9. Medical Complications of Pregnancy (À finir) Flashcards
Describe PREVENTION of iron defiency anemia (1)
Prevention (non-anemic): 30 mg elemental iron/d (met by most prenatal vitamins)
Describe TREATMENT of iron defiency anemia (3)
- 30-120 mg elemental iron/d
- 325 mg ferrous fumarate = 106 mg elemental Fe; 325 mg ferrous sulfate = 65 mg elemental Fe; 325 mg ferrous gluconate = 36 mg elemental Fe
- Polysaccharide-Iron Complex = 150 mg elemental Fe/capsule
Name complications of iron deficiency anemia (8)
Maternal:
- angina
- congestive heart failure CHF
- infection
- slower recuperation
- preterm labour
Fetal
- decreased oxygen carrying capacity leading to fetal distress,
- IUGR
- low birth weight
Iron requirements increase during pregnancy why? (3)
- due to fetal/placental growth (500 mg)
- increased maternal RBC mass (500 mg)
- and losses (200 mg) – more needed for multiple gestations
Describe prevention of folate deficiency anemia (2)
- Prevention: 0.4-1 mg folic acid PO daily for 1-3 mo preconceptually and throughout T1
- or 5 mg folic acid/d with past history of ONTD, DM, or antiepileptic medication use
Name complications: Folate deficiency anemia (6)
- Maternal:
- decreased blood volume
- N/V
- anorexia
- Fetal:
- neural tube defects in T1
- low birth weight, and
- prematurity
Folic acid is necessary for what? (1)
closure of neural tube during early fetal development (by day 28 of gestation)
Gestational Diabetes Mellitus is testing when? (1)
usually tested for around 24-28 wk GA
Describe etiology: GDM (1)
anti-insulin factors produced by placenta and high maternal cortisol levels create increased peripheral insulin resistance s leading to GDM and/or exacerbating pre-existing DM
Describe management of type 1 and type 2 DM: PRECONCEPTION (5)
- pre-plan and refer to high-risk clinic
- commence folic acid 3 mo prior
- optimize glycemic control (HbA1c <6%)
- counsel patient on potential risks and complications
- evaluate for diabetic retinopathy, neuropathy, and CAD
Describe management of type 1 and type 2 DM: PREGNANCY (5)
- for Type 2 DM, if already on oral medication, generally switch to insulin therapy
- continuing glyburide or metformin controversial
- teratogenicity unknown for other oral anti-hyperglycemics
- tight glycemic control
- insulin dosage may need to be adjusted in T2 due to increased demand and increased insulin resistance
-
monitor as for normal pregnancy, plus initial 24 h urine protein and creatinine clearance, retinal exam, and HbA1c
- HbA1c: >140% of pre-pregnancy value associated with increased risk of spontaneous abortion and congenital malformations
- increased fetal surveillance (fetal growth, BPP, NST) starting in the late T2 and T3, consider fetal ECHO in the T2 (if high HbA1c in T1 or just prior to pregnancy) to look for cardiac abnormalities
Describe management of type 1 and type 2 DM: LABOUR (4)
- timing of delivery depends on fetal and maternal health and risk factors (i.e. must consider size of baby, lung maturity, maternal blood glucose)
- induce by 38-39 wk, depending on glycemic control and presence of end-organ involvementent
- type of delivery
- increased risk of cephalopelvic disproportion (CPD) and shoulder dystocia with babies >4000 g (8.8 lbs)
- consider elective C/S for predicted birthweight >4500 g (9.9 lbs) (controversial)
-
monitoring
- during labour, monitor blood glucose q1h with patient on insulin and dextrose drip
- aim for blood glucose between 3.9-7 mmol/L to reduce the risk of neonatal hypoglycemia
Describe management of type 1 and type 2 DM: POSTPARTUM (2)
- insulin requirements dramatically drop with expulsion of placenta (source of insulin antagonists)
- monitor glucose q6h, restart insulin at two-thirds of pre-pregnancy dosage when glucose >8 mmol/L
Name: Risk Factors for GDM (9)
- Age >25 yr
- Obesity
- Ethnicity (Aboriginal, Hispanic, Asian, and African)
- FHx of DM
- Previous history of GDM
- Previous child with birthweight >4.0 kg
- Polycystic ovarian syndrome
- Current use of glucocorticoids
- Essential HTN or pregnancy-related HTN
Screen for GDM for who? (1)
- all pregnant women between 24-28 wk GA (or at any stage if high risk)
Describe screening options of GDM (2)
- 2-step screening
- Step 1: perform a random non-fasting 50 g oral glucose challenge test (OGCT)
- 1 h PG <7.8 mmol/L is normal
- 1 h PG ≥11.1 mmol/L is GDM
- if 1 h PG 7.8-11.0 mmol/L, proceed to Step 2
- Step 2: perform a fasting 75 g oral glucose tolerance test (OGTT), GDM if ≥1 of:
- fasting plasma glucose FPG ≥5.3 mmol/L
- 1 h PG ≥10.6 mmol/L
- 2 h PG ≥9.0 mmol/L
- Step 1: perform a random non-fasting 50 g oral glucose challenge test (OGCT)
- Alternative 1-step screening with fasting 75 g OGTT; GDM if ≥1 of:
- FPG ≥5.1 mmol/L
- 1 h PG ≥10.0 mmol/L
- 2 h PG ≥8.5 mmol/L
Describe management of GDM (6)
- first line: diet modification and increased physical activity
- initiate insulin therapy if glycemic targets not achieved within 2 wk of lifestyle modification alone
- glycemic targets:
- FPG <5.3 mmol/L
- 1 h PG <7.8 mmol/L
- 2 h PG <6.7 mmol/L
- oral agents can be used in pregnancy but is off-label and should be discussed with patient
- stop insulin and diabetic diet postpartum
- follow-up with 75 g OGTT between 6 wk-6 mo postpartum, counsel about lifestyle modifications
Describe prognosis: GDM (1)
most maternal and fetal complications are related to hyperglycemia and its effects
Name MATERNAL complications of DM: Obstetric (2)
- 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)
Name MATERNAL complications of DM: Diabetic Emergencies (3)
- Hypoglycemia
- Ketoacidosis
- Diabetic coma
Name MATERNAL complications of DM: End-Organ Involvement or Deterioration (occur in type 1 DM and type 2 DM, not in GDM)
(2)
- Retinopathy
- Nephropathy
Name MATERNAL complications of DM: OTHER (2)
- 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
Name FETAL complications of DM: Growth abnormalities (2)
- Macrosomia: maternal hyperglycemia leads to fetal hyperinsulinism resulting in accelerated anabolism
- IUGR: due to placental vascular insufficiency
Name FETAL complications of DM: Delayed Organ Maturity (1)
Fetal lung immaturity: hyperglycemia interferes with surfactant synthesis (respiratory distress syndrome)
Name FETAL complications of DM: Congenital Anomalies (occur in type 1 DM and type 2 DM, not in GDM) (5)
- 2-7x increased risk of
- cardiac (ventricular septal defect)
- neural tube defects NTD
- GU (cystic kidneys)
- GI (anal atresia)
- MSK (sacral agenesis) anomalies due to hyperglycemia
Pregnancies complicated by GDM do not manifest an increased risk of congenital anomalies why?
because GDM develops after the critical period of organogenesis (in T1)