pregnancy Fiona McKeeman-Credentialled Diabetes Educator 1 - - PowerPoint PPT Presentation

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pregnancy Fiona McKeeman-Credentialled Diabetes Educator 1 - - PowerPoint PPT Presentation

Diabetes in pregnancy Fiona McKeeman-Credentialled Diabetes Educator 1 Diabetes In Pregnancy Gestational Diabetes Pre-Existing Diabetes- Type 1 Diabetes Type 2 Diabetes The Endocrine Unit The advanced trainee/ Reg Pager


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Diabetes in pregnancy

Fiona McKeeman-Credentialled Diabetes Educator

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Diabetes In Pregnancy

 Gestational Diabetes  Pre-Existing Diabetes-

 Type 1 Diabetes  Type 2 Diabetes

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The Endocrine Unit

 The advanced trainee/ Reg  Pager 464 or through switch during working hours  The consultants -

 Drs Renouf, Matthiesson & Dutta  After hours -Contact the endocrinologist on call through switch

 The DNEs (Diabetes Nurse Educators)

 Sue, Fiona, Kylie, Debbie, Fadwa  Page 506 or ext 7625 (working hrs Mon-Fri)

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Carbohydrate glucose g g g g Insulin Pancreas g Muscle cell g g

2-3 times

g g

g g g

g

Placenta

Hormones

Gestational Diabetes

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What is GDM?

 Gestational Diabetes Melitis is glucose intolerance with onset

  • r first recognition in pregnancy

 Usually a temporary form of diabetes that occurs during

pregnancy.

 Rising levels of placental hormones (HPL and progesterone)

have opposite action to insulin causing release of glucose from cells into the bloodstream. These Hormones also cause insulin resistance.

 Insulin production from the pancreas needs to increase (2-3

times more) to match the effect of these placental hormones.

 Women who develop GDM have deficient insulin production

and/or significant insulin resistance.

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Foetal and maternal risks of GDM

 Risks to Baby

 Macrosomia  Neonatal Hypoglycaemia  Birth Trauma  Shoulder dystocia  Respiratory Distress  Hypocalcaemia  Polycythemia  Jaundice  Obesity, abnormal glucose

tolerance, GDM &Type 2 diabetes in adolescence and adulthood.

 Risks to Mother

 Pre-eclampsia  Polyhydramnios  Caesarean Birth  Future risk of GDM 50%

next pregnancy 70% if you have had it in first two pregnancies.

 Future risk of Type 2- 50%

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Testing for GDM

New recommendations ADIPS 2014 (nov) (RANZCOG Endorsed)  All women not known to have pre pregnancy diabetes or hyperglycemia in pregnancy should undergo 75gm OGTT at 24-28 weeks (Glucose Challenge Test (GCT) screening no longer recommended)  Those Identified as HIGHER RISK should undergo a 75gm OGTT early in pregnancy or at the fist opportunity after conception.  Women in the HIGHER RISK group who have a normal result on early pregnancy testing should have a repeat 75gm OGTT at usual time of 24-

  • 28wks. However a OGTT should be performed at any earlier time if

clinically indicated.

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GDM Risk Factors

 Higher risk groups- (any of below)

 Previous hyperglycaemia in pregnancy  Previously elevated BGL  Maternal age ≥40 yrs.  Ethnicity: Asian, Indian subcontinent, Aboriginal, Torres Strait

Islander, Pacific Islander, Maori, Middle Eastern, non-white African.

 Family History of Diabetes (1st degree relative or a sister with GDM)  Pre pregnancy BMI >30kg/m2  Previous macrosomia (baby birth wt >4500gm or >90th centile)  Polycystic ovarian syndrome  Medications: Corticosteroids, antipsychotics

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Diagnostic Criteria RANCOG Endorsed – recommended adoption Jan 1st 2015

Old Criteria: Fasting ≥5.5, 1hr- not considered, 2hr ≥ 8.0

GDM occurs in approx. 5-8% of Australian pregnancies (may increase to 12-14% with new diagnostic criteria)

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Carbohydrate glucose g g g g Insulin Pancreas Muscle cell g g g g

g g g

g

Placenta

Hormones

Embryo Image: library.thinkquest.org/.../glossary/Embryo.htm

Pre-Existing - Type 2 Diabetes g g g g

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SLIDE 11

Carbohydrate glucose g g g g Insulin Pancreas Muscle cell g g g g

g g g

g

Placenta

Hormones

Embryo Image: library.thinkquest.org/.../glossary/Embryo.htm

Pre-Existing - Type 1 Diabetes g g g g

Fat cell

FA

ketones

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Foetal and maternal risks of Pre-existing Diabetes

Risks to Baby

 Congenital abnormalities 2-3 higher risk

than gen pop

 Miscarriage/ foetal death  Intra uterine growth retardation- small for

gestational age

 Type 1 diabetes (greater if father has Type 1

diabetes) 2% mother vs 5% father

 Macrosomia  Birth Trauma  Shoulder dystocia  Neonatal Hypoglycaemia  Respiratory Distress  Polycythemia  Jaundice  Hypocalcaemia  Obesity, abnormal glucose tolerance &Type

2 diabetes in adolescence and adulthood.

Risks to Mother

Some complications of diabetes accelerated by pregnancy eg renal damage and retinopathy.

UTI’s

Hypoglycaemia

Ketoacidosis- Type 1 diabetes

Pre-eclampsia

Polyhydramnios

 Caesarean Birth

Normal BGLs are the aim pre pregnancy and throughout pregnancy

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Type 1 & Type 2 Diabetes Congenital Abnormalities

 Congenital abnormalities (heart, CNS, neural tube, kidneys,

GI ) 2-3 times higher risk than general population.

 Malformation rates are related to the degree of

hyperglycaemia

 Most congenital abnormalities occur 3-6 weeks after

conception -often before pregnancy is diagnosed.

 Can result in miscarriage, Foetal death in utero  Women conceiving with HbA1c less than 7% have

malformation rates comparable to non –diabetic women.

 Pre pregnancy counselling vital

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GDM (no DM before pregnancy)

Pre-existing diabetes

Type 1 Type 2

Diet and Exercise Rx Insulin Rx

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?? Metformin Rx

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 Treatment targets for self BG monitoring

 Varies between centres around Australia.  The Following are suggested by ADIPS Based on “best

available” data but need further research for RANZCOG endorsement.

 Fasting ≤ 5.0 mmol/l  (1 hour BG after commencing meal ≤ 7.4 mmol/l)- if can’t

wait to 2hrs

 2 hour BG after commencing meal ≤ 6.7 mmol/l

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Medtronic Paradigm pump

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On admission

 Check DMR for any admission instructions from

GDM clinic

 Check for Diabetes Labour management plan in

DMR

 Refer to Clinical Practice Guideline- Diabetes in

pregnancy (on intranet)

 Ring to inform endocrine unit

 during working hours if not urgent  at any time, if required urgently

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In labour- GDM and Type 2 Diabetes

 Withhold insulin when in labour  Aim is to keep the BGLs 4-7 mmol  This reduces the risk of neonatal hypoglycaemia  Check BGLs Hourly in labour  Contact Endocrinology unit If BGLs >7.0 an insulin

infusion may be required (stop after delivery of placenta)

 GDM -NO insulin after delivery  Type 2- Endocrinology review to assess if oral agents or

insulin is required.

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Type 1 DM in labour

 Hourly BGLs  Require an insulin infusion  Insulin pump patients – routinely cease pump and

commence infusion when in labour Type 1 After delivery

 Reduce insulin infusion to 1/5th at delivery of placenta

(do not stop infusion until restarting insulin injections)

 Ongoing Insulin doses will NEED TO BE REDUCED to

1/5th of previous pregnancy doses

 Do NOT withhold insulin or glucose even if not eating

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Elective Caesarean Section – On insulin

Clarify plan of management for pre, peri and post

  • peration with endocrinology and anaesthetist.

Ideally caesarean sections for patients with insulin requiring diabetes should be scheduled early on the morning list to minimise disturbance of glucose metabolism.

Normal insulin night prior to Caesarean. Withhold morning insulin

Type 2 and GDM monitor BGL early morning and pre-

  • p – if >7.0 insulin infusion may be required (cease

infusion after delivery)

Patients with Type 1 diabetes switch to insulin and dextrose infusion in morning. Reduce rate One Fifth rate after delivery of the placenta.

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Insulin Infusion 50units Actrapid in 50ml Normal saline 10% dextrose 12hrly rate

Insulin dextrose Intravenous Infusion

Extra 10units Actrapid in 10ml Normal saline to prime through tubing

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Preparing insulin infusion

Follow MR18B insulin infusion order -contact endocrinologist for or. Prepare Insulin Syringe Driver:

Make up 10 units (Actrapid) in 10mls normal saline (ie 1 unit per ml) prime infusion line with all of this solution before connecting – coats the tubing as insulin is sticky protein and will stick to plastic coating until fully coated.

Make up 50ml syringe with 50 units regular insulin (Actrapid) in 50mls normal saline (ie 1 unit per ml)

Connect to same cannula as dextrose infusion using Y lumen connector

Starting rate ordered by endocrinologist Prepare Dextrose Infusion

10% Dextrose to commence at 12hrly rate when BGL less than 15mmol

Aim is to keep BGL’s 4-7mmol during labour- specific instructions need to be handwritten by Dr in lower section of infusion protocol.

Hourly BGL’s

Follow hypo treatment as per insulin infusion protocol MR 18B

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Hypoglycaemia Treatment

 Routine hypo treatment (when not on insulin infusion)  If BGL<3.9mmol  100ml lucozade (if able to swallow and conscious)  Repeat BGL 10mim  If still < 3.9 repeat lucozade 100ml  Give longer acting carb snack once >4.0mmol  If altered conscious state- 25ml IV Dextrose 50% slow

push-retest in 5min- commence 8/24 10% dextrose.

 (If no IV access Glucagon IM 1mg)  (Refer to hypoglycaemia treatment CPG)

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Care post delivery

 GDM

 Diabetes educator review- advise risk of subsequent

risk of diabetes and GDM.

 Check QID BGL 24 hrs (diet controlled) 48hrs (insulin)

notify endo if above 10

 75 gm OGTT 6wks post partum  Review appointment GDM clinic or GP 8-10wks

postpartum

 1-2 yearly OGTT if not pregnant  Early OGTT in next pregnancy – first visit or 12-14

wks gestation

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Care Post Delivery

 Pre-Existing Diabetes

Continue QID BGL’s – Notify endocrinology if

BGL>10mmol or <3.5mmol

Diabetes Educator review- advise risk of

hypoglycaemia post delivery and after breastfeeding

GDM clinic review 2-4wks Ongoing follow-up at DIAB clinic or private

endocrinologist

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QUESTIONS?

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(HAPO) Hyperglycemia and Adverse Pregnancy Outcomes Study

 HAPO Study  5 year international study 23,000 women  AT ≈ 28wks subject had a 75g OGTT with fasting, 1 and 2 hour

samples . Subjects and healthcare providers blinded to results unless FBG >5.8mmol/l or 2 hour value >11.1 then out of study and treated.

 Conclusions:  BGL’s that are elevated but under diagnostic level of GDM have

increased risks usually associated with GDM.

 Data showed a continuous increase in risk as blood glucose levels

rise of:

 Large birth weight  High blood insulin levels in the newborn  Primary Caesarean birth  Pre-eclampsia and shoulder dystocia/birth injury  Was not significantly associated with hypoglycaemia in the newborn

requiring treatment

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The HAPO Study Cooperative Research Group. N Engl J Med 2008;358:1991-2002

Frequency of Primary Outcomes across the Glucose Categories

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References

RANZCOG July 2014 Diagnosis of Gestational Diabetes Mellitus (GDM) and Diabetes Mellitus in Pregnancy

ADIPS Consensus Guidelines for the Testing and Diagnosis of Gestational Diabetes Mellitus in Australia- Nov 2014

The HAPO Study Co-Operative Research Group 2008 “Hyperglycemia and Adverse Pregnancy Outcomes” NEJM May 2008 Vol358 no19

Nankervis A. 2001 “Diabetes and Pregnancy: Women’s Experiences and Medical Guidelines” Miravana Publishers Australia

Nankervis A 2007 “Gestational Diabetes” Diabetes Management Vol19 June

Siri et al NEJM vol 341 no 23 December 1999 “Current concepts: Gestational Diabetes Mellitus”

Diabetes-genetics.org 2009 “Genetics of Diabetes Mellitus”

MacNeil et al 2001 “rates and Risk Factors for Recurrence of Gestational Diabets” Diabetes Care Vol24 no4 April.

2007 National Institute of Diabetes and Digestive and Kidney Diseases: National diabetes statistics fact sheet: general information and national estimates on diabetes in the United States, 2007.

Hoffman et al, The Australian Diabetes in Pregnancy Society “Gestational diabetes mellitus- management guidelines” MJA1999 169:93-97

Gabbe SG et al Obstet Gynecol 2003:102 856-888. As cited in Pumps in Pregnancy Presentation Dr Alan O Marcus 2007

The Australian Diabetes in Pregnancy Society 2005 “Consensus Guidelines for the management of patients with Type1 and Type 2 diabetes in relation to Pregnancy guide” http://www.adips.org/content/ADIPS_PreGDM_Guidelines.pdf

Nankervis A Conn,J 2013 Gestational diabetes mellitus: Negotiating the confusion. Australian Family Physician Vol.42 No.8 August p528-531 30