Diabetes mellitus and thyroid diseases can impact pregnancy. The presentation discussed diabetes mellitus, its classification and effects during pregnancy. It can increase risks for the mother like hypertension and risks for the baby like macrosomia. Screening and care involve monitoring blood sugar via tests and working with a team. Gestational diabetes requires diet control or possibly insulin. Thyroid diseases like thyrotoxicosis also impact pregnancy and require treatment to control the condition and prevent risks. Care involves monitoring and treating any thyroid abnormalities in the mother or baby.

1. Presentation about :
Diabetus mellitus
and thyroid
diseases among
pregnancy
by :dr.esra Ali

2. Hello!
I am Esraa Ali Yahya
MBBS Uni. Of Ahfad University for women
AUW
2

3. 3

4. Objectives
✖ To define DM
✖ To determine the classification of DM
among pregnancy .
✖ To determine the effect of diabetes of
pregnancy and the effect of pregnancy
on diabetes .
✖ To know how to screen for DM among
pregnancy .
✖ to determine the Prenatal ,natal ,post
natal care of pregnancy with DM .
4

5. DM is ametabolic disorder of multiple
etiology characterized by chronic
hyperglysemia resulting from defects in
insulin secretion , insulin action ,or both
.
5

6. Varieties of abnormal glucose tolerance:
1. established or pre-existing Diabetes:
✖ IDDM
✖ NIDDM
2. Gestational Diabetes.
3. Impaired Glucose Tolerance- Chemical
D.M
6

7. Established diabetes
• affects 1–2% of pregnancies.
• Without good glycaemic control there is increased fetal and
neonatal morbidity and mortality.
• Management should be by a multidisciplinary team
including:
• obstetrician
• physician/diabetologist
• diabetic specialist nurse/midwife
• dietitian.
• Glucose metabolism is altered by pregnancy.
• Many pregnancy hormones are diabetogenic (human
placental lactogen, cortisol, glucagon, oestrogen, and
progesterone).
• Insulin requirements increas throughout and are maximal at
term.
7

8. Gestational diabetes
The World Health Organization (WHO)
now includes gestational impaired
glucose tolerance (IGT) with gestational
diabetes. A proportion of women
diagnosed in pregnancy will actually
have previously unrecognized type 1 or 2
diabetes (20–30%). WHO does not
advocate universal screening. Selective
screening should be based on risk
factors.
8

9. Risk factors for gestational diabetes
1. First degree relative diabetic
2. Any 2 of the following:
o Glycosuria 2+ is present.
o Body Mass Index > 30
o Previous baby > 4500g
o Previous unexplained stilbirth
o Polyhydrimnios
o Fetal macrosomia
3. 3+ glycosuria at any time
9

10. Screening for diabetes in pregnant women
All pregnant women should be screened for diabetes at their first
antenatal care visit (whatever the gestational age). This is done
by testing the fasting blood sugar (i.e 8hours) or RBS . If the
fasting result is below 95micrograms and RBS below 145 the test
should be repeated at 26 weeks of gestation. If the patient is at
low risk no further action should be taken. The test should be
repeated again for the third time at 34 weeks gestation for high
risk. If the results of the fasting blood sugar is above
95micrograms or RBS above 145 then a confirmation test is
carried out by giving 75/ 100g of glucose and results should be
as follows :
10

11. Fasting 95 or higher
At 1 hrs 180 or higher
At 2 hrs 155 or higher
At 3 hrs 140 or higher
If any two or more of these are elevated ,
the patient should be considered as
diabetic
11

12. The diagnosis is based on an oral
glucose tolerance test (OGTT) (Box
5.4), usually undertaken at 26–28wks
gestation. A normal result in early
pregnancy does not mean that
gestational diabetes will not develop,
and an OGTT should be repeated at
34wks if there are concern
12

13. Box 5.4 Oral glucose tolerance test
• Overnight fasting (8h minimum):
• water only may be consumed during this time
• no smoking.
• 75g Glucose load in 250–300mL water.
• Plasma glucose measured fasting and at 2h.
Results
• Diabetes:
• fasting glucose ≥7.0mmol/L
• 2h glucose ≥11.1mmol/L.
• IGT:
• fasting glucose <7.0mmol/L
• 2h ≥7.8 <11.0mmol/L.
Only one value needs to be abnormal to make the diagnosis.
13

14. Effect of diabetes on pregnancy
• Maternal hyperglycaemia: leads to fetal hyperglycaemia.
• Fetal hyperglycaemia: leads to hyperinsulinaemia
(through β-cell hyperplasia in fetal pancreatic cells).
Insulin acts as a growth promoter:
• macrosomia
• organomegaly
• i erythropoiesis
• fetal polyuria (polyhydramnios).
• Neonatal hypoglycaemia: caused by the removal of
maternal glucose supply at birth from a hyperinsulinaemic
fetus.
• Respiratory distress syndrome: more common in babies
born to diabetic mothers due to surfactant deficiency
occurring through reduced production of pulmonary
phospholipids.
14

15. Effect of pregnancy on diabetes
• Ketoacidosis: rare, but may be associated with hyperemesis,
infection,tocolysis (β-sympathomimetics), or steroid therapy.
• Retinopathy: there is a two-fold increased risk of development or
progression of existing disease. Rapid improvement in glycaemic
control leads to increased retinal blood flow, which can cause
retinopathy. All diabetic women should have assessment for
retinopathy in pregnancy, and proliferative retinopathy requires
treatment. Early changes usually revert after delivery.
• Nephropathy: affects 5–10% of women. Renal function and
proteinuria may worsen during pregnancy. This is usually temporary.
There is increased maternal risk of pre-eclampsia and fetal risk of
IUGR in this population and increased surveillance is required.
• Ischaemic heart disease: pregnancy increases cardiac workload.
Women with symptoms should be assessed by a cardiologist before
conception.
15

16. Complications of diabetes in pregnancy
Maternal
• UTI.
• Recurrent vulvovaginal candidiasis.
• Pregnancy-induced hypertension/pre-
eclampsia.
• Obstructed labour.
• Operative deliveries: CS and assisted
vaginal deliveries.
• i Retinopathy (15%).
• i Nephropathy.
• Cardiac disease.
16

17. Fetal
• Miscarriage*
• Congenital abnormalities:*
• neural tube defects
• microcephaly
• cardiac abnormalities.
• sacral agenesis
• renal abnormalities.
• Preterm labour.
• Polyhydramnios (25%).
• Macrosomia (25–40%).
• IUGR.
• Unexplained IUD.
17

18. Neonatal
• Polycythaemia.
• Jaundice.
• Hypoglycaemia.
• Hypocalcaemia.
• Hypomagnesaemia.
• Hypothermia.
• Cardiomegaly.
• Birth trauma: shoulder dystocia,
fractures, Erb’s palsy, asphyxia.
• Respiratory distress syndrome.
* In diabetics with poor control.
18

19. Anti Natal care
19

20. Pregnancy counselling
Offer to all diabetic women of reproductive age; include:
• Achievement of optimal control: keep fasting blood glucose between 3.5
and 5.9mmol/L and 1h post-prandial <7.8mmol/L (i risk of miscarriage
and congenital abnormalities with poor control).
• Assessment of severity of diabetes: check for hypertension, retinopathy
(fundoscopy, ophthalmology assessment), nephropathy (U&E,
urinalysis, urinary protein:creatinine ratio, 24h urine for protein,
creatinine clearance), neuropathy (clinical assessment), and cardiac
disease.
• Education: ensure understanding of effects of hyperglycaemia on fetus
and need for tight control—instruct to inform doctor as soon as
pregnancy confirmed; some drugs may need stopping (ACEIs).
• General health: stop smoking, optimize weight (aim for a normal BMI),
minimize alcohol (max 1–2U bd/wk).
• Folic acid: i risk of neural tube defects, so start on 5mg folic acid.
• Rubella status: offer vaccination if not rubella immune.
• Contraception: ensure effective contraception until good control
achieved and pregnancy desired.
20

21. Antenatal care
Manage by a multidisciplinary team with a diabetologist.
• Control: as for prepregnancy, aim for normoglycaemia. Monitor glucose
at least 4 times/day, usually before meals, but post-meal glucose may
give tighter control. Women can alter their own insulin based on their
glucose. Insulin can be given as SC injections 2 or 4 times/day or as a
continuous infusion. The latter is no better than injections.
• HbA1c every month: this gives an objective measurement of control
over the preceding 2mths.
• Dietitian review: low sugar, low fat, high fibre diet—low glycaemic
index.
• Dating ultrasound: to confirm viability and gestation.
X Down’s syndrome screening: consider nuchal translucency or invasive
testing. Serum screening is affected by diabetes (d AFP); therefore, less
accurate unless appropriate normograms used.
• Anomaly scan: 5–10-fold i risk of congenital anomalies. Risk depends
on glycaemic control prior to conception and early pregnancy.
• Fetal echocardiography: at 20–24wks.
• Antenatal surveillance: individualize care. Serial USS every 2–4wks to
detect polyhydramnios, macrosomia, or IUGR. Increased surveillance
if problems detected. The use of umbilical artery Doppler should be
restricted to cases of IUGR; it is not of value as a screening test.
• Hypoglycaemia: awareness of hypoglycaemia may be lost. Educate
patient and family and supply with glucagon.
21

22. labour and post-partum
care
22

23. Timing of delivery
Timing and mode of delivery should be
individualized and based on EFW and obstetric
factors (previous mode of delivery, gestation,
glycaemic control, and antenatal complications)
✖ Some obstetricians advise elective delivery by
induction of labour at38–39wks if there are no
maternal or fetal complications and good
glycaemic control. Outcomes may not be better
than awaiting spontaneous labour. Delivery
should be expedited if complications occur.
23

24. Mode of delivery
Vaginal delivery is preferred. Continuous electronic
fetal monitoring is advised in labour. Consider
elective CS if EFW is >4.5kg. If EFW is 4–4.5kg
use obstetric factors to influence decision. CS rates
are high: 50–60%. Give antibiotic and
thromboprophylaxis if CS is carried out.
✖ Shoulder dystocia is more common at all birth
weights than in the non-diabetic population.
Experienced obstetricians should perform
instrumental deliveries because this is an
independent risk factor.
24

25. Glycemic control
• Diet controlled: check blood glucose hourly. If
glucose >6.0mmol/L,
start sliding scale.
• Insulin dependent: continue SC insulin until in
established labour, then convert to insulin sliding
scale (Table 5.1). If induction of labour or CS,
continue normal insulin until day of procedure, then
start sliding scale in early morning.
Avoid maternal hyperglycaemia increase causes
fetal hypoglycaemia.
If steroids are given for threatened preterm labour,
monitor glucose closely—hyperglycaemia should be
anticipated.
25

26. Post-partum care
• Encourage breast-feeding.
Avoid oral hypoglycaemic drugs if
breastfeeding—metformin and insulin
are safe.
• Baby needs early feeding and glucose
monitoring
26

27. Contraception
• Avoid the COCP if breast-feeding or vascular
complications.
Progesterone-based contraception is safe and there
are no contraindications to an IUCD. This should be
fitted from 6wks post-partum onwards. Sterilization
or vasectomy should be considered if the family
is complete.
• Review sliding scale regularly.
• Renew insulin syringe every 24h.
• IV fluids should always be given with the sliding
scale:
• stable situations—5% glucose
• high blood glucose—normal saline.
27

28. Table 5.1 Insulin: IV sliding scale
Blood glucose (mmol/L) Insulin rate (mL/h)
<3.0 0
3.1–4 0.5
4.1–6 1.0
6.1–8 1.5
8.1–11 2.0
11.1–15 3.0
>15.1 Call doctor
Prescription: 50U human actrapid in 50mL normal saline (sodium
chloride 0.9%), via acontinuous infusion pump.
28

29. Post-partum insulin requirements
Insulin requirements fall dramatically after delivery
of the placenta.
Halve the sliding scale initially. Change back to SC
insulin when eating and drinking. Start with the pre
pregnancy dose of SC insulin. If this is not known, it
is roughly half the last dose. The dose may need to be
further reduced if breast-feeding. Stop the sliding
scale 1h after giving the SC dose.
Aim for blood sugar monitoring (BM) 4–9mmol/L in
the post-partum period
29

30. Management of gestational dm
• Management by a multidisciplinary team.
• Measure glucose 4–6 times/day (1h post-prandial measurements may
be more effective in preventing macrosomia than pre-meal glucose).
• Diet should be fi rst-line treatment:
• aim for normoglycaemia and avoid ketosis.
• weight should remain steady if diet followed
• compliance is often poor—dietitian input may help.
• Start insulin if:
• pre-meal glucose >6.0mmol/L
• 1h post-prandial glucose >7.5mmol/L.
• AC >95th centile despite apparent good control.
• There is no increased risk of miscarriage or congenital anomalies;
other fetal and neonatal risks are similar to established diabetes (IUGR
is less likely).
• Antenatal and intrapartum care as for established diabetes.
• Post-partum:
• stop insulin and glucose infusions
• check glucose prior to discharge to ensure normal (risk of
previously undiagnosed type 2 diabetes)
• arrange OGTT at 6wks post-partum
• education—50% risk of developing type 2 diabetes mellitus over
next 25yrs (this risk can be reduced by maintaining physical activity
and avoiding obesity)
30

31. Thyroid diseases
among
pregnancy
31

32. thyrotoxicosis
32

33. Thyrotoxicosis occurs in 1:500 pregnancies. The
most common cause is Graves’ disease (95%). This
is an autoimmune disease characterized by
the production of TSH receptor stimulating
antibodies. Most women have been diagnosed before
pregnancy and may be on treatment. Many
symptoms and signs occur in normal pregnancy. The
most discriminatory features are weight loss,
tremor, persistent tachycardia, and eye signs.
Diagnosis is made by a low TSH and high free T4 or
free T3 levels.
2 Use pregnancy-specific reference ranges for each
trimester. See Table 5.2.
33

34. Effect of pregnancy on thyrotoxicosis
• Usually improves in the 2nd and 3rd
trimester.
• Pregnancy is a state of relative
immunodeficiency, but with return of
normal immunity in the puerperium it is
likely to deteriorate.
34

35. Effect of thyrotoxicosis on pregnancy
• Maternal and fetal outcome usually
good if disease is controlled.
• Untreated or poorly controlled
thyrotoxicosis is associated with
subfertility (amenorrhoea due to weight
loss), i risk of miscarriage, IUGR,
and premature delivery.
35

36. With the stress of infection, labour, or
operative delivery a ‘thyroid storm’ can occur
in poorly controlled patients. This is a medical
emergency, characterized by pyrexia,
confusion, and cardiac failure. Neonatal/ fetal
thyrotoxicosis occurs in up to 10% of babies
born to women with current or past history of
Graves’ disease (transplacental passage of
thyroid receptor stimulating antibodies).
36

37. ✖ Check antibody levels in all women
with a history of Graves’ disease.
• If antibodies are present, monitor by
fetal heart rate, and serial USS for
growth and fetal goitre (treatments
include antithyroid drugs titrated
to fetal heart rate, or delivery).
• Antibodies have a half-life of around
3wks, therefore transient neonatal
hyperthyroidism may occur
37

38. Treatment
• Antithyroid drugs: carbimazole and propylthiouracil (PTU)
are the two drugs used. The aim of treatment is to achieve
clinical euthyroid withT4 at the upper limit of normal. Use
the lowest dose of drug to achieve this. Both drugs cross
the placenta and may cause fetal hypothyroidism in high
doses. PTU is preferred for new cases as there is less
transfer across the placenta and into breastmilk. β-
Blockers may safely be used for symptom relief in new
cases for a short period of time.
• Surgery: thyroidectomy can be safely done in pregnancy.
Indications
include dysphagia, stridor, suspected carcinoma, and
allergies to both antithyroid drugs.
Radioactive iodine is contraindicated in pregnancy and
breast-feeding
38

39. Causes of thyrotoxicosis
• Graves’ disease.
• Toxic multinodular goitre.
• Toxic adenoma.
• Carcinoma.
• Subacute thyroiditis.
• Amiodarone.
• Lithium.
Women with hyperemesis or a molar pregnancy
may mimic biochemical hyperthyroidism as hCG, at
high levels, can stimulate TSH receptors. They
usually have no clinical signs of thyrotoxicosis and
should not be treated.
39

40. Summary of Management
• Graves’ disease often improves in pregnancy, but relapses
postpartum.
• With treatment the outlook is good for mother and baby.
• Untreated thyrotoxicosis is dangerous for mother and baby.
• PTU and carbimazole may be used as treatment; both cross the
placenta.
• Avoid radioactive iodine.
• Check for TSH receptor stimulating antibodies.
• Monitor thyroid function every 4–6wks in new cases, less
frequently in stable cases.
• Monitor fetus by fetal heart rate and serial USS for growth and
presence of goitre.
• Breast-feeding is safe with doses of PTU <150mg/day and
carbimazole <15mg/day. Monitor TFTs in baby at higher doses
40

41. hypothyroidisim
41

42. Hypothyroidism complicates around 1% of pregnancies. Most
cases have been diagnosed previously and patients are on
replacement therapy. New diagnosis in pregnancy is rare. The
commonest cause is autoimmune and may be associated with
other autoimmune conditions.
• Classical symptoms and signs may be seen in normal pregnancy.
The most discriminatory features are cold intolerance,
bradycardia, and slow relaxation of tendon reflexes.
• The diagnosis is made by a low free T4. TSH is also raised, but in
isolation is not diagnostic.
Use pregnancy-specific reference ranges for each trimester
(Table 5.2).
Free T4 levels are normally lower in the 2nd and 3rd trimester.
TSH level is most useful.
42

43. Effect of pregnancy on hypothyroidism
No effect usually. Most women do not
need to alter their dose of levothyroxine.
The most common reason for increasing
levothyroxine is an inadequate
prepregnancy dose
43

44. Effect of hypothyroidism on pregnancy
• Untreated hypothyroidism is associated with
anovulatory infertility.
• Severe or untreated hypothyroidism in pregnancy
is associated with increased risk of miscarriage, fetal
loss, pre-eclampsia, and low birth weight.
• Hypothyroidism is also associated with gestational
diabetes.
• The fetus requires maternal T4 for normal brain
development before 12wks (inadequate replacement
may lead to reduced IQ in the offspring); after this
time T3/T4/TSH do not cross the placenta.
44

45. ✖ Aim for optimal control before
conception.
• Women on adequate replacement
therapy are euthyroid at the onset
of pregnancy and have good maternal
and fetal outcomes.
• Neonatal/fetal hypothyroidism is very
rare and caused by the transplacental
transfer of TSH receptor blocking
antibodies, which may be seen in
atrophic thyroiditis.
45

46. Treatment
• Most women should continue their maintenance dose of
levothyroxine; the dose should only be increased if they
are under-replaced (shown by TSH level).
• TSH levels need to be checked before conception and in
each trimester, unless there has been a dose adjustment,
in which case it should be repeated in 6wks.
• If the diagnosis is made in pregnancy, in the absence of
cardiac disease, consider a starting dose of 50 micrograms
daily.
• In practice, aim for a TSH level of <2.5µ/L in the first
trimester.
• Levothyroxine can be safely taken during breast-feeding
46

47. Causes of hypothyroidism
• Hashimoto’s thyroiditis.
• Atrophic thyroiditis.
• Congenital absence of thyroid.
• Iatrogenic:
• thyroidectomy
• radioiodine
• drugs (amiodarone, lithium, iodine,
antithyroid drugs).
• Pituitary cause (rare).
47

48. Other thyroid diseases
48

49. Post-partum thyroiditis
This is an autoimmune condition causing destructive thyroiditis. It
presentspost-partum due to return to normal immunity after the relative
immunosuppression of pregnancy. Preformed T4 is released, which may
cause transient hyperthyroid symptoms followed by hypothyroidism as the
reserve of T4 is used up.
It can present for up to a year after delivery, but usually occurs 3–4mths
post-partum. The incidence varies (5–10%) and it may manifest as
transient hypothyroidism (40%), hyperthyroidism (40%), or biphasic with
first hyperthyroidism then hypothyroidism (20%). There may be a family
history of thyroid disease in 25% of cases. Many women are asymptomatic
and often symptoms are vague and may be attributed to the post-partum
state. Initiation of treatment should be based on symptoms and not
biochemical results. Some women may not require any treatment. Most
recover spontaneously. Risk of recurrence in future pregnancy is 70%. Risk
of permanent hypothyroidism is 5%/yr for antibody-positive women (90%
of patients have thyroid peroxidase antibodies).
• The hyperthyroid phase should be treated with β-blockers (not
antithyroid drugs).
49

50. Differential diagnosis
• Graves’ disease.
• The hypothyroid state should be
treated with thyroxine; treatment
should be withdrawn after 6mths to
check for recovery.
• Hashimoto’s thyroiditis or Sheehan’s
syndrome.
Long-term follow-up should be with
annual TFT.
50

51. Thyroid nodules
• Thyroid nodules are common, affecting 5% of women in their
reproductive years.
A small proportion of thyroid nodules are malignant.
• Differential diagnosis is a solitary toxic nodule, subacute (de
Quervain’s) thyroiditis, or a bleed into a cystic lesion.
• Investigations:
• TFT and thyroid antibodies
• thyroglobulin level: suggests malignancy if >100 micrograms/L
• USS—cystic nodules are more likely to be benign than solid
nodules
• fine needle aspiration for cytology (cystic lesion)
• biopsy (solid lesion).
Radioiodine is contraindicated in pregnancy.
Malignant lesions can be surgically treated in the 2nd and 3rd
trimesters, and postoperatively thyroxine can be safely given to
completely suppress TSH in TSH-dependent tumours.
51

52. Thyroid nodules: symptoms or signs suggestive of
malignancy
• Past history of radiation to neck or chest.
• Fixed lump.
• Lymphadenopathy.
• Rapid growth of painless nodule.
• Voice change.
• Neurological involvement such as
Horner’s syndrome.
52

53. But It’s time for
transformation
53

54. “The most basic and
powerful way to connect to
another person is to listen.
Just listen.
Perhaps the most
important thing we ever
give each other is our
attention”
.
Dr. Rachel Naomi Remen
54

55. 55
Thanks!

56. References
✖ Oxford hand book of obstetric and
gynacology
✖ Guide line for best practice
✖ Guide line in obstetrics and gynecology by
jibril umar
56