Medical
Disorders in
Pregnancy
Dr. Brett Vair
Obstetrics & Gynecology
Family Medicine Academic Half-Day
August 20, 2015
Outline
Obesity
Hypothyroidism
Pregestational diabetes
Chronic hypertension
Seizure disorders
I. Obesity
“One of the most
blatantly visible, yet
neglected, public-health
problems that threatens
to overwhelm both more
and less developed
countries.”
- WHO
Defining obesity in pregnancy
 BMI should be calculated from prepregnancy height and
weight
 Those with a prepregnancy BMI >30 kg/m2 are considered
obese
 Other definitions:
 Women who are 110%-120% of their ideal body weight
 >91kg (>200 lbs)
A self-propagating phenomenon…
• Maternal obesity results in in-utero programming and
childhood obesity
Q: What is the suggested weight gain in
pregnancy for a woman who is obese (BMI
30.0-34.9)?
A.
B.
C.
D.
10 kg
3 kg
7 kg
15 kg
Suggested weight gain in
pregnancy
• Women should be encouraged to enter pregnancy with a BMI <30,
ideally <25
• All women without contraindications should participate in regular
exercise
Exercise in pregnancy (SOGC Clinical
Practice Guideline No. 129, June 2003)
 All women without contraindications should be
encouraged to participate in exercise as part of
a healthy lifestyle during pregnancy
 Reasonable goal: Maintain a good fitness level
throughout pregnancy without reaching peak
fitness or training for an athletic competition
 Initiation of an aerobic exercise program in
previously sedentary women:
 15 minutes continuous exercise 3x/week

 30 –minute sessions 4x/week
Exercise in pregnancy
 Absolute contraindications:
 Ruptured membranes
 Preterm labour
 Hypertensive disorders of pregnancy
 Cervical insufficiency
 IUGR
 Higher order multiple gestation (≥triplets)
 Placenta previa >28 weeks
 Persistent 2nd or 3rd trimester bleeding
 Uncontrolled type 1 diabetes, thyroid disease, or other serious
cardiovascular, respiratory, or systemic disorder
(SOGC Clinical Practice Guideline No. 129, June 2003)
Complications of obesity related to
pregnancy
 Infertility (OR 1.7-2)
 Spontaneous abortion (OR 2-3)
 Increased risk of recurrent pregnancy loss
 Prenatal risks:
 Hypertensive disorders in pregnancy (OR 2-3)
 Increased likelihood of a woman experiencing severe complications
from GHTN
 Gestational diabetes (OR 1.4-20)
 Testing women with risk factors early in pregnancy is recommended
 VTE (OR 2)
 OSA (OR 1.12)
Complications of obesity related to
pregnancy
 Risks to the fetus/neonate:
 Increased rate of fetal anomalies
 NTD (OR 1.7-2.2)
 Protective effects of periconceptual folic acid to not appear to benefit
obese women
 Recommended dose of 5mg daily (SOGC Clinical Practice Guideline No.
324, May 2015: 1.0 mg/day of folic acid recommended for those at
“moderate risk”)
 Also:
 Cardiac defects
 Orofacial clefts
 Ventral wall defects
Complications of obesity related to
pregnancy
 Risks to the fetus/neonate (continued)
 Macrosomia (>4000g) (OR 2.1)
 Birth injury, shoulder dystocia (OR 3.1)
 Fetal death (OR 2.0-3.6)
 The most prevalent risk factor for unexplained stillbirth is prepregnancy
obesity
 Antepartum fetal testing may be considered
 Childhood obesity (OR 1.9-2.2)
Complications of obesity related to
pregnancy
 Intrapartum risks:
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Macrosomia and shoulder dystocia
Longer labour
Difficulty with fetal monitoring
Difficulty with uterine monitoring
 Evidence of impaired uterine contractility
 Difficulty with regional anesthesia
 Anesthesia complications
 Cesarean delivery
 Higher rate of complications
 Postoperative complications
 Lower likelihood of successful VBAC
Use of ultrasound in obese
patients
 ~15% of normally visible fetal structures
will be suboptimally seen on the 18-22
week anatomic scan in women with a
BMI >90th percentile
 Structures less commonly seen include:
heart, spine, kidneys, diaphragm, umbilical
cord
 Obstetric care providers should take BMI
into consideration when arranging a fetal
anatomic assessment in the 2nd trimester
 U/S at 20-22 weeks may be best
 Error of ultrasound estimation of fetal
weight: >10% difference from actual birth
weight
Preconception Care
 The preconception visit may be the single most important
health care visit when viewed in the context of its effect on
pregnancy
 Identification and awareness by both patient and provider of
obesity is the first step in management and prevention of
pregnancy complications
 Discussion and education about obesity and its poor perinatal
outcomes should be provided
 Important interventions:
 Weight reduction prior to conception
 Prevention of excessive gestational weight gain
II. Hypothyroidism
Thyroid Physiology and Pregnancy
 Moderate glandular hyperplasia and increased thyroid vascularity are
physiologic
 Thyroid volume by U/S increases a mean of 18%
 Returns to normal postpartum
 Any significant goiter should be worked up
 TBG increases 200%
 High levels of hCG have some TSH-like activity and stimulate thyroid
hormone secretion
 Suppresses TSH
 Throughout pregnancy there is a 30-50% increase in T4 requirement
 Maternal thyroid hormone is transferred to the fetus throughout
pregnancy
 Important for fetal brain development
 Fetus is entirely dependent on maternal thyroid hormones prior to 12 weeks
Hyperemesis gravidarum &
gestational thyrotoxicosis
 Many women with hyperemesis gravidarum have abnormally
high thyroxine levels and low TSH levels
 Results from thyrotropin receptor stimulation from BhCG
 Transient condition called gestational thyrotoxicosis
 Antithyroid drugs are not warranted, even if associated with
hyperemesis
 TSH and FT4 levels will become more normal by midpregnancy
Complications of hypothyroidism in
pregnancy
 Untreated or partially treated clinical hypothyroidism is
associated with:
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Infertility
Miscarriage
Preeclampsia
Abruption
Preterm birth
Low birth weight
Fetal death
Impaired psychomotor function in infants whose mothers have
serum fT4 <10th %ile
 Possibility of lower IQ in children of women with untreated
subclinical hypothyroidism
Thyroid screening in pregnancy
 Universal screening for maternal hypothyroidism is not
recommended
 Women at high risk for hypothyroidism should be screened

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Symptomatic
Previous therapy for hyperthyroidism
History of high-dose neck irradiation
Goiter/palpable thyroid nodule
FHx of thyroid disease
Type I DM
Suspected hypopituitarism
Hyperlipidemia
Medications (amiodarone, lithium, dilantin)
Role of TPO Antibodies
 Present in:
 90% of women with Hashimoto’s thyroiditis
 10% of euthyroid women
 Crosses the placenta
 May increase risk of:
 Spontaneous abortion
 Placental abruption
 Increases incidence of postpartum thyroid
dysfunction
 Routine testing of TPO antibodies during
pregnancy is not recommended
 Serial levels of TPO in women treated for
hypothyroidism are not indicated because
treatment does not alter them
Management of hypothyroidism in
pregnancy
 Approximately 45-85% of women with preexisting
hypothyroidism need up to 45% increase in thyroxine
replacement dose during pregnancy

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Increased metabolism of thyroxine
Weight gain
Increased T4 pool
High serum TBG
Placental deiodinase activity
Transfer of T4 to the fetus
Management of hypothyroidism in
pregnancy
 Ferrous sulfate and calcium
carbonate interfere with T4
absorption and should be taken at
a different time of day from
thyroxine therapy
 Pregnant women should space their
levothyroxine and prenatal vitamin
by at least 2-3 hours
Q: How much time does it take for thyroxine
therapy to alter TSH level?
A. 48 hours
B. 1 week
C. 2 weeks
D. 4 weeks
Management of hypothyroidism in
pregnancy
 TSH and FT4 levels should be checked:
 Preconception
 At the first prenatal visit in the first trimester
 4 weeks after altering the dose of thyroxine replacement
 q4weeks until TSH is normal
 At least every trimester in pregnancy
 FHR should be assessed at each visit to rule out fetal
bradycardia
 Increased ultrasound surveillance is not recommended if
euthyroid
 May consider monthly ultrasounds for fetal growth, thyroid
assessment, and fetal heart rate if clinically hypothyroid
Postpartum thyroiditis
 Transient autoimmune thyroiditis occurs in 5-10% of women
during the first year after childbirth
 Up to 25% of women with DM Type I develop postpartum
thyroid dysfunction
 Diagnosed infrequently
 Typically develops months after delivery
 Vague signs and symptoms
Postpartum thyroiditis
 Two recognized clinical phases:
 (1) Thyrotoxicosis
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1-4 months
Small, painless goiter
Fatigue, palpitations
Treatment: B-Blocker for symptom management
Sequelae: 2/3 become euthyroid, 1/3 become hypothyroid
 (2) Hypothyroidism
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4-8 months
Goiter (more prominent)
Fatigue, inability to concentrate
Treatment: Thyroxine for 6-12 months
Sequelae: 1/3 permanently hypothyroid
 Overall, women who experience postpartum thyroiditis have a ~30%
risk of eventually developing permanent hypothyroidism
III. Pregestational Diabetes
Complications in pregnancy
 Incidence of complications is inversely proportional to glucose
control
 Poorly controlled DM is associated with:
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Spontaneous abortion
Congenital anomalies
IUFD
Preterm birth
Preeclampsia
Macrosomia
Operative delivery
Birth injury
Delayed lung maturity, RDS
Neonatal jaundice, hypoglycemia, hypocalcemia
Preconception Care
 Associated with better outcomes
 Multidisciplinary approach
 All women with DM type 1 and 2 should receive information on
reliable birth control and importance of good glycemic control
prior to conception
 Hgb A1C ≤7.0%
 Folic acid supplementation
 5mg (SOGC Clinical Practice Guideline No. 324, May 2015: 1.0
mg/day of folic acid recommended for those at “moderate risk”)
 Discontinue potentially harmful medications
 ACE Inhibitors
 ARBs
 Statins
Preconception care
 Lifestyle modification
 Efforts should be made to
reduce body weight
 Women with DM type 2
who are planning
pregnancy should switch
from oral antihyperglycemic
agents to insulin for
glycemic control
Assessment and management of
diabetic complications
 Women with preexisting vascular complications are more
likely to have poor pregnancy outcomes
 Retinopathy
 Women with DM type 1 and 2 should have opthalmalogical
assessments:
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Preconception
During the first trimester
As needed during pregnancy
Within the first year postpartum
 Risk of progression is increased with poor glycemic control in
pregnancy
Assessment and management of
diabetic complications
 Hypertension
 Incidence of hypertension complicating pregnancy is 40%-45% in
women with DM type 1 and 2
 Type 1 DM more often associated with preeclampsia
 Type 2 DM more often associated with chronic hypertension
 Poor glycemic control in early pregnancy is a risk factor
Assessment and management of
diabetic complications
 Chronic kidney disease
 Diabetic women should be screened for chronic kidney disease
prior to conception
 Estimation of GFR
 During pregnancy, random albumin:creatinine and serum
creatinine should be measured each trimester
 In women with an elevated serum creatinine, pregnancy can lead
to a permanent deterioration in renal function
Management of diabetes in
pregnancy
 Multidisciplinary care
 Glycemic control:
 Fasting PG <5.3
 1-hour post-prandial <7.8
 2-hour post-prandial <6.7
 Increased risk of hypoglycemia in pregnancy, particularly in
the first trimester
 Hypoglycemic unawareness due to loss of counterregulatory
hormones
 Glycemic targets may have to be raised
Management of diabetes in
pregnancy
 Frequent self-monitoring of blood
glucose is essential
 Pre- and post-prandial
 Pharmacologic therapy:
 Insulin
 Basal bolus therapy
 Continuous subcutaneous insulin
infusion
 Oral antihyperglycemic agents (DM
Type 2)
 No evidence to show increased risk of
congenital anomalies with glyburide or
metformin
 Use of oral agents is not currently
recommended in pregnancy
 Large RCT currently underway
Q: Insulin crosses the placenta…
True
False
Management of diabetes in
pregnancy
 Postpartum:
 Metformin and glyburide can be considered for use during
breastfeeding
 Long-term data are lacking
 High risk of hypoglycemia
 Careful monitoring
 Women with DM Type 1 should be screened for postpartum
thyroiditis
 TSH 6-8 weeks postpartum
 Breastfeeding should be encouraged
IV. Chronic Hypertension
Definitions
 Chronic hypertension:
 Either a history of hypertension preceding pregnancy or a blood
pressure ≥140/90 prior to 20 weeks’ gestation
 Severe hypertension:
 sBP ≥160 mmHg or dBP ≥110 mmHg
 Other disorders…
 GHTN, preeclampsia, superimposed preeclampsia, HELLP….
Recall maternal physiologic
changes in pregnancy…
 Increased blood volume
 Decreased colloid oncotic
pressure
 Overall decrease in total
peripheral resistance
 Physiologic decrease in
BP in 1st and 2nd
trimester may mask
chronic HTN
 A BP of ≥ 120/80 mmHg
in the 1st or 2nd trimester
is not normal
Risk factors and associations
 Renal disease
 Collagen vascular disease
 Antiphospholipid syndrome
 Diabetes
 Thyrotoxicosis
 Cushing’s disease
 Hyperaldosteronism
 Pheochromocytoma
 Coarctation of the aorta
Complications in pregnancy
Maternal
 Worsening HTN
 Superimposed preeclampsia
(20%)
 Eclampsia
 HELLP syndrome
 Cesarean delivery
 Pulmonary edema
 Hypertensive
encephalopathy
 Retinopathy
 Cerebral hemorrhage
 AKI
Fetal
 IUGR (8-15%)
 Oligohydramnios
 Placental abruption (0.71.5%; ~2-fold increase)
 PTB (12-34%)
 Perinatal death (2- to 4-fold
increase)
Q: Which of the following antihypertensive
drugs are safe for use in pregnancy?
 Methyldopa
 Diuretics
 ACE inhibitors
 ARBs
 Labetalol
 Atenolol
 Calcium channel blockers
Preconception counseling
 Appropriate counseling regarding possible complications
 Discontinuation of ACE inhibitors and ARBs
 Consider work-up for associated causes if not previously
done
Management
 Early pregnancy investigations (if not previously documented):
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Creatinine
Fasting blood glucose
Serum potassium
Urinalysis
EKG
 Baseline GHTN labs
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Transaminases
CBC
Creatinine
Urine protein:creatinine ratio
Urate
LD
 Consider IM consult
 New dx of HTN, investigation of associated causes
Management
 Home BP monitoring
 ASA 81 mg initiated after diagnosis of pregnancy but <16 weeks
gestation
 Consider for continuation until delivery
 Calcium supplementation (at least 1g/d) in women with low
calcium intake
 Lifestyle modification
 Insufficient evidence to make recommendations regarding:
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Dietary salt restriction
Exercise
Workload reduction, stress reduction
Bed rest
Management
 Antihypertensive drugs
 Methyldopa
 Labetalol
 Nifedipine
 Insufficient evidence to conclude that one antihypertensive is
better than the other
 Antihypertensive agents should probably be started (or
increased, or modified) in pregnancy when sBP ≥160 mmHg
or dBP ≥110 mmHg on two occasions
 A woman’s natural BP may be necessary for adequate
placental perfusion
 Goal of maintaining BP around 130-155/80-105 mmHg
 <140/90 mmHg with end-organ damage, renal disease, diabetes
V. Seizure disorders
Q: In pregnancy, there is evidence to
support a risk of increased seizure
frequency…
True
False
Complications in pregnancy
 Maternal complications:
 Insufficient evidence to support or refute a change in seizure
frequency in pregnancy or an increased risk of status epilepticus
in pregnant women with epilepsy
 Seizure freedom for at least 9 months prior to pregnancy is
probably associated with a high likelihood (84-92%) of remaining
seizure free during pregnancy
 90% of women with epilepsy have successful pregnancies and
deliver healthy babies
Complications in pregnancy
 Fetal complications:
 GTC seizures increase the risk of hypoxia and acidosis as well
as injury from blunt trauma
 May cause fetal heart rate abnormalities
 Risks associated with in utero exposure to AEDs:
 Fetal loss (1.3-14%)
 Perinatal death (1.3-7.8%)
 Congenital malformations (4-7%; ~twice the baseline risk)
 Most common: cardiac, NTDs, craniofacial, fingers, etc.
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Low birth weight (7-10%)
Prematurity (4-11%)
Developmental delay
Childhood epilepsy
AEDs and congenital anomalies
Data from the North American Antiepileptic Drug (NAAED) Pregnancy
Registry:
Antiepileptic drug
Rate of major malformations
Valproate
10.7%
Phenobarbital
6.5%
Lamotrigine
2.7%
Carbamazepine
2.5%
Effect of pregnancy on disease
 Concentrations of some AEDs fall
 Increase in hepatic cytochrome P450 enzyme activity
 Increased renal clearance
 Changes in volume distribution
 Decreased protein binding results in higher levels of unbound
biologically active AEDs
 May cause toxicity
Preconception counseling
 Conception should be deferred until seizures are well
controlled on minimum dose of medication
 Monotherapy is preferable
 Good compliance with AEDs is essential
 Inform women about risk of congenital malformations in
infants exposed to AEDs in utero
 4-8% risk
 Avoid category D drugs if possible in the first trimester
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Carbamazepine
Phenobarbital
Phenytoin
Valproate
Topiramate
Preconception counseling
 Neurologic consultation
regarding possibility of tapering
off and stopping AEDs if the
patient has been seizure free for
>2 years and EEG is normal
 Observe for 6-12 months before
attempting conception
 Preconception folic acid 5 mg
 (SOGC Clinical Practice
Guideline No. 324, May 2015: 1.0
mg/day of folic acid
recommended for those at
“moderate risk”)
 Enzyme-enhancing AEDs
enhance the metabolism of
OCPs
Postpartum
 Breastfeeding is not contraindicated
 For most AEDs, the pharmacokinetics in the mother will
return to prepregnancy levels within 10-14 days postpartum
 Monitor AED levels 8 weeks postpartum and adjust doses
accordingly to avoid toxicity
 Sleep deprivation may exacerbate seizures
 Counsel patients regarding seizure precautions
Referral options in Calgary
 OB
 MFM
 MDIP
 DIP
 ACCP
Suggested References
 Obesity in pregnancy. SOGC Clinical Practice Guideline No. 239,
February 2010.
 Exercise in pregnancy and the postpartum period. SOGC Clinical
Practice Guideline No. 129, June 2003.
 Diabetes and pregnancy. Canadian Diabetes Association Clinical
Practice Guideline. Can J Diabetes 37(2013), S168-S183.
 Diagnosis, evaluation, and management of hypertensive disorders of
pregnancy: executive summary. SOGC Clinical Practice Guideline No.
307, May 2014.
 Pre-conception folic acid and multivitamin supplementation for the
primary and secondary prevention of neural tube defects and other folic
acid-sensitive congenital anomalies. SOGC Clinical Practice Guideline
No. 324, June 2015.
Questions?