Post on 07-May-2015
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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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