DM pdf - D. Aseel - Muhadharaty

Definitions :

 Diabetes mellitus : Is a metabolic disorder in CHO metabolism with

impact on fat and protein metabolism due to insulin deficiency or

insufficiency in its action .

 Gestational diabetes : It is diabetes discovered for the 1

time during

pregnancy despite severity or persistence after pregnancy .

Incidence :

 Before insulin therapy , DM with pregnancy was very rare because

diabetes at usually infertile and amenorrheic Now , the incidence of

pregestational DM is 0.1 – 0.5 % .

Classifications :

1. Pregestational :

a. Type = 1 Insulin dependent DM ( IDDM ) which was named juvenile DM .

b. Type II = Non-insulin dependent DM ( NIDDM ) which was named maturity

or DM .

c. Type III = 2

DM .

2- Gestational DM :

Etiology :

1. IDDM : It occurs due to " immunological destruction " of the B-cells

Langerhans the pancreas in genetically predisposed individuals triggered

by autoimmu disorder , viral infections and drugs .

2. NIDDM : Occurs mainly due to decreased insulin sensitivity . In general ,

it is ( common with pregnancy as it usually occurs ( over 40 years of

age ) .

B- Gestational diabetes :

* Class A1 : Fasting plasma glucose < 105 mg / dl and 2hr PP < 120 mg/dl .

* Class A2 : Fasting plasma glucose > 105 mg/dl and / or 2hr PP > 120 mg/dl.

Effects of Pregnancy on Diabetes :

1. Pregnancy is diabetogenic due to the action of pregnancy hormones and

placental insulinase enzyme .

2. Increased insulin requirements for cases with pregestationl DM .

3. Higher incidence of diabetic complications as ketoacidosis ,

hyperglycemic coma starvation ketosis and hypoglycemic coma ( diabetic

state is unstable and difficult to control .

4. Progression of diabetic nephropathy and retinopathy .

Effects of Diabetes on Pregnancy :

A Material effects :

I- During pregnancy :

1. Hypertensive disorders ( 4 times ) :

* The exact mechanism is not clear but may be due to :

a. diabetic vasculopathy .

b. Inability of the vascular endothelium to produce sufficient amounts

prostacyclin .

c. Increased levels of renin and angiotensis II . .

2. Hydramnios ( 10 – 20 % ) :

* It may be due to :

a. Fetal polyuria due to fetal glycosuria as a result of maternal and fetal

hyperglycemia .

b. Congenital anomaly which cause inability of the fetus to swallow .

c. Increased osmotic pressure of the liquor due to maternal and fetal

hyperglycemia .

d. Other causes as maternal vascular disease and irritation of amniocytes to

secrete more liquor due to excessive fetal urine .

3. Generalized maternal edema mainly in cases complicated with

vasculopathy .

4. Infections : Such as UTI , vulvovaginitis specially monilia , wound

infection after episiotomy or CS and LAI .

5. Habitual abortions : Due to IHD , HF , severe retinopthay or nepropathy .

6. Hypoglycemia ( blood glucose < 50 mg/ dl ) , hyperglycemia or ketosis

causing coma .

7. Peripheral , visceral or autonomic neuropathy .

II- During labor :

1. Preterm labor :

a. Polyhydramnios .

b. Congenital anomalies .

c. Fetal macrosomia .

d. Induced preterm labor due to diabetic complications as preeclampsia ,

accidental hemorrhage , diabetic IHD , diabetic nephropathy or progressive

retinopathy .

2. Intertia : Due to :

a. Abnormal uterine action .

b. Macrosomia and malpresentations .

c. Overdistention of the uterus by hydramnios .

3. Dystocia and obstructed labor : Due to :

a. Macrosomia .

b. Malpresentation .

c. Congenital anomalies .

4. Increased incidence of instrumental deliveries and CS .

5. Increased incidence of ketoacidosis during labor .

6. Increased incidence of post partum hemorrhage .

III- During puerperium :

1. Hypoglycemia due to rapid drop in insulin requirements after placental

separation and disappearance of placental anti insulin factors .

2. Post partum hemorrhage .

3. Failure of lactation .

4. Increased postpartum infections .

B. Fetal affects :

1. Congenital anomalies ( 7% ) : In uncontrolled cases . The mosr common is

VSD , NTD but the most specific anomaly is sacral agenesis .

a. Hyperglycemia b. Ketosis . c. Growth factor inhibitors .

2. Macrosomia :

* The fetus of uncontrolled diabetic mother is at higher risk for macrosomia

4000 g or 4500 g at birth .

* Macrosomia has its own dangers which are :

a. Malpresentation and malposition .

b. PROM , prolonged labor or obstructed labor .

c. Shoulder dystocia and increased risk of birth trauma .

d. Higher risk for development of obesity later in life .

3. IUGR : If maternal diabetes is accompanied with vascular disorder .

4. IUFD near term ( 1-4% ) are unexplained

a. Increased incidence of fetal hypoxia due .

b. Maternal or fetal hormonal imbalance .

c. Congenital anomalies .

d. Maternal hypoglycemia when severe .

Screening During Pregnancy :

 Screening of DM is essential since 1

visit because the early the condition

is diagnosed and treated , the less the complications . If the tests are (+)

ve , the diagnostic OFTT is indicated , while if all tests are (-) ve , repeat

the screening at 24-28 Ws .

 Screening Tests :
1. 50 gram GTT : This is the most investigated and accepted screening test .

Plasma glucose level is measured 1 hour after ingestion of 50 gram

glucose . A value > 140 mg/dl is considered abnormal .

2. Random whole venous blood glucose level .

3. 400 Kcal & 600 kcal mixed meal loading tests .

4. Urinary Glycosuria and ketonuria : not reliable due to :

a. Alimentary glucosuria is normal finding in early pregnancy .

b. Renal glucosuria is normal during mid pregnancy .

c. Glucosuria is usually intermittent , so multiple testing is required .

d. Morning urinary sample is the commonest sample to be tested while it is

the least sample to have glycosuria . However , heavy glycosuria and

ketonuria should not be overlooked .

Diagnosis :

1. 100 gram 3-hour OGTT :

* This test should be done for every case screened (+) ve for glucose

intolerance . However , it is not indicated when FBS > 120mg/dl and is C/I

when > 200mg/dl .

* Steps :

a. The woman should not restrict her CHO diet for at least 3 days before the

test . Thiazide diuretics should be stopped 2 Ws before the test ( thiazides

decrease B-cell response to glucose ) .

b. After 8 hours fasting , a venous sample is taken to determine fasting glucose

level then 100 gram glucose are taken orally . Venous blood samples are

taken 1 , 2 & 3 hours after glucose load .

2. 75 gram OGTT .

3. 50 grams OGTT .

4. Fasting blood glucose level : If > 120mg % or > 105 mg% on 2 occasions ,

GM is diagnosed and no need for OGTT .

Treatment during pregnancy :

I- Preconceptional counseling : Any diabetic cases needing pregnancy should

undergco preconceptional counseling .

1. Full history and examination .

2. Determination of blood glucose level .

3. Discussion of the special care for the diabetic pregnant women ,

II- Management during pregnancy :

Management of diabetic pregnancy as well as other medical problems

associating pregnancy should be carried out by a team work of an obstetrician

and an internist , labor , an anesthetist and a neonatologist should attend the

delivery for dealing with the baby .

1. Frequency of antenatal visits : Depends mainly on the type diabetes , class of

diabetes and past obstetric history . For cases with GDM , many authors

believe not increases the visits over normal , while in cases with uncontrolled

pregestational DM , visits may be double the normal cases .

2. Antenatal visit :

a. Full history and examination for diagnosis of pregnancy , condition ,

complications of diabetes , C/I of pregnancy , and other associations with

diabetes .

b. Weight of the woman .

c. Hb % , Rh typing , complete urine examination specially for sugar , acetone

and bacteriuria ,. FBS and 2hr PP glucose level .

d. Determination of the HbA

level to evaluate the effectiveness of diabetic

control during the previous 4-8 Ws . This is very important in estimating the

metabolic environment around the early developing embryo which has a

significant relation to the development of congenital anomalies . Normally ,

the level of HbA

is 4-6% . Values above 10% indicates bad diabetic

control with high risk for congenital anomalies . HbA

increases also in

cases of non hemolytic anemias and in CRF , so in false .

3. Control of diabetes :

A. Diet :

* Proper dieting is an essential step in treating GDM and is usually the only

treatment for class A1 .

* Caloric intake should be individualized according to maternal original weight

However , pregnancy is not the time for weight reduction and the woman

should gain 10-12 kg during pregnancy .

* In general , caloric requirement during pregnancy is 30-35 Cal/Kg/day of the

idal body weight . Diet should contain 50-60% CHO , 12-20 protein , <10%

saturate FA and up to 10% polyunsaturated FA . Some add 300 Cal . Late in

pregnancy .

* As regard the number of meals / day . In type II and GDM ( 3 meal + Bed

time snack ) .

* Avoid alcohol , smoking and excess coffee and tea .

* Supplementary vitamins & minerals after the 1

trimester .

* If diabetes is not controlled within 2Ws of dieting , insulin therapy is indicate

However , prophylactic insulin therapy is not proved to be beneficial .

Insulin therapy :

 Initially , the dose is calculated empirically by the formula FBS/5 . The

calculate dose is given as 3 doses of regular insulin / day before meals and

then adjusted to keep FBS < 105 mg/dl and 2hr PP <120 mg/dl ( 140 –

160 mg/dl for cases with frequent hypoglycemia attacks ) .

 2/3 of the total dose before breakfast consisting of 2/3 NPH and 1/3

regular insulin .

 The remaining 1/3 is given before dinner consisting of 1/2 NPH and 1/2

regular insulin .

4- Follow up of the mother :

* FBS & 2hr PP levels are done every visit . Daily home monitor using the

glucose reflectance meter is getting popular nowadays . The records are

plotted on which is examined by the physician every visit .

* Routine measures every visits in the form of BP measurement & weighing

woman to diagnose preeclampsia as early as possible .

* Fundus examination , urine examination for albumin and pus cells and renal

function tests are done every trimester .

* The woman is instructed to report any symptom special visual or neurological

symptoms , vaginal fluid or blood , pain or fever .

a. For adjustment of insulin dose .

b. At 16 – 18 Ws to diagnose fetal anomalies .

c. At 24 – 28 Ws to start fetal surveillance .

d. At any time when complications occur .

5. Follow up of the fetus :

a. Tests for detection of congenital anomalies .

b. Tests for fetal well being starting usually at 24 – 28 Ws .

Management of delivery :

1. Timing of delivery :

* It depends on :

- Control of DM .

- Prev. obstet. History .

- Presence of diabetic or obstetric complications .

- Size of the fetus .

2. Mode of delivery :

* Vaginal delivery is indicated whenever possible , either spontaneous or

induced . Induction is done either by amniotomy + Oxytocin or by PGs +

Oxytocin in le favorable cases .

* Diabetes itself is not an indication for CS , so CS is done mostly for the

ordinary obstetric indications as previous CS , malpresentations , failed
uterine response , obstructed labor , precious baby …. Etc . In general , the

incidence of CS in diabetics is 50% ( including repeat CS ) .

5- Postnatal Care :

* The glucose / insulin infusion of delivery should be stopped after labor .

Encourage the patient to take highly nutritive light fluids . Insulin is not

restarted except if blood glucose level is > 200 mg/dl .

6. Contraception :

* All diabetic females should avoid combined pills . However , the low dose

pills can used for cases with no hypertension or vasculopathy ( no reported

increase in risk CVS ) . Minipills and long acting gestagens .

* IUCD is also an effective method for contraception however , in diabetics

there increased risk of menorrhagia & genital infection .

* Local methods offer an alternative to the above methods , however they have

high failure rate and higher incidence of infection .

* Stermzation :

Specific problems of the infant of diabetic mother :

a. Respiratory distress syndrome ( RDS ) :

b. Hypoglycemia .

c. Hypocalcemia ( Ca

< 7 mg/dl ) .

d. Hypomagnesemia .

e. Polvcythemia ( Hct > 60 % ) .

f. Hyperbilirbunemia .

g. Poor feeding related top prematurity .

h. Birth trauma .

i. Increased risk of development of IDD later in life .