DIABETES MELLITUS IN

PREGNANCY

BY DR. JOHN OJULE

DEPARTMENT OF OBSTETRICS &
GYNAECOLOGY
U.P.T.H. PORT HARCOURT
 SYNOPSIS
A. HISTORICAL PERSPECTIVE
B. DEFINITION OF TERMS
C. CLASSICATION
D. PATHOSIOLOGY
E. RISK FACTORS
F. EFFECTS OF PREGNANCY ON
DIABETES
G. COMPLICATIONS
H. CONCLUSION
 HISTORICAL PERSPECTIVE
Early 20th century & beyond – pregnancy rare
in diabetics.
40% of gravid diabetics died in pregnancy, the
rest died with in 2years.
Fetal wastage - then in excess of 50% .
1921- insulin discovered→ scenario changed;
 fertility-restored
 Dramatic reduction in MM-2.3%
 Perinatal mortality- unchanged
5.1930 - Elective timing of delivery→
↓ in perinatal mortality.
6. 1949 - Individualized timing of delivery-
further reduction in PNM
7. 1950s &1960s - improved surveillance→
PNM- reduced to 20%
8. 1960 to date—further refinements in mgt. of
diabetic mothers, the fetus and neonates
*PNM→ that of normal pregnancy—2-4%
 DEFINITION
DIABETES MELLITUS- metabolic disorder of
multiple aetiology characterised by chronic
hyperglycaemia with disturbance of CH2O,
protein & fat metabolism, resulting from defects
in insulin secretion, action or both.
INSULIN - polypeptide hormone secreted by the
beta cells of the pancreas with profound
metabolic actions on carbohydrate, protein &
lipid metabolic
 DEFINITION
INSULIN RESISTANCE- Defined arbitrarily as
the requirements of 200 or more units of
insulin/day for control of hyperglycaemia &
prevention of ketosis.
3. Types of Resistance;
* Pre-receptor resistance
* Receptor resistance
* Post-receptor resistance
GESTATIONAL DIABETES- carbohydrate
intolerance of variable severity with onset or first
recorgnition during the index pregnancy.
 EPIDEMIOLOGY OF DM
IN PREGNANCY
Most common medical complication
Occurs in all races, but relatively more in
Blacks, Hispanics & Asians
DM complicates about 0.75-5% of
pregnancies
80-90% of these- GDM
True prevalence GDM in Nigeria-
unknown
UPTH- GDM prevalence-2.98/1000 preg.
 CLASSIFICATION OF DIABETES
IN PREGNANCY
A. PRE-GESTATIONAL DIABETES
known diabetics before the pregnancy:
1. Type 1.-Insulin dependent diabetes mellitus- IDDM
2. Type 2.-Non insulin dependent diabetes mellitus-NIDDM
B. GESTATIONAL DIABETES- As defined earlier.
* glucose level normalises after pregnancy
*Insulin may or may not be required for R.
*40-60% GDM dev. Type 2 in 10-20 years
* Global prevalence of 0.15-3%
 MODIFIED WHITE’S
CLASSIFICATION OF DIABETES IN
PREGNANCY
Class A- Chemical diabetes diagnosed before
pregnancy- managed by diet alone
Class B- Insulin Rx necessary before
pregnancy & onset after 20years 0f age
Class C- Age of onset 10-19years or duration
of DM 10-19 years
Class D- onset b/4 10, duration of 20yrs,
chronic hypertension or background
retinopathy
 MODIFIED WHITE’S
CLASSIFICATION continued.

5. CLASS F- Renal disease

6. CLASS H- Coronary artery disease
7. CLASS R- Proliferative retinopathy
8. CLASS T- Renal transplant
 PATHOSIOLOGY
With each feeding & rise in blood glucose, mother
undergoes series of hormonal actions- insulin, glucagon
& cathecolamines
These adjustments ensure enough, but not excessive
supply of glucose to both mother & fetus
Key features of this complex interaction include:
*pregnant women tend to develop Hypoglcaemia btw
meals & during sleep- as the fetus continous to draw
glucose from the maternal blood, even during fasting.
* The levels of placental hormones - estrogens,
progestrones, HPL,GH, rises linearly throughout
pregnancy.
 PATHOPHYSIOLOGY
* Because these hormones confer
increasing tissue insulin resistance, the
demand for increased insulin requirement
escalates progressively during pregnancy.
* If the maternal pancreatic insulin
response is inadequate, maternal, and
therefore fetal hyperglycaemia results
manifesting as recurrent postprandial
hyperglycaemic episodes.
 PATHOPHYSIOLOGY
Surging maternal & fetal glucose levels
are accompanied by episodic
hyperinsulinaemia → nutrient storage
resulting in macrosomia, with decreasing
fetal oxygen →hypoxia
Hypoxia is accompanied by surges in
catecholamines →increased
erythroppetin, RBC hyperplasia,
polycythaemia, vascular sludging &
hyperbilirubinaemia.
 RISK FACTORS
Maternal age 35 years & above.
Strong family Hx. of NIDDM OR GDM
Maternal obesity- wt greater than 90kg
Previous Hx. of GDM
Previous unexplained stillbirth
Previous macrosomic baby
 EFFECTS OF PREGNANCY ON
DIABETES
• Difficult control due to increasing insulin
resistance= hcG, HPL, cortIsol, prolactin
• Increased exogenous Insulin requirement
• Increased risk of acute metabolic
complications
*DKA
*Hyperosmolar non ketotic coma
*Hypoglycaemia
 EFFECTS OF PREGNANCY ON
DIABETES MELLITUS

4. Worsening chronic complications

* Gastroparesis
* Retinopathy
* Nephropathy
* Neuropathy
* Vascular angiopathy
MATERNAL COMPLICATIONS
Acute metabolic complications
Increased risk of infections-UTI/CANDIDA
Pregnancy wastage
Pre-Eclampsia
Polyhydramnious
Pre-term labour
Difficult delivery/shoulder dystocia
 Maternal complications

Increased risk of operative delivery-c/s

Increased risk of postpartum hypoglycaemia
Increased maternal morbidity & mortality
Increased risk of NIDDM later in life
 Fetal complications

Increased risk of congenital malformations

Fetal macrosomia
Intra uterine growth restriction
Intrauterine fetal death
 Neonatal complications
Increased risk of birth injuries
Birth asphyxia-aspiration syndrome, wet lung
syndrome & Hyaline membrane disease
Hypoglycaemia - glucose 40mg/dl or below
Hypocalcemia-7mg/dl or below
Polycythemia - PCV 65% or more
Hyperbilirubinaemia - 200mmol/l or more
Increased risk of NN intensive care
 Complications later in life

Impaired intellect
Risk of development of DM in 10%
 Congenital malformations
CVS- Transposition of the great vessels, endocardiac
cushion defects, PDA, coarctation of aorta, cardiomegaly
CNS-Caudal regression syndrome-sacral agenesis, neural
tube defects, anaencephaly, microcephaly
SKELETAL- Polydactyly
RENAL- Hydronephrosis, Renal agenesis, double ureter
GASTROINTESTINAL- Duodenal atresia, Anorectal atresia,
small left colon syndrome
OTHERS- Single umbilical artery.