Transcript DIABETES IN PREGNANCY

DIABETES IN PREGNANCY
BY
DR. SHUMAILA ZIA
DIABETES IN PREGNANCY
INCIDENCE -- 3—4/1000 pregnancy.
CARBOHYDRATE METABOLISM
DURING PREGNANCY:
• Increased tissue resistance to insulin.
• Normally glucose level stays constant b/w 4-4.5
mmol/l except after meals.
• With increasing insulin resistance, homeostasis
can only be maintained by doubling insulin
secretion from the end of 1st to 3rd trimester b/c
insulin resistance increases with gestation.
• Exact etiology unknown, most probably b/c of
increased production of preg. associated
hormones or free cortisol, like HPL (Human
placental lactogen) most important.
INFLUENCE OF PREGNANCY ON CHO MET.
1. Increased insulin resistance –increased production
of insulin by pancreas (hyperplasia/ hypertrophy)
• Adequate insulin production may become
inadequate to meet increased demand during
pregnancy –gestational DM
• Abnormally high tissue insulin resistance.
2. Known diabetic controlled on diet may need insulin
3. Medicine dependent need enhanced medication.
CHO. DERANGEMENTS IN PREGNANCY
1. Established DM:
- Type- 1----IDDM (more common in peg.)
- Type- 2----NIDDM
2. Gestational DM:
- Appear in preg. mostly disappear after preg.
3. Impaired Glucose tolerance:
- CHO metabolism altered
- Some develop frank DM in later half
- So, should be managed as DM
White’s classification
Class A1
Abnormal glucose tolerance test with normal
fasting capillary (95 mg/dl) and postprandial
(120 mg/dl) glucose levels Controlled with
diet alone
Class A2
Abnormal glucose tolerance test with abnormal
fasting or postprandial glucose levels Treated
with diet and insulin
Class B
Insulin-treated diabetic
Onset over age 20 years
Duration less than 10 years
No vascular disease or retinopathy
Class C
Insulin-treated diabetic
Onset between ages 10 and 20 years
Duration between 10 and 20 years
Background retinopathy
Class D
Insulin-treated
diabetic
Onset under age
10
Duration more
than 20 years
Background
retinopathy
Class F
Diabetic
nephropathy
Class H
Cardiac disease
Class R
Proliferative
retinopathy
EFFECTS OF DM ON PREGNANCY
• Fetal glucose level follows maternal one closely
until facilitated diffusion saturated or maternal
glucose reaches 11-13mmol/l then fetus dose not
follow—Fetal protective mechanism
• Insulin appear in fetal circulation at 10-12 wk.
• In maternal DM, fetus has hyperinsulinemia- acting
as growth promoting hormone-- fetal macrosomia
• F. hyperinsulinemia rather than F. hyperglycemia is
responsible for adverse effects.
ADVERSE FETAL EFFECT OF DM.
1. Congenital Malformation:
4—10 times higher than normal.
Exact mechanism of teratogenicity not known.
Said to be directly related to conc. Of glucose at
time of organogenesis.
So, in known diabetics ---more chance of
Cong. abnormality.
ADVERSE FETAL EFFECT OF DM. Cont-• Structural abnormalities:
CVS, Skeletal, CNS, GIT.
• Fetal caudal regression syndrome:
Abnormality of vertebrae below T10.
• Sacral agenesis: missing sacrum.
• Dislocation of hips.
• Talipes.
• Spina bifida.
• Renal anomalies.
• Urinary or fecal incontinence.
Cong. An. of infants of diabetic mother
• Skeletal and central
nervous system
Caudal regression syndrome
Neural tube defects
Microcephaly
•Renal
Hydronephrosis
Renal agenesis
Urethral duplication
• Cardiac
Transposition of the great
vessels
Ventricular septal defects
Coarctation of the aorta
defects or patent ductus
arteriosus
Atrial septal defects
Cardiomegaly
•Gastrointestinal
Duodenal atresia
Anorectal atresia
Small left colon
syndrome
•Other
Single umbilical artery
ADVERSE FETAL EFFECT OF DM. Cont-2.Spontaneous miscarriage:
Due to cong. Anomalies.
3.Fetal macrosomia:
- Due to f. hyperinsulinaemia. body wt 4kg.
- f. macrosomia----large for dates.
- Prolonged obstructed labour.
- Shoulder dystosia.
4.IUGR:
- placental function compromised.
- poor prognosis.
ADVERSE FETAL EFFECT OF DM. Cont-5. Polyhydramnios:
- fetal. polyuria—osmotic diuresis.
- premature labour.
- malpresentation.
6.Pre-eclempsia:
- perinatal mortality double.
7.RDS:
- diabetes delays production of surfactant.
8. Unexplained intrauterine death.
9. Perinatal mortality:
- 5times higher.
Infant of diabetic mother.
MANAGEMENT.
I. INITIAL MANAGEMENT:
A:known diabetic:
- Pre-pregnancy care
- Early booking --- optimal control
--- USG
B:Gestational diabetes:
- Many women go unrecognized
&diagnosed after poor obs. Outcome.
EFFECTS OF PREGNANCY ON DM
CONTROL
More difficult
RETINOPATHY Proliferative retinopathy may
progress so careful ophthalmic assessment.
NEPHROPATHY
• No permanent deterioration in renal function.
• Fetal outcome good if preclampsia does not
supervene & glucose control good.
• End stage renal disease – termination of
pregnancy.
INITIAL MANAGEMENT Cont-SCREENING:
a. Clinical Features:
cheap way of screening.
women at high risk of gest. D.M.
*diabetes in 1st degree relatives.
*maternal obesity. Wt.90kg.
*persistent glycosuria.
* previous hx. of large baby.
*previous hx. of unexplained still birth.
*previous birth of cong. malformed baby.
*polyhydramnios /macrosomia in current
preg.
INITIAL MANAGEMENT Cont-b. Random glucose test.
cut of value 6.4 mmol/l with in 2 hr&
5.8mmol/l after 2 hrs of meal-----OGTT.
c. Fasting glucose test.
cut of value 4.8mmol/l-----OGTT.
d. Glucose challenge test:
At 28wks.
50g glucose given.
1hr later blood taken--if >7.8mmol/l-OGTT.
DIAGNOSTIC TEST.
• Oral glucose tolerance test.
Gold standard investigation.
If screening test is +v
O’SULLIVAN METHOD.
- after an overnight fast >8hrs.
- a fasting blood sample taken.
- Give 100g glucose in 250ml water.
- Take blood sample ½ hrly for next 3 hrs.
• Abnormal results:
if values exceeds this:
fasting= 5.0mmol/l
1hr = 9.2mmol/l
2hr = 8.1mmol/l
3hr = 6.9mmol/l
WHO OGTT
75 grams glucose in 250ml water after
fasting sample
Blood Sample
Glucose Level
Remarks
Fasting
< 6 mmol/l
D M excluded
6- <7.8 mmol/l
Impaired glucose tolerance
> 7.8 mmol/l
Frank D M
<7.8 mmol/l
D M excluded
> 7.8-< 11 mmol/l
Impaired glucose tolerance
>11 mmol/l
Frank D M
2 Hours PP
II. Further Management.
• Medical management.
• Obstetrical management.
MEDICAL MANAGEMENT:
combined care –obstetrician + endocrinologist.
a) TREATMENT MODLITIES:
- diet.
- diet + insulin.
1. Diet:
Three meals and three snacks
30-35 Kcal/Kg ideal body weight
No more than 10-12 Kg weight gain
50% of energy carbohydrates (unrefined), 30%
fat and 20% proteins
Review diet history to identify major areas of
reduction of caloric intake
Insulin: see later
Alert the patients and relatives about the
possibility of hypoglycemia and measures to
counteract
2.INSULIN THERAPY.
• Tm of choice - does not cross placenta.
- Short acting.
- Long acting.
• Insulin regimen:
• four times daily regimen;
- short acting insulin---3 times after meal.
- long acting---------------at night.
2.INSULIN THERAPY Cont-BIPHASIC REGIMEN:
• Fixed combination of medium & short acting
insulin 70:30 is given in 2DD dosage.
• One before breakfast and other before dinner
• 2/3rd of daily dose before breakfast.2/3p.insulin+1/3-NPH.
• 1/3rd in evening.1/2+ 1/2. p.insulin+NPH.
DOSAGE SCHEDULE
A. In insulin dependent, adjust dose especially
in later half of pregnancy
B. If started during preg. Initially start 6 hourly
short acting 6 units/dose but at night long
acting 10 units
For biphasic regimen start 20units/day
C. In NIDDM control on diet, start insulin if
Pre-prandial glucose persistantly > 6mmol/l
OTHER FORMULAS TO CONTROL
DIABETES.
1.wt× 0.7------6_15 wks. Wt× 0.8 ---15_25wks
wt×0.9 ---25_35wks. Wt×1 u----36-40 wks.
2.wt/2. total dose.
3. Sliding scale.
4. BSL -5/20= single dose.
5. Mean of all readings of bld sugar profile/5.
MONITORING
• Objective is to maintain
- Fasting glucose------< 5.5 mmol/l
- P P ---------------------<7.5 mmol/l
a. Blood glucose level:
- In U K ---- test 4 times (3 pre-meal & 1 at bed time)
- In U S A – after meal measurements also taken
b/c it correlate better with fetal wt.
- Pre-breakfast high measurement may be due to
rebound phenomenon after nocturnal hypoglycemia
b. HbA1C (glycosilated Hb.):
Glucose irreversibly bound to Hb.
- Indicates previous 2 months glucose control
- Repeat monthly basis
- For good control should be <8%.
OBSTETRICAL MANAGEMENT
1. ANTENETAL CARE:
A. -1ST trimester : - good glucose control &
- USG
- 2nd trimester: - USG at 18-20 wk.(cong. An.)
- USG at 20-22wk.(cardiac An.)
- 3rd trimester: - Care for
. Polyhydramnios
. PIH
. F. macrosomia
. IUD
. Pre-term labour
2. DELIVERY:
a) Time of Delivery:
- Well controlled DM --- 39-40 weeks
- Uncontrolled DM ----- 38 weeks
b) Mode of Delivery:
- Vaginal delivery is mode of choice
- Low threshold for C- section
c) Management During Labour:
*Insulin therapy: Give I/V insulin 1 unit/h if,
. Labour established
. Induction of labour
. Elective C-section
Dilute insulin 20 U (0.2ml) in 19.8 ml N/S . Infuse 1
ml (1 U)/ hour. Measure glucose 1 hourly
Aim: Maintain glucose between 4.5-5.5 mmol/l
Give also 10% D/W in other I/ V line @ 1L/8 hourly
* OBSTETRIC Mx:- Induction of labour – as usual
- good pain relief
- avoid milking of U cord
- Early clamping of U cord
- call neonatologist
2. VISIT FREQUENCY:
-Fortnightly from 24-32 wk. followed by weekly
3. FETAL SURVEILLANCE:
a) USG: - AC– good indicator of fetal wt. so,
- AC+ AFI from 24 weeks , fortnightly
b) CTG: - 2-3 times/week from 36 weeks onward
c) Doppler:
d) Biophysical Profile:
POST PARTUM CARE
CARE OF THE MOTHER
Fall in insulin requirement in the puerperium.
CARE OF THE BABY
1. RESPIRATORY SYSTEM
1.
2.
Resp distress syndrome
Transient tachypnoea of the newborn
2. HYPOGLYCAEMIA
1.
2.
3.
Blood glucose checked at 2,4,6& 12 hours of age.
If <1.4mmol/l at 4 hours, I/v 10% dextrose.
Start feeding by 2 hours & continue at 3-4 hours interval.
3. HYPERBILI RUBINAEMIA
1.
2.
3.
4.
Vit K 1mg Inj.
Phenobarbitone 2.5-5mg /kg daily
Phototherapy
Exchange transfusion
NEWBORN MAANAGEMENT
• SERIALLY ASSESS CAPILLARY GLUCOSE OF THE
NEONATE ESPECIALLY IN THE FIRST 12 HOURS.
REPLACE GLUCOSE IF THE GLUCOSE LEVEL IS
LESS THAN 45 MG/DL
• IF THE HEMATOCRIT VALUE EXCEEDS 70,
EXCHANGE TRANSFUSION
• SERIALLY MONITOR BILIRUBIN LEVEL.
CONTRACEPTION
• Estrogen containing allowed with need for
tight control unless vascular disease
• Progestin only allowed
• IUCD allowed increased method failure
• Barrier methods allowed
• Sterilization should be considered especially
women with contraindications to pregnancy
(proliferative retinopathy, cardiopathy,
nephropathy, gastropathy and other vascular
lesions)
DON’T FORGET
• OGTT at 6 weeks to confirm disappearance of
impaired glucose tolerance
SUMMARY
• DM is a common and serious problem for the
mother and fetus
• Prompt management of preexisting DM
should start BEFORE pregnancy
• Insulin dosage schemes differ but the
therapeutic aim is the same
• GDM should be sought in all pregnant women
with few exceptions
THANK YOU