Diabetes in pregnancy

1. Dr ALIYU Labaran Dayyabu.
FWACS, MSc O & G Uss
O & G Department College of Medicine BUK:

2. //???????//
What makes diabetes in pregnancy different from
diabetes in the general population?
What maternal and fetal problems does diabetes pose?

3. Definition
Diabetes is a metabolic disease that results from lack
of insulin.
WHO expert committee defined diabetes in terms of
blood glucose levels.
RBS level of ≥ 11 mmol/l in a pt with polyuria,
polydipsia, wt loss and occasional glycosuria
 A Pt without the above Sxs and signs has a fasting
blood glucose value >8.0 mmol/l and a 2 hr glucose
level following a 75g OGTT is > 11mmol/l

4. Classification
1) Established diabetes
(Diabetes predates pregnancy)
2)Gestational diabetes
(Diabetes develops in pregnancy)
3)Impaired glucose tolerance
(Women with impaired glucose tolerance)

5. Incidence
Incidence is increasing with life style changes
More commonly seen were routine screening is
adopted
LUTH 15 undiagnosed diabetic women per 1000
antenatal population
1.5% found by Gilmar in a London Hospital
Generally incidence is 0.25 to 2.5%

6. Pathophysiology
Absolute or relative lack of insulin leads to;
Hyperglycaemia
Protein catabolism
Lipolysis → Ketogenesis
In pregnancy there is significant alteration in
carbohydrate and fat metabolism which increase the
risk of ketoacidosis in the diabetic

7. Cont:
These changes in CHO and fat metabolism is hormone
dependent
Oestrogen & progesterone facilitate insulin release→
peripheral utilization of glucose
Fasting hypoglycaemia is thus common in pregnancy
Glucose readily crosses the placenta but Insulin does
not

8. Cont:
In pregnancy ↑ production of HPL, cortisol and
prolactin is seen in pregnancy
These hormones counter the effects of insulin (Insulin
resistance)
Because of these some pregnant diabetics may require
↑ doses of insulin
In diabetics absence or insufficient insulin leads to less
glucose utilization by peripheral tissues

9. Cont:
The liver responds by ↑ glycogenolysis →
hyperglycaemia → ↑osmotic pressure in extracellular
fluid causing intracellular dehydration
The hyperosmotic pressure in the kidneys leads to
diuresis and extracellular dehydration
Persistent maternal hyperglycaemia → fetal
hyperglycaemia

10. Cont:
The response is pancreatic hypertrophy→ ↑ insulin
secretion. Since insulin can not cross the placenta it
accumulates in the fetus leading to fetal
hypoglycaemia
In late pregnancy this may explain sudden
unexplained fetal demise.

11. Effects of pregnancy on diabetes:
↑ insulin dose requirements
The need for tight glycaemic control
Increased severe hypoglycaemia
Risk of worsening pre-existing retinopathy
Risk of deteriorating established nephropathy

12. Effects of diabetes on pregnancy:
↑ risk of miscarriage
Risk of congenital malformation
Risk of macrosomia/Microsomia
↑ risk of pre-eclampsia
↑ risk of stillbirth
↑ risk of infection especially UTI
↑ risk of operative delivery

13. Factors associated with poor
pregnancy outcome in diabetes:
Low socioeconomic status
No folic acid intake pre-pregnancy
Suboptimal preconception care
Suboptimal glycaemic control at any stage
Suboptimal maternity care in pregnancy
Suboptimal fetal surveillance

14. Who are potential diabetics?
Those with;
Hx unexplained stillbirth
Hx of fetal macrosomia
Previous malformed infants
Polyhydramnios in current pregnancy
Diabetes in 1st degree relative
Glycosuria in current pregnancy
[Hx can identify about of diabetics and those with IGT]

15. Pre-conception care for diabetics:
The aim is to optimize pts to help them embark on
pregnancy in a relatively healthy state and achieve
good maternal and fetal outcomes
Information
Folic acid supplement prior to pregnancy and up to 12
weeks in pregnancy
Good glycaemic control
HbA1c level in early pregnancy correlates with early
fetal loss and congenital anomalies
Manage retinopathy/nephropathy

16. Maternal/Fetal complications of
DM:
Maternal;
Worsening retinopathy/Nephropathy
↑ risk of Ketoacidosis
Vulvo-vaginal candidiasis
Urinary tract infection
PIH/PET
Hydramnious

17. Cont:
Fetal complications;
Congenital malformations[40% PM]
Traumatic delivery from shoulder dystocia
Intrauterine fetal death
Miscarriage
At birth
Polycythemia → hyperbilirunaemia → Neonatal
jaundice
Hyperglycaemia/hypoglycaemia
RDS

18. Management:
Multidisplenary approach is adopted in managing
patients with DM in pregnancy.
These involves;
The obstetrician
The diabetic physician
Neonatologist
Others

19. Principles of management:
Thorough clinical evaluation
Admission for stabilization
Comprehensive fetal evaluation and surveillance
Strict glycaemic control
Surveillance and treatment of emerging conditions

20. Cont:
Obtain pt’s bio data
Age, Gravidity, Parity, No of children alive, LMP
Disease Hx [Duration since diagnosis, Rx,
complications, others]
Examination
General
Obstetrics
Specific by physician/Others

21. Investigations:
Urinalysis
FBC
Urea, electrolytes and creatinine
Others for;
Retinopathy
Nephropathy
e.t.c

22. Cont:
Ultrasound
To determine Viability, GA, Anomaly, fetal growth,
others
Fetal Doppler to screen for Pre-eclampsia
Admit for stabilization at;
Booking
At 28 weeks
At 36 weeks

23. Cont:
From 28 week fetal surveillance
Fetal kick charting by the woman
Fetal cardiotocograph
Biophysical profile
If on oral hypoglycaemic convert to insulin after
determining insulin requirements [6 point glucose]
depending on the trimester

24. Antenatal visits:
Individualize based on pt’s disease
Generally 2 weekly till 32 weeks then weekly till
delivery
At each visit take Hx
Evaluate her glycaemic control
Urinalysis each visit
Urine mcs at each visit
Do not allow pt to pass her date
Vaginal delivery should be the objective
C-section based on obstetric indications

25. Cont:
Admit pt when there sign of
 Infection or
 Poor glycaemic control

26. Labour Management:
When labour is confirmed inform
The peri-operative nurse on duty
The anaesthesiologist
The neonatologist
Labour should strictly monitored partographically
It should not be allowed to be prolonged

27. Cont:
On admission in labour take sample for;
FBC
Electrolytes and Urea
ABO and Rh if not known
Keep an open line with a wide bore Cannular
Actively manage labour
One on one
Partograph
Pain relief

28. Cont:
Glycaemic control is maintained by;
Administration of 5% glucose and insulin IV [where
available with an infusion pump] giving soluble insulin
1-2 units per hour
The blood glucose is measured every hour
The rate of glucose infusion is varied as required
Where infusion pump is not available ½ the dose of
the patient requirement is given and infusion of 5% set
up

29. Cont:
Thereafter a sliding scale with blood glucose
estimation is used in giving the necessary dose of
insulin
After delivery hand over the infant to the
Neonatologist for further evaluation and management

30. Postpartum:
Insulin requirement falls
Maternal hypoglycaemia may occur
Monitor blood glucose regularly to avoid this
Giving contraceptive counselling before discharge
Permanent contraceptive should be advocated after 2-3
children
For short term contraception use OCPs or IUDs

31. Prognosis:
Maternal and Fetal prognosis is improved when
preconception care is adopted
Prognosis is also better with good ANC and good
glycaemic control
Bad prognosis is associated with poor glycaemic
control and non compliance by patients

32. Conclusion:
Diabetes is a serious metabolic disorder and take its
toll in pregnant women without proper care through
out pregnancy
Better outcomes are observed in those who strict and
meticulous care in pregnancy

33. Thanks for your time.