Diabetes in

pregnancy
PRESENTER: ANNAKAY
HUDSON

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Objectives
Define diabetes

Pre-gestational diabetes

Gestational Diabetes
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 A chronic metabolic disorder
characterized by hyperglycemia
secondary to the inability of the
pancreas to produce sufficient
insulin or from inefficient use of
Definition insulin by the body.

Type 1 Diabetes Mellitus

Type 2 Diabetes Mellitus
Gestational Diabetes Mellitus
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What is insulin?

Insulin is a peptide
hormone secreted by the β
cells of the pancreatic islets
of Langerhans and
maintains normal blood
glucose levels by
facilitating cellular glucose
uptake, regulating
carbohydrate, lipid and
protein metabolism.

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 Type 1 DM – insulin-dependent diabetes. Pancreas
produces little to no insulin due to autoimmune destruction
of the beta cells of the pancreas. - Young Patients

Types of Type 2 DM – marked by insulin resistance and relative

underproduction of insulin – older and obese patients
Diabetes
Gestational DM - any degree of glucose intolerance with
onset or first recognition during pregnancy. It is diabetes
that develops in pregnancy and resolves after the foetus is
delivered.

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 In 2016, 2,339 persons died from diabetes in Jamaica,
accounting for 12.7% of all deaths. (STATIN)

Approximately 11.9% (9% men, 14.6% women) or

236,200 of Jamaicans 15 years and older have
diabetes .
In Jamaica:
The prevalence of diabetes has increased by 41.1%
from 2001 to 2017 among Jamaicans 15 to 74 years old.

Approximately 11.9% (9% men, 14.6% women) or

236,200 of Jamaicans 15 years and older have diabetes
(Jamaica Health and Lifestyle Survey III, 2016-17)

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Making
the
diagnosis

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WHO’s
Diagnostic
Criteria for
Diabetes

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Pre-gestational
A WOMAN WHO HAS BEEN DIAGNOSED WITH DIABETES
PRIOR TO BECOMING PREGNANT.

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Pre- conception
Counselling = Risk Reduction
The aim in persons known to have diabetes is planned pregnancies.
“Aim to empower women with diabetes to have a positive experience of
pregnancy and childbirth by providing information, advice and support
that will help to reduce the risks of adverse pregnancy outcomes for
mother and baby” NG3, 2008
Achieve the best possible glycaemic control
Education on the effects of diabetes on pregnancy: possible
complications and its potential effects on labor (induction, C-section)

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CONTRACEPTIVE counselling is important

Patients with BMI > 27 kg/m2 should be

referred to dieticians and weight loss advised

High dose folic acid (5 mg/day) until the first

12 weeks

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 the need for assessment of
The risks of hypoglycaemia
The importance of diet, diabetic
and impaired awareness of
weight and exercise on the retinopathy/nephropathy
hypoglycaemia during
pregnancy before and during
pregnancy
pregnancy

the importance of maternal the possibility of temporary

blood glucose control during
labour and birth and early
feeding of the baby, in order
to reduce the risk of
neonatal hypoglycaemia
health problems in the baby
during the neonatal period,
which may require
admission to the neonatal
unit

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Targets (PRE- pregnancy)
HbA1c < 6.5%
Fasting glucose(upon waking): 5-7 mmol/l
Pre-meal Glucose : 4 -7 mmol/l

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complications
Foetal
Congenital abnormalities (Neural tube defects
Maternal and cardiac defects)
• Hypertension/preeclampsia (especially if there is
the presence of previous nephropathy) Polyhydramnios
• Diabetic ketoacidosis
• Retinopathy
Macrosomia – traumatic delivery, shoulder
dystocia
• Nephropathy
• Increased risk of miscarriage(pre- existing IUGR (long standing disease- arterial
diabetes) complications)
• Infections (especially pyelonehritis)
Foetal lung immaturity
Sudden unexplained late stillbirths

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 Respiratory Distress Syndrome

Hypoglycemia

Neonatal Hypocalcemia

Hypomagnesaemia

Hyperbilirubinemia ( neonatal jaundice)

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Management in pregnancy
Aims of antenatal Care:
Glycaemic control: fasting: 4-5.5 mmol/l

1 hour after meals: <7.8 mmol/l

2 hours after meals: 4-6.5 mmol/l

-Renal and retinal screening

-Foetal surveillance
-Plan for delivery

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Gestational diabetes
mellitus

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 Anti – insulin factors are produced by the placenta leading to
increased peripheral insulin resistance.

Anti- insulin factors include: human placental lactogen

Pathophysiology prolactin
progesterone
glucagon
cortisol
placental insulinase

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Normally this diabetogenic state is counterbalanced by an increase
in insulin (almost twice non-pregnant levels)
Most women are therefore able to maintain normoglycaemia
5-9% can not which leads to Gestational Diabetes
Usually starts in the 2nd or 3rd trimester
Disappears after delivery
50% of patients with Gestational Diabetes will develop overt
Diabetes after about 25 years

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Risk factors
Maternal Foetal
Family history of diabetes Previous macrosomic foetus
Maternal age > 30 years Polyhydramnios
Increased BMI
High parity
Previous GDM
Polycystic Ovarian Syndrome
Steroid use
Hypertension related disorders

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 Does not usually cause any noticeable
signs and symptoms hence the
importance of screening tests

Signs and Rarely there may be increased thirst

symptoms and urination

The presence of polyhydramnios may

be a sign of hyperglycaemia so the
necessary investigations should follow

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Screening test
O’ Sullivan’ s Test
Screening for GDM occurs between the 24th to 28th week of pregnancy or at any
point if considered high risk
Random Non fasting test
50 g glucose solution given and the blood glucose measured 1 hour after.
Results: < 7.8 mmol/l – Normal
7.8 – 11.1 mmol/l – OGTT
> 11.1 mmol/l – diagnostic for GDM

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Oral glucose tolerance test (ogtt)
Diagnostic test for diabetes
On the morning of test fasting plasma glucose taken
75 g glucose solution given to patient (should be had in 5 minutes)
Blood glucose levels measured at 1 hour and 2 hours after
Diagnostic of GDM if there are glucose levels exceeding any of the two (2) cut off intervals
Results:
Fasting < 5.3 mmol/l
1 hour < 10 mmol/l
2 hour < 8.6 mmol/l
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 1. Glycosuria: urinalysis. Unreliable as a measure of
hyperglycaemia since the renal threshold for glucose is
said to fall in pregnancy.

2. Random Blood Sugar

Other tests
3. Glycosylated haemoglobin: HbA1c
Good for long term control and not as a screening tool for
gestational diabetes
Values of > 8% indicative of hyperglycaemia in the previous 3
months

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Glycaemic control
Initially the aim is to achieve control with diet modification and exercise
If control is not achieved within 2 weeks of conservative management, insulin therapy is added
to the regimen

TARGETS:
FPG < 5.3 mmol/l
1 hr < 7.8 mmol/l
2 hr < 6.7 mmol/l

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Management

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Antenatal care
Aims:
-Glycaemic control
*Type 1: increased doses of insulin
* Type 2: switched from oral hypoglycaemic agents to soluble insulin
* lifestyle: physical activity and diet (3 meals, 2 snacks)
- the aim is for 1600-1800 kcal diet per day which should be high in fiber,
protein, unrefined carbohydrate and low in fat

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* home glucose monitoring
* clinic visits – recommended: every 2 weeks until third trimester where seen
every week

-Renal and Retinal Screening (Type 1 and 2 DM ) – offered at booking

* (according to NICE guidelines they should be offered preconception)

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Insulin therapy
The total daily dose of insulin used is dependent on the current weight of the patient and the
stage of the pregnancy.
So it is calculated as follows:
1. 1st trimester: 0.7 U/kg/ day
2. 2nd trimester: 0.8U/kg/day
3. 3rd trimester: 0.9U/ kg/day

The total daily doses are given in a split dose regime and adjusted based on results of glucose
monitoring.

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Insulin therapy( con’t)
Given in a split – dose/ split mixed regime
1. 2/3 of the total insulin requirement is given in the morning in the ratio of 2:1 short acting:
intermediate acting, of morning requirements. That is 2/3 of the total MORNING
requirement is given as short acting and the remainder as intermediate acting (1/3).
2. The remaining 1/3 of TOTAL DAILY insulin requirement is given in a 50:50 split between short
and intermediate acting.

Remember insulin requirements increase as pregnancy progresses.

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Antepartum care (continued)
Foetal Surveillance
*accurate dating
* Nuchal translucency Scanning (first trimester)
* anomaly scan (18 – 20 weeks)
* CTG, foetal movements and foetal growth
* Foetal Echo
* Triple/ Quad Screen (alpha fetoprotein, hCg, estriol, inhibin A) – for patients with
type 1 or 2 diabetes. (later in pregnancy)
* Fetal Biometry – Monitors growth

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 * Aim: 38 – 39 weeks

* biophysical profile to ensure foetal well being at 37- 38 weeks in

preparation for labour
Plan for
Delivery * Vaginal delivery if there are no contraindications present

* If there are complications in the pregnancy (severe pre-

eclampsia, renal failure, progressive proliferative retinopathy)
elect to do earlier.

*Give Betamathasone if pre-term labour to allow lung maturity

(steroids are diabetogenc so may need an insulin sliding scale)

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 Induction of labour at 38 to 39 weeks once there is no
contraindication present
Otherwise Caesarean Section at 37-39 weeks
Failure to progress: C- Section

Monitoring blood glucose:

- every 30 mins (general anaesthesia)
Intrapartum - Every 1 -2 hours (vaginal delivery)
Aim: 4- 7 mmol/l

Role of insulin and dextrose solution (5%) – dextrose started at

the beginning and blood glucose checked as above and insulin
given on a sliding scale to maintain glucose in the therapeutic
dose

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postpartum

Return to oral
Reduced insulin hypoglycaemic agents- Contraceptive
Stop insulin use (GDM)
therapy (Type 1) metformin, counselling
glibenclamide ( Type 2)

Post natal visit (6 Counselling for patients

weeks): OGTT repeated Fasting plasma glucose with pre-pregnancy
HbA1c yearly
for patients who had (6 – 13 weeks) diabetes on continued
GDM medical care

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references
Roopnarinesingh Textbook of Obstetrics, 3rd edition
Obstetrics by Ten Teachers. Kenny L, Baker P.19th Edition. Hodder Arnold: Hodder Education. 2011
https://www.nice.org.uk/guidance/ng3
http://apps.who.int/iris/bitstream/10665/43588/1/9241594934_eng.pdf
http://apps.who.int/iris/bitstream/10665/85975/1/WHO_NMH_MND_13.2_eng.pdf?
ua=1%2520%2520
http://www.acog.org/Womens-Health/Gestational-Diabetes
https://www.nice.org.uk/guidance/ng3/chapter/1-Recommendations#preconception-planning-and
-care-2

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1204764/

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