Done by: Al-Yaqdhan Al-Atbi81559

DIABETES IN PREGNANCY

Iman a 41 year leady G10P6A1E2 at 13 weeks of gestation, LMP: 27/10/2012

k/c/o DM on metformine in 2011Presented to the OPD with FBG 9.9 admitted

for glycemic and VPG control.She complain of polydepsia, polyphagia, and

labiality of moodShe diened any nausea, vomiting, dysurea,

vaginal discharge or fever.

Case

OBS Hx:

1st: uneventfull2nd: spontaneous abortion, 23 y, at 14 weeks, D&C done,

no complication3rd , 4th ,5th: uneventfull6th: LSCS (big baby), 1998, 40+ weeks, GDM on diet,

4.39 Kg, girl7th: ectopic pregnancy, 2003, at 8 weeks, Lt

salpingoectomy done8th: ectopic pregnancy, 2011, at 8 weeks, treated with

methotraxate. After this ectpoics she diagnosed with DM on metformine

9th: LSCS (preeclempsia), 2012, at 37+ weeks, DM on insulin and HTN on tablet, 3.4 Kg,.

Current: DM on insuline, at 13 weeks, antenatal scan and investigations were normal.

Menstrual Hx:regular, 5/28days, small amount, mild pain, no

intramenstrual bleeding, age of Menarche 14 y, LMP: 27/10/2012

PMH: apart from OBS Hx, unremarkable

Allergy: nil

Family Hx: No consanguinity strong Family Hx of DM and HTN in first degree

relativesSocial HX:

Not smoker or alcohol consumer

General examination:

Looks well, comfortable, obese, afebrile, alert and cooperative not in distress.

- BMI: 32- There no pallor , jaundice, dehydration- BP: 139/90

Physical examination:

Abdominal examinations:Inspection:

The abdomen is distended symmetricallyUmbilical is invertedscarsNo Striae gravidarum No Linea nigra No visible veinsNo obvious massesNo change in skin colourNormal hair distribution

Palpation:No tenderness on light or deep palpation Uterus at 1cm above pubis symphysis

Other systems are normal

Investigations:Hb: 11.9, platelet normalLDH, LFT, coagulation, and electrolytes

normal VPG at the day of admission:

Post dinner

Post lunch Post breakfast

Pre breakfast

8.7 8.6 7.4 4.9

Gestational Diabetes MellitusGDM

DIABETES IN PREGNANCY

Diabetes mellitus refers to a chronic disorder of metabolism that due to an absolute or relative lack of insulin

It is characterized by hyperglycaemia in postprandial or fasting state or both.

GDM is defined as glucose intolerance of variable degree with onset or first recognition during the present pregnancy.

Gestational diabetes affects 3-10% of pregnancies

Introduction

TRADITIONAL

Type 1 – IDDM – Juvenile diabetes

Type 2 – NIDDM – Maturity onset diabetes

Type 3 – Gestational diabetes

CLASSIFICATION OF DIABETES

Type 1. Immune mediated & idiopathic B cell dysfn

Type 2. DM of adult onset due to insulin resistance & relative insulin deficiency, or from a secretory defect.

Type 3. Specific types of diabetes 1.Genetic defect of B cell function 2.Genetic defect in insulin action 3. Diseases of exocrine pancreas.

Type 4. Gestational diabetes

NEW CLASSIFICATION

WHITE’S CLASSIFICATION OF DIABETES IN PREGNANCY

A1 Gestational diabetes – FBS and Postprandial plasma glucose normal

A2 Gestational diabetes- FBS > 105mg/dl or 2- hr PPBS >120mg/dl

B Overt diabetes developing after 20yr & duration <10yr

C Overt diabetes developing before 20 yr/ duration > 10yr

D Overt diabetes developing between age 10 and 19yr or duration 10-19 yr and or background retinopathy

F Overt diabetes at any age/ duration with nephropathy

R Overt diabetes at any age/duration with prolif. retinopathy

H Overt diabetes at any age/duration + arteriosclerotic HD

Pathophysiology of GDM

Normal pregnancy

Gestational diabetes

increase insulin resistance insulin resistance

worse

increase insulin secretion

decrease pancreatic B cell production of

insulin

The precise mechanisms causing GDM remain unknown

In the pathophysiology of GDM we have to consider one main point.Role of feto-placental unit in GDM.

Pathophysiology of gdm

pregnancy-associated hormones

estrogen, progesterone, cortisol, and placental

lactogen

decrease insulin sensitivity

Increase Insulin resistance

• As pregnancy progresses and the placenta grow larger, hormone production also increases and so does the level of insulin resistance.

•At birth, when the placenta is delivered, the hormone production stops and so does the condition.

Role of feto-placental unit in GDM

Although some scientists have considered that HCG may participates in the development of insulin resistance during pregnancy it shows higher level in women with GDM in comparison

with normal pregnancies

Diabetic action of steroid hormones

Meternal age > 25 yearsobesityFamily history of diabetes

in a first-degree relativePrevious large babyPrevious still birth, or a child with a birth defectPolyhydramniosPrevious pregnancy with

GDM

Risk Factors:

Screening is generally performed between 24-28 weeks of gestation.

Method: oral glucose screening test (OGST) or OGCT

Need no preparation: not fasting 50 gm glucose is giving in glass of water Venous plasma glucose taking before the test and after 1

hr

Results:<7.8 mmol/L = no GDM≥7.8-10.3 mmol/L = further investigation with

OGTT≥10.3 mmol/L= (185 mg/dL) = GDM

Diagnosis

There are six different ways of performing OGTT.

NICE guidelines recommend WHO method

How to do?

Overnight fasting

75 gm glucose giving in 300 ml of water

Venous plasma glucose taking before the test and

after 2hr

OGTT

OGTT on 75 mg oral glucose loadDiabetes Mellitus

FBS ≥ 7.8 mmol/l2 PPBS ≥ 11.1 mmol/l

GDMFBS ≥ 5.5 mmol/L2 PPBS ≥ 9 mmol/L

ORAL GLUCOSE TOLERANCE TEST

WHO criteria for the 2-hour OGTT

Whole blood venous

(mmol/L)

Whole blood capillary (mmol/L)

Plasma venous

(mmol/L)

Plasma capillary (mmol/L)

Fasting >=6.1 >=6.1 >=7.0 >=7.0

2 hours >=6.7 >=7.8 >=7.8 =>8.9

At booking (14 weeks) if at high risk:Family history of DMPrevious GDObesityPrevious still birthMacrosomiaCongenital malformationmultiparty

When to do OGTT?

Done in day care unit or in the wardPatient on diet or insulin

4 venous sampling are collected: Fasting…5.5 mmol/ll 2 hr post breakfast…8 mmol/l 2 hr post break lunch…8 mmol/l 2 hr post break dinner…8 mmol/l

Venous plasma glucose profile

Management

Diet providing 30 kcal/kg –normal pregnant, 24 kcal/kg – over wt pregnancy women . Postprandial hyperglycemia - decreased by CHO

restricted, low glycemic index diets & small frequent meals

Increase Exercise improve blood sugar control 30 minutes a day recommended by NICE

guidelinies

Diet and Exercise

If already on medication, generally switch to insulin therapy: continuing glyburide or metformin controversialteratogenicity unknown for other oral anti-hyperglycemics

Tight glycemic control diet management first line therapy post-prandial blood glucose values seem to be the most

effective at determining thelikelihood of macrosomia or other adverse pregnancy outcomes

aim for Fasting Plasma Glucose (PG) ≤5.3 mmol/L 1-hour post prandial PG ≤7.8 mmol/L2-hour post prandial PG ≤6.7 mmol/L

Management of DM in pregnancy

If blood glucose not well controlled, initiate insulin therapy

Insulin dosage may need to be � adjusted in T2 due to increased demand and increased insulin resistance

Insulin requirement- 0.6, 0.7 & 0.8 units / kg /day- 1st, 2nd & 3rd trimesters

Given as 2 injections/day (some require 3- 4 injections)

INSULIN THERAPY

2/3rd am 1/3rd pm

2/3rd N 1/3rd R½ N ½ R

Available insulin preparations

Type Onset Peak (hours) Duration (hours)

Rapid Lispro* Aspart* Glulisine

< 15 min< 15 min

1 – 21 – 2

3 – 43 – 4

Short regular insulin 0.5 – 0.7 hour 2 – 4 5 – 8

Intermediate NPH(neutral protamine

hagedorn)

Lente

1 – 2 hours

1 – 2 hours

6 – 12

6 – 12

18 – 24

18 – 24

Long acting Ultralente Glargine*

4 – 6 hours 2 – 4 hours

16 – 18peakless

20 – 36 18 – 24

TARGETS OF GLYCEMIC CONTROL

FASTING POST B.F. POSTLUNCH

PREDINNER

POSTDINNER

876543210

MM/L

V.P.G PROFILECut values

Pre: 5.5

Post: 8.0

Monitor as for normal pregnancy plus initial 24-hr urine protein and creatinine clearance

Retinal exam, HbA1C

HbA1C: >8.5% of pre-pregnancy value associated with increased risk of spontaneous abortion and congenital malformations

Increased fetal surveillance (BPP, NST)

Management of DM in pregnancy

Increase incidence of preterm labourIncrease incidence of pre-eclampsia Polyhydramnios - AFI >240mm Macrosomia >4000gm Poorly controlled DM- subfertility, miscarriage,

congenital anomalies, UTI Shoulder dystocia Perinatal mortality

Complications of Diabetes

Maternal Complications

•Obstetric:• Hypertension/preeclampsia

(especially if pre-existing nephropathy/proteinuria)

• Polyhydramnios

Diabetic Emergencies• Hypoglycemia• Ketoacidosis• Diabetic coma

End-organ involvement or deterioration(occur in DM1 and DM2, not in GDM)• Retinopathy• Nephropathy

•Other• Pyelonephritis/UTI

• Increased incidence of spontaneous abortion (in DM1 and DM2, not in GDM)

Fetal Complications

Growth Abnormalities• Macrosomia: maternal hyperglycemia leads to fetal hyperinsulinism resulting in accelerated anabolism

• (IUGR): due to placental vascular insufficiency

Delayed Organ Maturity• Fetal lung immaturity

Congenital Anomalies (occur in DM1 and DM2, not in GDM)• 2-7x increased risk of cardiac (VSD), NTD, GU (cystic kidneys), GI (anal atresia), and MSK (sacral agenesis) anomalies due to hyperglycemia

Fetal Complications

•Labour and Delivery• Preterm labour/prematurity:• Preterm labour is associated with poor glycemic control • Increased incidence of stillbirth• Birth trauma: due to macrosomia, can lead to difficult vaginal

delivery and shoulder dystocia

•Neonatal• Hypoglycemia: due to pancreatic hyperplasia and excess insulin

secretion in the neonate• Hyperbilirubinemia and jaundice: due to prematurity and

polycythemia• Hypocalcemia: exact pathophysiology not understood, may be

related to functional hypoparathyroidism• Polycythemia: hyperglycemia stimulates fetal erythropoietin

production

Caused by a complete lack of insulin but usually

precipitated by something else e.g. infection, infarction

associated with fetal loss rates in excess of 50% and

maternal mortality rates are generally less than 1%.

Signs and Symptoms of DKA:

Malaise Nausea/Vomiting

Headache Polyuria/polydypsia

Dry mouth Shortness of breath

Weight loss Abdominal pain

Dehydration Mental status changes

Diabetic Ketoacidosis in pregnancy

DIAGNOSIS (need all 3 features) 1- Raised blood glucose

2- Ketonuria 3- Acidosis

Goals of therapy Re-hydration Correction of acidemia Normalization of serum glucose Restoration of electrolyte homeostasis Elimination of the underlying cause

Antepartum Care

GoalsMinimize/eliminate the risk of fetal deathEarly detection of fetal compromise Prevent unnecessary premature delivery

Fetal Surveillance

Frequent ANC Confirm viability & Gestational Age by early

scan Detailed anomaly scan ( 18-20 wks) Fetal echo cardiogram ( 24 weeks) Growth scans ( after 30 wks) BPP & Doppler ( after 34 wks)

FETAL SURVEILLANCE

Monthly VPG profile HbA1c once every 3 monthes FBS & PPBS every visit

ASSESSMENT OF GLYCEMIC CONTROL

Timing and mode of delivery

Patient well controlled on diet only to be delivered by 40 weeks.

GDM well controlled to be delivered at 38 weeks.

NICE guidelines recommends that pregnant women with diabetes be offered elective birth after 38 completed weeks gestation

Timing of Delivery

o Spontaneouso Induced – PG/ARM/Syntocino Caesarean section

Mode of delivery

Hourly reflos – keep Blood Sugar ( 5-8 mmols)< 5 mmols – start 5% dextrose> 8 mmol - I.V insulin pump –1unit/hr & titrate

Continous CTGWatch for progress of labourAnticipate & prepare for shoulder dystocia

Spontaneous labour

Continue regular dose of insulin till the time of induction.

Reflo 4 hourly initially and 1-2 hourly in established labour.

Continue infusion of regular insulin in 5% dextrose at rate of .5 to 2 U of insulin/ hr and insulin dosage adjusted accordingly to maintain plasma glucose level (5-8 mmol)

Induction of labour

NICU facility should be availableNeonatologist present for deliveryNo need for routine admission to NICUCheck for hypoglycemia .Watch out for other problems

Care of the newborn

Insulin requirements dramatically drop with expulsion of placenta (source of insulinantagonists)

No insulin is required for 48-72 hours postpartum in most Type 1 DM

Monitor glucose q6h, restart insulin at two-thirds of pre-pregnancy dosage when glucose >8 mmol/L

GDM on diet ( no reflows/diet required)GDM on insulin ( reflows on Normal Diet if high Diabetic Diet

)NIDDM ( Diabetic Diet - reflows – pre-pregnancy. Oral agent.)IDDM ( Diabetic Diet –reflows -pre-pregnancy dose.)

Post delivery care

Evaluation of glycemic control HbA1c – gives control 2-3 months If high – control diabetes before conceptionEvaluation of B.PEvaluation of retinal statusEvaluation of renal functionChange to Insulin prior to / when pregnancy is

diagnosed.

Planning next pregnancy

1. Toronto Notes 2011; OB13

2. Pubmed

3. Uptodate.com

4. Hacker/Moore,2010 essentials of Obstetrics & Gynecology,saunders, fifth edition

5. Obstetrics Guidelines, University of Illinois at Chicago, Sept 2008

6. Pathophysiology of Gestational Diabetes Mellitus: The Past, the Present and the Future,Mohammed Chyad Al Noaemi1 and Mohammed Helmy Faris Shalayel2 1Al-Yarmouk College, Khartoum,2National College for Medical and Technical Studies, Khartoum,Sudan

7. Diabetic ketoacidosis in pregnancy,D Kamalakannan, V Baskar, D M Barton, T A M Abdu

References:

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