3. Type Ia- immune mediated beta cell destruction
Type Ib-idiopathic beta cell destruction
Type II-insulin secretory defect with insulin
resistance
Type III-other cause
A-genetic deficiency in beta cell fn
B-genetic deficiency in insulin action
C-ds of exocrine pancreas
D-endocrinopathies
E-drug induced
F-infection
G- Uncommon forms stiff man’s syndrome
Anti - insulin receptor antibody
H- Other genetic syndrome associated with Diabetes Mellitus
Type IV- Gestational Diabetes
4. It is defined as carbohydrate intolerance with onset or
recognition during pregnancy.
The prevalence of gestational diabetes mellitus (GDM)
in India varies from 3.8 to 21% in different parts of the
country, depending on the geographical locations and
diagnostic methods used.
GDM has been found to be more prevalent in urban
areas than in rural areas.
5. • Women diagnosed to have GDM are at an increased
risk of future diabetes predominantly type 2 DM and
increase in the foetal/neonatal morbidity, future
development of obesity, and diabetes in the offspring.
• The most common presentation of gestational
diabetes in mothers is antenatal glycosuria.
6.
7. CLASS DEFINITION
A1 Diet controlled gestational DM
A2 GDM requiring insulin
B Pre-existing DM without complications. Dur:<10yrs. Onset:
>20yrs
C Pre-existing DM without complications. Dur:10-19yrs,
Onset:<10-19yrs
D Pre-existing DM. Dur:>20yrs. Onset:<10yrs
F Pre-existing DM with Nephropathy
R Pre-existing DM with retinopathy
T Pre-existing DM with post op renal transplant status
H Pre-existing DM with heart diseases
8. Most important reason for exacerbation of diabetic
tendency in pregnancy Progressive increase in
insulin resistance.
Other reasons increased lipolysis and altered
gluconeogenesis.
1st
and early mid trimester increased insulin
sensitivity due to high levels of estrogen
HYPOGLYCEMIA.
9. During 2nd
trimester production of human placental
lactogen, increase in cortisol, estriol and progesterone
& due to increased destruction of insulin by kidney
and placenta progressive insulin resistance and
renal glycosuria HYPERGLYCEMIA
During 3rd
trimester further insulin resistance
decreased hypoglycemic effect of given dose of insulin
HYPERGLYCEMIA ( reason for GDM to occur
commonly after 26 wks of gestation).
10. Lack of Insulin
Hyperglycemia
Glycosuria
Osmotic Diuresis
Salt and Water
depletion
Increased secretion:
Glucagon
Cortisol
Catecholamines
Growth Hormone
Increased Catabolism
Glycogenolysis
gluconeogenesis
lipolysis
Hyperketonemia
Acidosis(DKA)
Fatigue
Vulvitis
Polyuria
Polydipsia
Tachycardia
Hypertension
Wasting
Weight
loss
Peripheral
vasodilatation
Hyperventilation
Glycosuria
HPL, PROLACTIN,ESTROGEN & PROGESTERONE- DIABETOGENIC
11. More insulin needed to achieve metabolic control.
Progression of Diabetic Retinopathy.
Worsening of Diabetic Nephropathy.
Increased risk of death in patients with diabetic
cardiomyopathy.
12. On mother:
• Preeclampsia: affects 10-25% of all pregnant diabetics.
• Infection: High incidence of chorioamnionitis & post
partum endometritis.
• Post partum bleeding: High incidence due to
exaggerated uterine distention.
• Cesarean section: High incidence in pregnant
diabetics.
15. Congenital anomalies:
Most frequent cause of neonatal mortality and
morbidity.
Potentially preventable through strict control of
maternal glycemic levels in periconceptional period.
Hypoglycemia
Neonatal hypoglycemia is secondary to excessive
insulin production by the neonatal pancreas in
response to maternal hyperglycemia.
Can lead to seizures, coma and brain damage.
16. Postnatal hyperbilirubinemia
Occurs in appox. 25%, double that of normal.
Due to immaturity of the neonate’s liver function.
Phenobarbital administration antenatally may help
in preventing this condition.
Respiratory distress syndrome
5-6 fold increased frequency.
May be due to a delay in lung maturation or simply
due to the increased frequency of preterm
deliveries
Polyhydramnios
Amniotic fluid volume >2000 mL
Increased risk of placental abruption and preterm
labor.
17. • There are no reliable signs and symptoms to diagnose
Gestational Diabetes.
That is why it is necessary to screen the entire
obstetric population or at least the women at high
risk to determine their need for definitive test to
determine the presence of GDM.
18. Low risk( Bl. Glucose screening not routinely required):
Members of an ethnic group with a low prevalence of
GDM.
No known 1st
degree relatives with diabetes.
Age < 25 yrs.
Weight normal before pregnancy.
Weight normal at birth.
No history of abnormal glucose metabolism.
19. Average risk ( Bl. Glucose testing at 24 – 28 wks):
Members of an ethnic group with high prevalence of
GDM.
Diabetes in a 1st
degree relative.
Age >/= 25 yrs.
Over weight before pregnancy.
Weight high at birth.
20. High risk( perform glucose testing as soon as feasible):
Marked obesity.
Age > 35yrs.
Smokers
Previous h/o birth of large babies(>4.5kgs).
H/o PCOD.
Strong family history of type 2 DM.
Previous history of GDM, impaired glucose
metabolism or glycosuria.
21. Non challenge blood glucose test:
Fasting glucose test
2 hr post prandial test
Random glucose test
Screening glucose challenge test
Oral glucose tolerance test
22. Non challenge blood glucose test:
At the 1st
antenatal Visit and on the subsequent day, if
the fasting plasma glucose level is found to be >
126mg/dL or RBS > 200mg/dl, the diagnosis of GDM is
confirmed.
23. Screening Glucose challenge test/ O’ Sullivan test:
It is a simplified version of OGTT.
Performed between 24-28wks.
50g of oral glucose is given and blood sugar is
measured 1 hr later.
If cut off point is set to 140 mg/dL, 80% of women with
GDM can be detected.
If threshold is reduced to 130mg/dL, 90% of GDM
cases can be detected.
No fasting is required for this test.
24. Oral Glucose Tolerance Test(OGTT):
It requires over night fasting of 8-14 hrs.
Usually 75g or 100 g of oral glucose is given.
Blood glucose levels are measured at start of test and
then at set intervals of time.
25. American Diabetic Association guideline values for
100g OGTT:
Fasting >/= 95mg/dL
1hr >/= 180mg/dL
2hr >/= 155mg/dL
3hr >/= 140mg/dL
• At least 2 out of 4 positive values confirms the
diagnosis of GDM.
26. Indian National diabetic data group criteria :
Fasting 105mg/dL
1hr 190mg/dL
2hr 165mg/dL
3hr 145mg/dL
27. 1. Symptoms of diabetes
Polyuria
Polydipsia
Unexpected weight loss
2. Fasting plasma glucose > 126 mg/dl
3. 2 Hour plasma glucose >/= 200mg/dl after taking 75 gm
glucose load
28. Diet
Provide adequate maternal &fetal nutrition
Restricted fat & cholesterol
Increase in dietary fiber
3 meal & 1-3 snacks , last snack being taken at bed time
Desirable wt. gain 200-450 gm / week until full term
Total wt gain 10-13 kg during normal & diabetic pregnancy is
recommended
Calorie intake 25-35 kcal/kg
Monitoring
Self monitoring of Bl.Sugar – 4 times/day
Daily urine ketones testing when Bl.Sugar >200mg% or pt is unable to
eat.
30. GLYBURIDE:
Sulfonylurea. Primary mechanism of action is
stimulation of release of insulin from the storage
granules of the pancreatic beta cells.
Also decreases insulin resistance.
Non teratogenic, no noticed fetal effects and effective
control of maternal blood glucose levels are the
reasons for its use in treating GDM.
Side effect: Hypoglycemia.
Dose: 1.25 to 2.5 mg OD or BD. Daily max dose 20 mg.
Peak plasma level: 2-4 hrs. Duration of action: 10-
12hrs
31. Gold standard
Does not cross placenta
Pt on oral hypoglycemic should be changed to insulin
GDM on diet control will require insulin if fasting
glucose >95mg% or pp>130 mg%
Started with 0.5-0.8 u/kg/day in three divided doses
with regular insulin
35. Most common during 2nd
and 3rd
trimester.
Caused mainly due to the deficit in insulin and the
response to that deficit by counter regulatory
hormones.
If uncorrected, may lead to maternal and fetal death.
37. If severe, the picture could include
Kussmaul hyperventilation,
signs of volume depletion (e.g., hypotension and
oliguria),
lethargy to coma,
normal-to-cold body temperature and
fruity odour noticeable in the patient’s breath.
38. Findings for diagnosing DKA:
Bl. Glucose > 250mg/dL.
DKA may develop in pregnancy with bl. Glucose
<250mg/dL and occasionally in the normal range
( EUGLYCEMIC KETOACIDOSIS).
Ketone bodies in urine and plasma.
Arterial pH<7.3
Sr. bicarbonate < 15mEq/L.
Increased anion gap.
39. It is associated with the following factors:
(1) bacterial infection;
(2) omission of insulin doses in the presence of
gastroenteritis because of the parturient’s concern
about the possibility of an insulin reaction due to
anorexia, nausea, and vomiting;
(3) pump malfunction in patients receiving continuous
subcutaneous insulin infusion therapy and
(4) tocolytic therapy with β- sympathomimetic agents,
with or without concomitant glucocorticoid therapy
41. i.v line
O2 by Face mask
Asses level of glucose& electrolytes
Replacement of fluid
Average fluid deficit 3-5 L
1-2 L in first hr- isotonic N saline followed by
250-500 ml/hr maintenance.
Insulin therapy
The initial insulin dose is a continuous IV insulin infusion using an
infusion pump, at a rate of 0.1 U/kg/h.
A mix of 24 units of regular insulin in 60 mL of isotonic sodium
chloride solution usually is infused at a rate of 15 mL/h (6 U/h)
until the blood glucose level drops to less than 250 mg/dL; the rate
of infusion then decreases to 5-7.5 mL/h (2-3 U/h) until the
ketoacidotic state subsides.
42. Glucose administration– 5% dextrose(when plasma
glucose reaches 250mg/dL, to prevent hypoglycemia).
K+ administration– after 3-4 hr of insulin therapy 10-20
mEq/hr.
Bicarbonate– if arterial ph <7.1
S. Hco3 <5 mEq/l
51. Preop. Advise
Nil Per Oral
pt to be taken as first case in OT
Fasting Blood Sugar, Urine sugar ,ketones,
Serum electrolytes
Aspiration prophylaxis
Pt is adviced to eat their usual evening meal and bed
time snack the evening prior to induction or cesarean
delivery. Should also take their evening insulin dose.
Should omit their morning dose of insulin on the day of
surgery.
52. To facilitate changes in insulin, electrolytes and fluid
administration, it is ideal to have 2 I.V lines.
One to be used for the purpose of administering
insulin and,
The other is connected to a 2 way system with one
bag containing fluid and electrolytes and other
containing fluid and electrolytes with 10% dextrose.
This allows a rapid response to manipulations in total
fluids, insulin, electrolytes and dextrose
administration.
55. Choice of Anaesthesia
Depends on status of mother and fetus
Regional anaesthesia: If no evidence of peripheral
neuropathy
Epidural labour analgesia:
Decreased Pain
Decreased plasma catecholamine level
Improved uteroplacental circulation
Minimises the need for GA in event of CS
58. Post operative care:
Intra op insulin infusions and serial blood glucose
monitoring has to be continued into the post
operative period.
There may be initial hypoglycemia in the early post
op period which has to be managed by careful
monitoring and titration of insulin infusion.
59. References:
Miller’s Anesthesia 7th
edition.
Stoelting’s Anesthesia and co-existing disease 5th
edition.
Practical guide to high risk pregnancy and delivery(Fernando Arias) 3rd
edition.
Obstetric anesthesia(Dr. Sunanda Gupta) reprinted 1st
edition.
Wylie and churchill Davidson principles and practice of anesthesia 5th
edition.
www.en.wikipedia.org
www.ncbi.nlm.nih.gov
www.onlinelibrary.wiley.com
www.diabetes.co.uk
www.diabetes.org
www.diabetesindia.com
www.diabetesaustralia.com.au
www.diabetesupdate.blogspot.in
www.emedicine.medscape.com
www.apiindia.org