Presenter: Dr. P.

Usha Rani
Resident,
ASRAMS, Eluru
 Clinical syndrome
characterized by
deficiency of insulin or
insensitivity to insulin
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

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.
• 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.
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
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.
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).
 Lack of Insulin

Increased Catabolism
Fatigue Hyperglycemia Increased secretion:
Glucagon
Cortisol Wasting
Vulvitis Glycogenolysis
Glycosuria Catecholamines Weight
gluconeogenesis
Growth Hormone loss
lipolysis

Polyuria Osmotic Diuresis

Polydipsia
Hyperketonemia

Tachycardia Salt and Water

Hypertension Peripheral
depletion Acidosis(DKA)
vasodilatation
Hyperventilation

HPL, PROLACTIN,ESTROGEN & PROGESTERONE- DIABETOGENIC

More insulin needed to achieve metabolic control.

Progression of Diabetic Retinopathy.

Worsening of Diabetic Nephropathy.

Increased risk of death in patients with diabetic

cardiomyopathy.
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.
On Fetus:
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.
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.
• 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.
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.
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.
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.
Non challenge blood glucose test:
Fasting glucose test
2 hr post prandial test
Random glucose test
Screening glucose challenge test
Oral glucose tolerance test
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.
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.
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.
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.
Indian National diabetic data group criteria :
Fasting 105mg/dL
1hr 190mg/dL
2hr 165mg/dL
3hr 145mg/dL
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
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.
ORAL AGENTS
Transplacental passage
Teratogenic
Prolonged hypoglycemia
SECOND GEN. SULFONYL UREA (glyburide) - Does
not cross placenta, achieve satisfactory glucose
control
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
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
Therapeutic objective for plasma glucose level
Fasting 60 – 90 mg/dl
After meal
1 hr < 130 – 140 mg/dl
2hr < 120 mg/dl
1. withhold a.m insulin
2. start glucose infusion– 5% dextrose 125 ml/hr ( 6.25
g glucose/hr)
Begin regular insulin infusion 0.5 U/hr(25 U Iin 250
ml NS)
Monitor glucose every 1 – 2 hr
Adjust insulin infusion
 Acute Chronic
 DKA Macrovascular
(Atherosclerosis)
 Hyperosmolar  Coronary
Hyperglycemic non-  Cerebrovascular
 Peripheral Vascular
ketotic coma (HHNC)
Hypoglycemia Microvascular:
 Retinopathy
 Nephropathy
Neuropathic:
 Autonomic
 Peripheral neuropathic
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.

Classical presentations include
anorexia,
nausea,
vomiting,
polyuria,
 polydipsia,
 tachycardia and
 abdominal pain or muscle cramps.
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.
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.
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

(5) decreased caloric intake,
(6) poor medical management,
(7) patient non-compliance.
 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.
 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
 Symptoms–
 thirst
 Polyuria
 Malaise
 Lab finding
 Plasma glucose > 600 mg%
 Ph >/= 7.3
 Hco3 > 20
 Osmolality > 330 mosm/ l
 Treament
 0.95% NS 15-20 ml/hr
 0.15 u/kg i.v bolus regular insulin
 O.1 u/kg/hr infusion
 K replacement
Symptoms of rapidly decreasing blood glucose
 Sweating
 Increase heart rate
 Tremor
 Nervousness
 Irritability
 Weakness
 Tingling
Symptoms of constantly low bl glucose
 Headache
 Visual disturbances
 Mental dullness
 Confusion Amnesia
 seizure
Unconscious-
 100ml of 25% dextrose i.v.
 Or 0.5- 1 mg glucagon i.m/ s.c
Conscious
 Liquid carbohydrate
Fetal Maternal
Fetal distress before •Pregnancy complicated with
start of labour PIH
•Severe vaginal moniliasis
Shoulder dystocia
•Unfavourable cervix
Macrosomia
•Proliferative
Abnormal fetal retinopathy
presentation •Diabetic Retinopathy
Malpresentation
Preoperative evaluation
History
 Family h/o DM
 H/O obesity
 Previous h/o large birth wt. of baby
 h/o drug intake
 Thiazide diuretic
 Beta blocker
 Phenytoin
 Steroid
History Of :
 Fatigue
 Polyuria
 Polydipsia
 Palpitation
 Headache
 Inc RR
 Wasting
 Wt loss
 Diminution of vision
 Tingling
 numbness
Examination
Pulse Rate
Blood Pressure
Temperature
Joint mobility
Bed side test for autonomic function
Investigations:
Blood Sugar  fasting, post prandial
Serum electrolytes
Urine  albumin, sugar, ketones
Blood urea, serum creatinine
ECG
X ray chest
ABG
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.
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.
Monitoring:
Non Invasive Blood Pressure
Pulse Rate
SPO2
ECG
Urine Output
Blood Sugar
Temperature- If autonomic dysfunction
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

Premedication– aspiration prophylaxis
 Ranitidine/metoclopramide

Induction –RSI
Difficult intubation trolly
 Ketamine not used(hyperglycemia)

Maintenance– inhalation agent (ether& trilene

causes hyperglycemia)
Fluid – NS or 10%D and insulin(separately).
Reversal – neostigmine/atropine
 Conversion : 18 x mmol/L = mg/dL
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.
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