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Introduction
Pregnancy is a period of metabolic stress with a challenge to Betal cells of pancreas, Pregnancy may unmask the impaired glucose tolerance state or cause deterioration of pre-existing diabetic state. Diabetic pregnancies account for 1 to 2% of all the pregnancies. Diabetic pregnancy carries both maternal and neonatal morbidity & mortality.
Carbohydrate metabolism in Pregnancy
In diabetic pregnant women there is increased Insulin secretion and there is a state of Insulin resistance. This is probably mediated through increased cortisol, abnormal binding of Insulin, human placental lactogen, increased oestrogen and progesterone levels.
Detection of D.M. in Pregnancy
Whom to screen for Diabetes mellitus?
a) Strong family history of Diabetes mellitus
b) H/O Delivery of large babies over 4000gms.
c) Recurrent abortion.
d) Mother delivering Infant with multiple congenital anomalies,
e) Unexplained stillbirth.
f ) Recurrent candidal vaginitis or UTI.
g) Obesity over 20%.
h) Poly hydramnios.
i ) Uterus larger than date.
j ) Excessive weight gain
k) Hypertension with pregnancy
1) Unexplained other vascular disturbances.
Effect of pregnancy on diabetes mellitus
| |
Changes noted |
Possible cause |
| Ist Trimester |
Improve carbohydrate metabolism, hypoglyce-mic-reactions, increase sensitivity to insulin. |
1. Poor intake due to hyperemesis gravid orum. 2. Glucose from maternal circulation crosses Placenta & reaches foetus Exogenous Insulin need decreases |
| 2nd Trimester |
Insulin need increase Ketosis prone |
Anti insulin hormones are acting like HPL, cortisol and degeneration of insulin by placenta occurs. |
3rd Trimester
|
Greater intensification of Diabetic state. |
Same as above. |
| Labour |
Hypoglycemia increased sensitivity to insulin |
Due to increased physical activity, insxilin sensitivity increases. |
| Post parhini |
Remission in D.M. or amelioration. Insulin need fall. |
Once the placenta is out, anti-insulin effect has gone. |
Foetal fuel requirement :
Foetal blood sugar is 20-30 mgm less than the mother. The glucose need of foetus is 6 mgm/kg body weight per minute at term. Foetal insulin is present by 12th week of gestation. Maternal hyperglycemia leads to premature maturation of pancreas, Beta cell hyperplasia and foetal hypoglycemia. Across placenta glucose diffuses by facilitated diffusion while maternal insulin does not cross placenta. Changes observed in newborn infants born to diabetic mothers:
A) Foetal hyperinsulinism leads to obesity, increased deposition of fat and glycogen
occurs. Hence, increase in birth weight noted.
B) At birth there is increased risk of hypoglycemia due to relative hyper insulin.
C) Premature kidney function seen leading to increase of water and electrolyte excretion.
D) Neonatal tetany with hypoglacemia.
E) Hyper viscosity and polycythemia.
F) Neonatal hyperbilirubinemia.
G) Respiratory distress syndrome.
H) Congenital malformation.
Investigations
a) Urine Exam for sugar:
Test Low renal
threshold Due to diabetes Lactosurta
Positive mellirus 3rd trimester
Positive
Positive
by non-
specific test
Positive Positive Positive Positive
b) Blood Sugar:
i) Fasting/2hr post prandial Blood Sugar
ii) Oral glucose tolerance test : 75 gm to be given or
1.75gm/kg. Response-Normal, impaired, Overt D.M.
c) Glycosylated Haemoglobin.
Diagnostic Criteria of Diabetes in Pregnancy
O'Sullivan & Mahan Criteria:
Fasting Ihr 2hrs 3hrs
>90 >165 >145 >125 mgm
Classification of Diabetes in Pregnancy:
Modified White's classification:
Class A : Asymptomatic, Abnormal OGTT, managed
by diet alone.
B : With symptoms, Insulin treated 0-9 yrs
duration. No angiopathy.
C : Insulin treated, 10-14 yrs duration of D.M.,
No angiopathy
D : Insulin treated, over 19yrs, Diabetic Retinopathy
E : IDDM, pelvic vascular disease on X-ray.
F : Diabetic Nephropathy
G : IDDM with multiple obstetric failure +F
H : IDDM, CAD with nephropathy
R : IDDM with malignant proliferative retinopathy.
T : Pregnancy after renal transplantation in IDDM.
Class B to R- perinatal mortality is high.
Gestational Diabetes mellitus: appears during pregnancy and reverses to normal with
termination of gestation.
Factors interfering with control of diabetes mellitus in pregnancy
1) Nausea & Vomiting - During 1st trimester.
2) Alteration in carbohydrate tolerance.
3) Lowered Renal threshold for glucose.
4) Increased energy requirement during labour.
5) Worsening of diabetic retinopathy in pregnancy.
6) UTI/skin infection increase in pregnancy with D.M.
7) Hypertension may get aggravated.
 Pre-existing neuropathy, nephropathy, micro vascular lesions & retinopathy intensified
during pregnancy.
Effects of diabetes upon the course of pregnancy
1) Toxemia
2) Still birth
3) Abortions
4) Intrauterine growth retardation
5) Premature labour
6) Poly hydramnios
7) Ketoacidosis with pyelonephritis
Endomyometritis. Puerperal infection occur.
9) Placental abnormalities: Calcification, glycogen deposition and fibrosis. With severe
long standing diabetes. Placenta is immature. Vascular thrombosis, thickening, & infarct
may be seen.
Perinatal monitoring for foeto-placental insufficiency
1) Foetal activity score.
2) Urinary Oestriol weekly or biweekly determination. Less than 12mg in 24 hrs specimen
mean foetal distress.
3) Decrease in Oestriol values of 35% or more than from the mean previous 2 values.
Signals foetal distress.
4) Increase Oestriol/creatinine ratio in 24hrs urine will rarely be associated with foetal
death.
5) Lecithin'/Sphingornyelin ration (L/S ratio) less than 2 indicates respiratory distress
syndrome.
6) Ultrasonography to assess gestational age.
Management
A) Dietary prescription for the pregnant diabetic women :
Total calories - 30.35 cal. per kg body weight
Distribution - Protein 100-125 gm Carbohydrate
& Fat 50% of calories each
- Division Breakfast 25%
- Lunch 30%
- Dinner 32% .
- Bedtime 12%
Note: Protein to be restricted if there is Nephropathy.
B) Insulin therapy :
a) Strict control.reduces foetal mortality.
b) Maintain blood glucose less than 100m.gm.per dl.
c) Use purified insulin.
d) Use regular insulin, multiple injections or combination of intermediate insulin with
short acting insulin.
C) Timing of delivery :
Preterm delivery leads to still birth. Delivery after 38 weeks foetal loss greater due to excessive foetal size. White's timing of delivery at Joslin Clinic.
Class A around 38 weeks A - Drawback of this method is high
B & C 37 weeks rate of neonatal loss due to
prematurity
D 36 weeks and respiratory distress syndrome.
F&R 35 weeks B -High caesarean section.
Current concept of timing of delivery in Diabetic pregnancy is by determining foetal placental function and identify foetal distress and in such cases do early delivery.
Self monitoring of blood sugar
This is done by glucometer and the patient can herself check her blood sugar several times a day. This helps in adjusting diet and insulin time to time and it achieves good control of blood glucose which results in successful delivery of a normal healthy child. A sudden drop in insulin requirement without any accountable cause should arouse concern and probably means impending foetal demise. Intensive antipartum surveillance is needed in all classes of diabetic pregnancy except Class-A.
Management of delivery
High rate caesarean delivery noted. Vaginal delivery may be difficult due to macrosomic infant or there may be inability to induce progressive labour. Respiratory distress syndrome is more with a abdominal delivery. Insulin requirements usually fall after delivery 1/3 rd to 1/2 dose of pre-pregnancy doses to be given after delivery. Start I/V 5% Glucose at 125 cc per hour to avoid maternal hypoglycemia.
Should the diabetic woman attempt pregnancy?
Pregnancy in diabetic woman carries risk both to her and the newborn. Hence she has to make a conscious decision. She should be committed to rigorous self care and it is better to get pregnant early and limit the family.
Summary
Physiological adaptation of normal pregnancy creates a demand for extra insulin. In women with inadequate islet cell reserve abnormal glucose tolerance occurs. If this gestational diabetes mellitus is not recognised perinatal death occurs. In great majority immediately after delivery this abnormal glucose tolerance returns to normal.
Pregnancy in overt diabetics if well controlled is not a hazard. Perinatal mortality has been reduced with strict control of blood sugar and vigilant foetal monitoring. Strict control of Diabetes mellitus is key to successful outcome.
REFERENCES
1) John Bonner. Diabetes Mellitus in pregnancy- Recent Advances in Obstetrics &
Gynaecology 14th Edition, 1983 page 95411.
2) Malcolm Nattess and Julio V. Santiago, Diabetes in pregnancy Recent advances in
Diabetes Meliitus 1) Churchill Livingstone 1984 page 239.
3) M.R.Krishna menon, K. Bhaskar Rao: Diabetes in pregnancy, 3rd Ed. year 1986
page 70-80.
4) James Green and Richard Sweet: Diabetes in pregnancy Clinical diabetes- Modern
management by Podolsky Appleto-Century- crofts, New York, 1984, 581-598.
5) Alexander Marble, Priscilla White, Robert, F. Bradlay, Led P.Krall-Joslin's Diabetes
Mellitus, llth Edition Lea and Fibiger'-Philadelphia 1971, page 581- 597.
6) A Elmore Seeds - Diabetes in pregnancy Clinical Obsterics and Gynaecology,
Harper & Row March, 1981 Vol. 24 No.l.
7) Steven, G. Gabbe- Diabetes in pregnancy, Clinical Ostetrics and Gynaecology,
Harper & Row, Sept 1985, Vol.28, No.3.
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Pre-existing neuropathy, nephropathy, micro vascular lesions & retinopathy intensified