DIABETES IN PREGNANCY

All You Need To Know About The Management Of

Gestational Hyperglycaemia

�1

by "Associate Professor Dr Hanifullah Khan

Hyperglycemia in Pregnancy

�2

What is DM? A metabolic condition characterized by chronic hyperglycemia as a result

of defective insulin secretion, insulin action

or both

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• Type 1(IDDM) • Type 2(NIDDM) • Gestational diabetes • Others -genetic defects in insulin processing or action -endocrinopathies -drugs -exocrine pancreatic defects -genetic syndromes associated with DM

Pregnancy predisposes to persistent hyperglycaemia

• Glucose is made available to the fetus – ↑ placental hormones – ↑ plasma cortisol – A state of insulin resistance – Further aggravated by ↑

body weight and ↑ caloric intake during pregnancy

�4

• Pregestational diabetes becomes worse during pregnancy

• GDM develops when the pancreas cannot overcome the effect of these hormones

Diabetes & Pregnancy

the prevalence of women with preexisting T2DM getting pregnant (diabetic pregnancies) seems to be rising

�5

nowadays, more and more women go into pregnancy with increased body weight and caloric intake

This prevalence

is increasing

• Glucose intolerance of variable severity with onset or first identification during the pregnancy

– Generally occurs in the latter half of pregnancy

– Previously, found to constitute 90% of diabetes in pregnancy

�6

• resolving after delivery

Important facts

To understand the effects of hyperglycaemia on the fetus, it should be remembered that glucose crosses the

placenta freely but maternal insulin does not

�7

Thus, maternal hyperglycaemia leads to fetal hyperglycaemia with a consequent rise in fetal insulin

secretion

Pregnancy is a state of insulin resistance, especially towards term

What does chronic hyperglycaemia lead to?

�8

Pathogenesis of tissue injuryHyperglycaemia leads to the production of reactive oxygen species (ROS)!

ROS lead to tissue damage through various mechanisms!

This ultimately leads to micro- and macrovascular complications

�9

Giacco F. Circulation Research, 2010

Maternal Complications - antenatal

• Pre-eclampsia$

• Recurrent infection-vaginal candidiasis,UTI$

• Polyhydramnios—PPROM, discomfort$

• Anomalies & abortions$

• Sudden IUD

�10

Maternal Complications - delivery

• Increased instrumental rates$

• Birth trauma$

• Operative delivery

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• Polyhydramnios—premature membrane rupture, cord prolapse

Maternal Complications - postpartum

Increased risk of developing DM later in life

�12

Past history of GDM increases the risk of recurrence in subsequent pregnancies

Retnakaran R. Diabetes Care, 31, 1275–1281

Maternal Complications - Medical

• Retinopathy$

• Nephropathy$

• Neuropathy $

• Micro/macroangiopathy

�13

Fetal complications!

Congenital anomalies (4 fold) - sacral agenesis, NTD, cardiac and renal anomalies$Macrosomia$Malpresentation$Shoulder dystocia$

!

Prematurity$Respiratory distress syndrome$Hypoglycemia$Polycythemic -jaundice

�14

“strong continuous associations of several perinatal outcomes with maternal glucose levels below those diagnostic of diabetes”$

HAPO study 2008

Fetal macrosomia

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The child - later on….

Obesity$

Diabetes mellitus$

Reproductive problems$

Metabolic syndrome

�16

Why is it important to differentiate between gestational

& pregestational DM?

�17

This is important

because each diagnosis imparts a different clinical

significance

�18

future development of T2DM

The significance of GDM

mothers are at risk of

adverse obstetrical outcomes!

- esp. fetal overgrowth

�19

growth restriction

The significance of pregestational DM

Most of the risk is to the fetus

complications during

organogenesis!�20

similar to GDM

Pregestational diabetic pregnancies

• carry a graver consequence$

• should be managed immediately once identified$

• Ideally, evaluation for DM should occur before pregnancy$

• to prevent complications during organogenesis (1st trimester)

�21

Hyperglycaemia in the 1st trimester

confers a significantly increased risk of major malformations

�22

Type of Diabetes

in pregnancy

T1DM$(n=221)

T2DM$(n=317)

GDM$(n=1822)

Risk of Major

congenital abnormality

(%)

5.9 4.4 1.4Farrel T 2002

Fetal malformations & Glycaemic control

• HAPO study $

• a continuum of increasing risk of perinatal outcomes as glucose levels increase$

• even within levels that were previously defined as normal

�23HAPO study. NEJM 2008

Hyperglycaemia later in pregnancy

• High blood glucose increases fetal growth$

• Postprandial normoglycemia can reduce the rate of macrosomia

FBG>5mmol/L, HbA1c>5.3%

MACROSOMI

A!

�24HAPO study. NEJM 2008

Issues of concern

1. The frequently undiagnosed nature of T2DM before pregnancy

�25

2. Lack of preconception care

3. The increase in complications of pregnancy due to the coexistence of obesity and T2DM

Difference between GDM & DM

• GDM$– early pregnancy BS normal – Usually no effect on

organogenesis – less likely to have congenital

defects – diabetes disappears after

delivery – macrosomia more likely

• DM + Pregnancy$– elevated BS since before

pregnancy – effect during organogenesis – more likely to have

congenital fetal defects (up to 8x more than normal pregnancy)

– fetes may be growth restricted

�26

overall though, perinatal outcomes are worse whatever the cause of the hyperglycaemia

How do we detect those asymptomatic mothers with

DM?

�27

Pregnant women with DM are

frequently asymptomatic

They need to be identified before harm can come to the fetus

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Screening

• this process of looking for asymptomatic diabetics is termed screening

elevations of maternal blood glucose are deemed harmful to the fetus

• during antenatal check-ups, mothers with unknown elevations of blood glucose need to be identified

�29

• The benefits and importance of screening for GDM have been proven (ACHOIS & HAPO study)

Crowther NEJM 2005

In Malaysiawe base our screening strategy on

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• screen selectively those considered high risk (1-step testing)

Who are those considered high risk?

�31

Added criteria• In recent time, this list has been expanded$

• Include factors such as $

• physical inactivity$

• certain dietary patterns$

• polycystic ovarian syndrome (PCOS)$

• biochemical markers such as adiponectin & C-reactive protein

�32

Retnakaran R. Clin Endocrinol 2007 Lo JC. Diabetes Care, 2006

PCOS• Ex-GDM mothers investigated for PCOS$

• A majority of them displayed characteristic polycystic ovarian morphology

�33

Kousta E. Clin Endocrinol, 2000

What is done now• At booking - assess risk$

• if risk present, do OGTTCurrent'screening'protocol'

First Obstetric Visit - check risk status '

Risk Factors

Absent

Present

Consider'normal'

Risk Factors •Age >=40 yrs •Unexplained SB •P/H recurrent miscarriages •P/H BW >=4.0 kg •Weight >100 kg •P/H oligomenorrhoea •Strong maternal/sibling F/H

Note: OGTT not performed in: Known pre-existing DM cases & Cases with P/H of GDM

OGTT performed after 24 weeks

gestation

Consider'GDM'if'diagnostic'criteria'met'

�34

Schedule for screeningBetween 24-28 weeks of gestation

or earlier if there are stronger indications

If the glucose tolerance remains

normal at 34 weeks, stop testing

If the original OGTT is negative, recommend periodic repeat testing (may be required

until 34 weeks of gestation)

�35

Recent Recommendations• Based on HAPO study data - even the slightest

hypoglycaemia increases pregnancy adversity$

• IADPSG formulated recommendations

�36IADPSG. Diabetes Care 2010

• In a bid to achieve international consensus$

• Try to catch as many patients with pregnancy hyperglycaemia as possible

IADPSG strategy

�37IADPSG. Diabetes Care 2010

IADPSG screen

• 1st phase - early pregnancy$• aimed at detecting previously undiagnosed overt diabetes$

• HbA1c or plasma glucose (fasting or random) measurements$

• carried out on high-risk women (adult non-pregnant criteria)

�38

2 discrete phases

• 2nd phase - 24-28 weeks$

• if 1st phase normal$

• 2-hour 75 g OGTTIADPSG. Diabetes Care 2010

Adult non-pregnant risk factors

�39ADA. Diabetes Care 2013

The OGTT

�40

OGTT• The first-line diagnostic test$

• Initially developed to identify the diabetic in the general population

because of the many controversies surrounding this topic, numerous

iterations of the OGTT abound with different criteria for diagnosis

�41

O’Sullivan, Mahan. Diabetes 1964.

Procedure

�42

Procedure for OGTT

�43

IADPSG. Diabetes Care 2010

75 grams of oral glucose is given 3 readings -fasting glucose level, 1 hr and 2 hr post glucose

Diagnostic Values

5 4 5 4

Table 1: Values for Diagnosis

Fasting Random

Venous Plasma Glucose ≥ ≥ 11.1 mmol/L

Table 2: Diagnostic values for Type 2 Diabetes Mellitus/Glucose Intolerance – oral glucose tolerance test (OGTT) [IDF 2005] 5 (Level III)

OGTT Plasma Glucose Values (mmol/L)

Category 0-hour 2-hour

DM ≥ ≥ 11.12

Recommendations: Screening and Diagnosis

in those with risk factors and those ≥30 years. [Grade C]

initiated at 10 years old or at onset of puberty if puberty occurs at a younger age. [Grade C]

3. More frequent and/or earlier testing with either a FPG or 2-hour plasma glucose in

[Grade C]

≥6.1 to 6.9 mmol/L in order to identify individuals with IGT or diabetes. [Grade C]

screening for other cardiovascular risk need to be done or planned. [Grade C]

�44

More recent diagnostic criteria

Commonly referred to diagnostic criteria for the 75 gram OGTT include the WHO and the ADA criteria

More recently, the IADPSG have adopted stringent criteria based on the HAPO study

�45

IADPSG. Diabetes Care 2010

23

12:20:10

Postpartum considerationsPostpartum considerationsP/H GDM woman

Postpartum oGTT

Normal GTAbnormal GT

IGT/DM

Manage as appropriate

Diet & exerciseF/U Blood Glucose

Stable glucose

75g oGTTDiet & exercise

F/U Blood Glucose

Raised glucose

Normal GT

�46

Should be carried out after 2 months

postpartum

Is there any other way to diagnose DM in pregnancy?

�47

Yes, but…

• Only in early pregnancy$

• Glycated haemoglobin (HbA1c) and plasma glucose (random or fasting)$

• HbA1c has been validated for the diagnosis of DM outside of pregnancy (≥6.5%) with many authorities favouring its use in pregnancy as well

�48

International Expert Committee. Diabetes Care 2009

HbA1c limitations$•costs!•unavailability!• inaccuracy in anaemia

Plasma glucose

• Fasting or random$

• FPG level of ≥7.0 mmol/L is diagnostic of overt diabetes$

• RPG of ≥11.1 mmol/L has to be confirmed with either an FPG or A1c value ≥ the threshold

�49

How do we manage hyperglycaemia in

pregnancy?

�50

Strategy

• Rapid normalisation of blood glucose$

• Limited weight gain$

• Monitoring for anomalies and complications$

• Avoiding macrosomia$

• Planned delivery

�51

Optimization of metabolic control

• BS control dependant upon diet modification, exercise and hypoglycaemic medications

�52

• Lifestyle modification (dietary advice & appropriate exercise) should be the primary interventions considered

• Resort to medications only when these fail to achieve the desired targets

What is the dietary advice for diabetes in pregnancy?

�53

Less weight gain

• In overweight or obese mothers$

• No specific guidelines for women with diabetes$

• Less weight gain is safe and has a beneficial effect on perinatal outcomes in obese women$

• Access to dietitian

�54

Individualised counselling• From a registered dietician experienced with pregnancy

and diabetes$

• Basic plan - based on dietary recommendations for all pregnant women, adjusted to the individual needs of the patient

�55

• Carbohydrate and caloric contents - modified based on the woman’s height, weight, and degree of glucose intolerance

Caloric restriction• A 33% reduction of calories results in clinically relevant

improvement in glycemic parameters $

• 30-35 kcal/kg/day = 1200 Kcal/d is safe$

• 50% of these calories should be from complex carbs$

• Exact amount unknown - carbohydrates, like calories, should be determined based on individual needs$

• mother’s weight, activity, home & personal circumstances$

• Base calculations on home blood glucose levels

�56

Specific targets• Avoid concentrated sweets and highly processed foods -

contribute to unwanted weight gain$

• soft drinks, ice cream, cakes and sweets$

• restrict CHO to those found in vegetables and dairy products like cheese and cottage cheese

�57

Hone J. J Clin Endocrinol Metab 2010

• Small frequent meals (4 hourly) instead of fewer larger meals $

• reduces the amount of insulin needed at any one time, resulting in lower glucose excursions$

• also reduce hunger and prevent overeating

Some more targets• Breakfast should be especially small and low in carbs because

insulin resistance is highest in the morning$

• High-fiber and low-GI foods should be substituted wherever possible for simple sugars $

• higher fiber/low GI may assist in delaying absorption of food, thus allowing the insulin peak to “catch up”$

• Foods rich in antioxidants have a role in reducing the incidence of fetal anomalies$

• fruits and vegetables are recommended

�58

Folic acid

• Supplemental $

• Proven to reduce the risk of neural tube defects$

• The prescription should begin at least 3 months preconceptionally and through the first trimester $

• Minimum dose of 4 mg daily

�59

Medical

Nutritional

Therapy -

MNTIf MNT

doesn't work?

Medication is implemented if 2 or more glucose values are elevated after 1 wk of

lifestyle management

�60

What to do if dietary intervention does not work?

�61

Oral medication?

• Previously, next step would be insulin therapy $

• because oral medications were thought unsafe, ineffective & teratogenic$

• enough data to show the utility and safety of oral hypoglycaemic agents (OHAs) in pregnancy

�62

When to start OHAs?

• When fasting or premeal BS values constantly exceed 5.5 mmol/L$

• OHAs should be started without hesitation whilst encouraging dietary and exercise efforts

�63

Glibenclamide

• The first OHA to have proven efficacy and safety in pregnancy $

• At a dose of 2.5 mg daily to a maximum of 20 mg per day$

• Similar birth outcomes can be achieved when comparing glibenclamide use to insulin initiation in pregnancy

�64

Langer et al. N Eng J Med 2000

Metformin• The starting dose is 500 mg once daily & increasing to

500 mg tds$

• Similar outcomes between metformin and insulin initialisation$

• Although 46% of mothers on metformin required additional insulin supplementation for blood sugar optimisation$

• An early indicator that metformin therapy alone might be inadequate to achieve target values is a higher fasting glucose

�65

Rowan et al. N Eng J Med 2008

General considerations• OHA dosage should be increased every 4-5 days to

achieve the desired blood sugar target values

�66

Rowan et al. N Eng J Med 2008

• Although both metformin and glibenclamide cross the placenta, there have been no reports of fetal adversity so far

• The long term effects of these OHAs are still under study but there is optimism that their safety will be proven$

• decreased overall weight gain has been noted in pregnant mothers on metformin

When do we use insulin?

�67

When MNT & OHA fails to achieve glycemic goals after 1 wk

�68

An example of a therapy guide

�69

14

lifestyle, and personal circumstances. Food intake should be adequate to maintain maternal and foetal nutrition. An energy prescription of 30-35 kcal/kg pre-pregnant ideal body weight is recommended, though this should be flexible to correct for any alteration in activity levels. Those women whose body weight exceeds 120% of their ideal body weight may require a lower energy intake per kilogram in order to limit their weight gain during pregnancy. Frequent small meals may facilitate improved blood glucose control. Complex carbohydrates should provide about 50% of the total calories. This should be distributed in the form of 10-gram exchanges as regular main meals and snacks throughout the day. Levels of dietary fibre of 30-50g per day should be advised. Foods rich in antioxidants - fresh fruits and vegetables - may have aa role in reducing malformations. All foods containing refined sugars, eg cakes, ice cream, sweets, soft drinks, should be strictly avoided preferably by all pregnant women irrespective of their carbohydrate metabolism status. Foliate supplements (4 mg/day) should be routinely prescribed preconceptionally and in the first trimester to reduce the risk of neural tube defects. Exercise helps maintain control and women should be encouraged to walk for about 30 minutes per day. Hypoglycaemic agents need to be introduced when lifestyle and dietary measures fail to control the glycaemia. In cases of GDM, it is appropriate to consider starting oral hypoglycaemic agents in the first instance whenever the fasting or pre-meal blood glucose levels consistently exceed 5.5 mmol/l, definitely if the value exceeds 7.0 mmol/l. Recent research has confirmed the safety and clinical efficacy of glibenclamide [gliburide] during pregnancy. Glibenclamide should be started at 2.5 mg daily with the dose increased every 4-5 days to a maximum of 20 mg/day. If control is not achieved, then the sulphonylurea should be replaced by insulin. An alternative oral hypoglycaemic agent if metformin, though the use of this is still under investigation. This should be started as a 500 mg daily dose, increasing the dose to 500 mg t.d.s. depending on gastrointestinal symptoms.

Class Fasting/preprandial Blood glucose

2-hour postpradial Blood glucose

Management option

A1 Always <5.1 mmol/l Always <6.7 mmol/l Diet alone A2 5.1-7.0 mmol/l 6.7-7.0 mmol/l Diet +/-

pharmacological Rx B1 >7.0 mmol/l >7.0 mmol/l Diet + Insulin

Management options

Savonna-Ventura. UMMS Malta 2011

How do we use insulin?

�70

Insulins

• Each type of insulin has an onset time, a peak and duration of action$

• The onset time is delineates how soon the blood glucose lowering action comes into effect and is commonly used to classify this class of medications$

• either rapid-, short-, intermediate- or long-acting

�71

A basic understanding of the dynamics and actions

Development of Insulins• Originally, from animals$

• Biosynthetic preparations in the 1970s - more effective and cheaper preparations$

• The first such insulins - regular insulin (or “human” insulins)$

• classed as short-acting, $

• mainstay of diabetes treatment in pregnancy in the 1980s $

• not fully satisfactory due to a late peak (2-3 h after injection) - not very effective for postprandial control$

• too long duration of action - tending to cause hypoglycaemia

�72

Insulin analogues• They provide more optimal glucose control during pregnancy$

• technically not insulin, but something similar that retains the hormone’s glucose lowering function$

• They are considered safe for pregnancy use - no teratogenic or embryotoxic effects have ever been demonstrated$!

• They act rapidly, peak in about 1 hour with a duration of action between 2-4 hours. $

• The first such insulin developed was insulin lispro followed soon after by insulin aspart

�73

NPH insulin

• An intermediate acting insulin originally developed in the 1930’s $

• now synthetically produced to give better absorption rates when injected subcutaneously$

• May be mixed with shorter acting ones in the same syringe to complement its longer duration of action and to allow for better dosing and blood sugar control$

• NPH remains in the market today specifically for the reason that it can be marketed in premixed formulations for ease of use

�74

More recent insulin analogues

• Insulin glargine and detemir$

• Absorbed more steadily after injection, providing a “peakless” mode of action, followed by a rapid decline and all the while producing a more constant glucose lowering effect$

• Duration of action is approximately 24 hours, thus needing only once-daily administration - long-acting insulins$

• also induce less hypoglycaemia and weight gain compared to conventional insulins$

• Despite these attractive features, they are currently unlicensed for pregnancy use due to lack of systematic data although several reports have not demonstrated any adverse effects or teratogenicity.

�75

Summary of insulins

�76

Table&1&Commonly&used&insulins&and&their&properties&

Type&of&insulin&

Generic&name& Onset& Peak& Duration&

!

Rapid'acting!!

!

Insulin!lispro!

15!minutes!30'90!minutes!

3'5!hours!Insulin!aspart!

!Short'acting!

!

Regular!

insulin!

30'60!

minutes!2'4!hours! 5'8!hours!

Intermediate!acting!

!

NPH!insulin! 1'3!hours! 8!hours! 12'16!hours!

Long'acting!

Insulin!

glargine!1!hour! Peakless!! 20'26!hours!

Insulin!detemir!

!

!Modes&of&administration&

By! dint! of! being! protein! in! origin,! insulin!medications! cannot! be! taken!

orally! and! have! to! be! injected.! The! most! frequent! mode! of! parenteral!administration!is!via!subcutaneous!injection!using!repeat'use!insulin!pens!with!

fine! needles.! Intravenous! administration! is! frequently! seen! in! intensive! care!settings.!Of! late,! insulin!pumps!have!been!providing! fine'tuned! insulin!delivery!

and!consequent!better!blood!glucose!control.!This!mode!of!insulin!delivery!may!

supersede! others! once! financial! and! a! host! of! technical! considerations! can! be!overcome.!

&Regimes&&

The!philosophy!behind!insulin!delivery!is!to!mimic!physiologic!secretion!

of!insulin!by!the!pancreas!as!close!as!possible.!In!pregnancy,!this!entails!multiple!injections! of! various! combinations! of! rapid,! short! and! intermediate'acting!

insulin.!!

To! limit! the! effects! of! persistent! hyperglycaemia! on! the! fetus,! insulin!should! be! instituted! as! early! as! possible! once! failure! of! nutritional! and! OHA!

therapy! is! recognized.! A! tried! and! tested! insulin! combination! is! a! rapid'acting!and!NPH!one.!!

The! daily! insulin! requirement! of! the! pregnant! mother! is! based! on! her!

weight!and!gestation!as!follows:!first!trimester!,!0.7!U/kg/day;!second!trimester!0.8!U/kg/day;!third!trimester!(wk!29!–34),!0.9!U/kg/day;!and!term!(wk!35–39),!

1.0!U/kg/day.!Jovanovic&L,&Peterson&CM.&1982!Optimal!insulin!delivery!for!the!pregnant! diabetic! patient.! Diabetes! Care! 5! (Suppl! 1):24–37.! LapollaA,&DiCianniG,&BruttomessoD,&Dalfra`MG,& FresaR,&MelloG,&Napoli&A,&Romanelli&T,&Sciacca&L,&Stefanelli&G,&Torlone&E,&Mannino&D.&2009!Use!of!insulin!detemir!in!pregnancy:! a! report! on! 10! type! 1! diabetic!women.!Diabet!Med! 26:1181–1182.!

Slightly! higher! starting! doses! may! be! used! for! obese! patients.! It! must! be!

remembered!that!these!values!are!a!safe!guide!to!insulin!initiation!and!must!be!

Modes of administration

• The most frequent mode of parenteral administration is via subcutaneous injection $

• using repeat-use insulin pens with fine needles$

• Intravenous administration - in intensive care settings$

• Insulin pumps provide fine-tuned insulin delivery & consequent better blood glucose control$

• financial & technical considerations

�77

How do we calculate the amount of insulin to use?

�78

Philosophy behind insulin• Mimic physiologic secretion of insulin as close as

possible$

• In pregnancy, this entails multiple injections of various combinations of rapid, short and intermediate-acting insulin

�79

A tried and tested insulin combination is a rapid-acting and NPH one

Starting values

• Slightly higher starting doses may be used for obese patients$

• These values are a safe guide to insulin initiation $

• Must be optimised rapidly to achieve the target blood glucose values by using (home blood glucose monitoring) HBGM

�80

Starting dose calculationTime of pregnancy Dose

Prepregnancy 0.6 U/kg/day

First trimester 0.7 U/kg/day

Second trimester 0.8 U/kg/day

Third trimester$(29-34 wks) 0.9 U/kg/day

Term (35-39 wks) 1.0 U/kg/day

�81

Jovanovic. Diab Care 1982$Lapolla et al. Diab Med 2009

Starting doses• The regimens are based on predicted total daily insulin

requirements - based on current weight and stage of pregnancy $

• 50% of the total dose is given as a basal dose using NPH insulin (intermediate-acting)$

• at bedtime or bedtime+breakfast time$

• the other 50% of the total dose - given as boluses before meals using insulin analogues (rapid-acting)$

• before meals (within 15 minutes) in divided doses (1/6 of the total dose per meal)

�82

Adjustments

• These doses are starting doses only$

• Necessary to rapidly adjust dose to achieve glucose goals using HBGM data & A1C testing$

• Serial blood sugars - carried out between 3-7 days after starting & the dosage of insulin adjusted commensurately

�83

How do we know if the diabetes is under control?

�84

Pillar of assessment

• Glycaemic adequacy is assessed through regular blood glucose estimations$

• Tight glucose control achieved through dietary, physical and pharmaceutical interventions

�85

Adequate BS control is proven beneficial to the pregnancy. Despite this, no clearly established

glucose targets exist.

Crowther et al. N Eng J Med 2005

Techniques of assessment

• 2 techniques of assessment - HBGM & HbA1c $

• Most data regarding target values in pregnancy - derived from pregnant T1DM & T2DM patients

�86

Kitzmiller et al. Diab Care 2008

Target Values - FPG

• FPG of ≤5.0 mmol/L $

• Associated with a reduction in the risk of macrosomia, neonatal hypoglycemia, and maternal preeclampsia in GDM during the third trimester

�87

Prutsky et al. JCEM 2013

Target Values - FPG & postprandial

• FPG of ≤4.9 mmol/L & and 2-hour postprandial glucose between 5.9–6.4 mmol/L$

• risk of birthweight greater than 4 kg, prematurity, neonatal hypoglycaemia & preeclampsia are all lowered

�88

Rowan et al. Diab Care 2010

Target Values - HbA1C

Amongst pregnant Type 1 diabetic mothers, maintaining HbA1c levels to less than 6% before and during pregnancy

predicated outcomes similar to non-diabetic pregnant mothers

�89

Wyatt et al. Diab Med 2005

Recommendations

�90

Timing Glucose Level

Premeal, bedtime, overnight 3.3–5.4 mmol/L

Postprandial 5.4-7.1 mmol/L

HbA1c 6.0%

ADA.Diabetes Care 2013

Monitoring • Regular blood glucose monitoring - mainstay of objective

optimization of metabolic control$

• between 3-4 times a day$

• a prebreakfast and postprandial (2 hours post-lunch and dinner) and/or night test$

• Initially, clinic attendance - primarily for patient education purposes$

• Subsequently, self-monitoring of blood glucose is the optimum$

• Assessment of long-term control and further optimization - 4-6 weekly by measuring HbA1c levels$

�91

Postprandial blood glucose monitoring

• Glycaemic control has been shown to be improved by limiting postprandial glucose excursions$

• Postprandial glucose correlates well with HbA1C$

• By measuring and controlling the postprandial and fasting sugars, the occurrence of neonatal hypoglycaemia and macrosomia may be reduced

�92de Veciana M. NEJM 2013

Do This

Assessment of the pregnancy

The pregnancy must be treated as a whole$

Take precise history - maternal well-being, FM$

Examine for complications - remember; maternal, fetal & placental$

Investigations - in order of priority$

ultrasound scan, urine, blood tests, CTG

�93

Patient complaints!

Do not manage the blood sugar, manage the patient!

�94

Physical Examination!

Ultrasound scans!

Are you able to manage a patient with diabetes in

pregnancy?

�95

You can if..• You routinely manage antenatal patients$

• You know how to screen for & diagnose this condition$

• You know how to implement & monitor treatment$

• You know how to monitor for complications

�96

Do not hesitate to seek help!

Case Studies

Test Yourself!

�97

Case 1

• A 34-year-old Malay woman, known DM, who is in her second pregnancy and has had one live birth is seen for prenatal care at 8 weeks gestation

• Her weight is 96 kg, and her blood pressure is 130/80 mmHg. Uterine size is appropriate for gestational age. Her family history reveals that her mother has type 2 diabetes mellitus. A urine dipstick shows 3+ glycosuria and negative ketones$

Q. . What tests should be done to evaluate the patient's glucose tolerance?

Q. How is the diagnosis of GDM established?

Q. What would be the best treatment and follow-up strategy?

�98

Case 2

• 25 year old G1P0 at 10 weeks gestation. No significant past medical, surgical or reproductive history. No family history of DM. A regular patient of the GP, antenatal booking bloods includes a diabetic screen utilizing HbA1c. HbA1c was 6.2%. $

Q. Is this patient GDM?$

Q. Does she need to be started on insulin

�99

Case 3 • 35 year old G2P1 at 8 weeks gestation. Her first pregnancy –

delivered LSCS for obstructed labour 4 years prior – 3.6 kg baby girl. No contraception prior to this pregnancy. $

• Routine ANC by GP – incorporate HbA1c – 8%. Diagnosed as DM with pregnancy. Based on local knowledge and guidelines, this patient requires insulin but patient refuses.

�100

Q. What should the GP do next?

Q. Should this patient be started on oral medication immediately?

Case 4

• 38 year old G4P3 at 35 weeks, known DM diagnosed since last pregnancy, on metformin 850 mg bd. Since the patient is already on treatment, the GP has continued the oral medication. Regular serial sugar estimations are carried out – pre-breakfast, post-lunch and dinner – 6.2/7.7/7.8$

• Maternal and fetal well-being established$!

Q. Should she be started on insulin now?

�101

�102

Thank You