications for Intrapartum Antibiotic GBS Prophylaxis
Centres for Disease Control and Prevention. Prevention of Perinatal Group B Streptococcal Disease. MMWR 2010;59(RR-10):14
• Previous infant with invasive GBS disease.
• GBS bacteriuria during any trimester of the
current pregnancy
• PositiveGBSvaginal-rectalscreeningculturein
late gestation during current pregnancy
• UnknownGBSstatusattheonsetoflabour (culture not done, incomplete, or results
unknown) and any of the following:
• Deliveryat<37wkgestation
• Amnioticmembranerupture≥18h
• Intrapartumtemperature≥38.0°C
( ≥100.4 °F)
• Intrapartumnucleic-acidamplificationtest
positive for GBS
• type1andtype2DM:riskofprogressiveretinopathyandnephropathy • GDM:50%riskofdevelopingtype2DMinnext20yr
Group B Streptococcus Epidemiology
• 15-40%recto-vaginalcarrierrate
Risk Factors (for neonatal disease)
• GBSbacteriuriaduringcurrentpregnancy,eveniftreated • previousinfantwithinvasiveGBSinfection
• unknownGBSstatuswith:
■ pretermlabour<37wk
■ ruptured membranes ≥18 h before delivery ■ intrapartum maternal temperature ≥38°C
• positiveGBSscreenbetween35-37weeksGAincurrentpregnancy
Clinical Features
• notharmfultomother
• riskofverticaltransmission(neonatalsepsis,meningitisorpneumonia,anddeath)
Investigations
• offerscreeningtoallwomenat35-37wkwithvaginalandanorectalswabsforGBSculture
Treatment
• treatmentofmaternalGBSatdeliverydecreasesneonatalmorbidityandmortality
• indicationsforantibioticprophylaxis:positiveGBSscreen,GBSinurine,orpreviousinfantwithGBS
disease or GBS status unknown + one of the other risk factor
• antibioticsforGBSprophylaxis(shouldbegiven4hpriortodeliverytobeconsideredadequate)
■ penicillin G, 5 million IU IV, then 2.5 million IU IV q4h until delivery
■ penicillin allergic but not at risk for anaphylaxis: cefazolin 2 g IV then 1 g q8h