The document discusses the fetal skull, its areas and diameters, sutures, fontanelles, and screening and management of gestational diabetes mellitus (GDM) and pregestational/overt diabetes in pregnancy. It describes that the fetal skull is compressible and made of thin, flat bones. It is divided into the vertex, brow, and face. It discusses the diameters and sutures of the skull. For GDM screening, it recommends testing based on risk factors. It outlines management of GDM including diet, exercise and insulin therapy if needed. For pregestational diabetes, it discusses increased risks and the need for tight glycemic control before and during pregnancy.
2. INTRODUCTION
Fetal skull is to some extent
compressible, and made mainly of
thin pliable tabular (flat) bones
forming the vault.
3. AREAS OF THE SKULL
It is divided into several zones of
obstetrical importance, these are,
• Vertex
• Brow
• Face
4. VERTEX
• It is a quadrangular area bounded
Anteriorly -by bregma and coronal
sutures, Posteriorly -lamda and
lambdoid sutures. Laterally – by lines
passing through the parietal
eminences.
5. • it is an area bounded on one side
by the anterior fontenelle or
bregma and coronal sutures and
the other side by the root of the
nose and supra orbital ridges of
either side.
BROW
6. FACE
It is an area bounded on one side by
the root of the nose and supra –
orbital ridges and on other side by
the junction of the floor of the
mouth with neck.
7. SUTURES
• Flat bones of the vault are united
together by non- ossified membranes
attached to the margins of the bones.
These are called sutures.
8. TYPES
4types:
a) The saggital suture or longitudinal suture:
it lies between two parietal bones.
b) The coronal suture: runs between parietal
and frontal bone on either side.
c) The frontal suture: it lies between two
frontal bones
d) The lambdoid suture: it represents the
occipital bone and the two parietal bones.
9. FONTENELLE
• A wide gap in the suture line is called
fontenelle.
Types: 2types
• Anterior fontenelle(bregma)-diamond in
shape, diametre-4cm, time of ossification-
18months.
• Posterior fontenelle- triangular in shape,
diametre- 1.2cm, time of ossification- 1 half
months.
10. DIAMETERS OF SKULL
• 1. sub-occipito bregmatic: (9.5cm)
It extends from the nape of the neck to the centre of
the bregma.
2. sub-occipito frontal : (10cm)
It extends from the nape of the neck to the anterior
end of the anterior fontenelle or centre of sinciput.
3. Occipito – frontal : (11.5cm)
It extends from the occipital eminences to the root of
the nose.(glabella)
11. • 4. Mento- vertical : (11.5cm)
It extends from the mid point of the chin to
the highest point on the saggital suture.
5. sub- mento vertical: (11.5cm)
It extends from the junction of floor of the
mouth and neck to the highest point on the
saggital suture.
6. sub- mento bregmatic: (9.5cm)
It extends from unction of floor of the mouth
and neck of the bregma.
14. Screening strategy for detecting GDM
• Low risk:
* Blood glucose testing not routinely required in:
– Member of an ethnic group with low prevalence
– No known diabetes in 1st degree relatives
– Age < 25yrs
– Weight normal before pregnancy
– Weight normal at birth
– No history of abnormal glucose metabolism
– No history of poor obstetrical outcome
15. Screening strategy for detecting GDM
• Average risk
* Blood glucose testing at 24-28 wks (1 step/2step)
– Member of an ethnic group with high prevalence
– Diabetes in a first degree relative
– Age ≥ 25yrs
– Overweight before pregnancy
– Weight high at birth
16. Screening strategy for detecting GDM
• High risk
* Blood glucose testing as soon as feasible
– Severe obesity
– Strong family history of type 2 diabetes
– Previous history of GDM
– Impaired glucose metabolism
– Glucosuria
17. Screening (OGTT)
• Plasma glucose level measured 1 hr after 50g glucose load
• Without regarding to time of day/ time of last meal
• Plasma glucose level > 130mg/dl; sensitivity 90%
• Plasma glucose level > 140mg/dl; sensitivity is 80%
18. Diagnosis of GDM by OGTT
Time 100 g Glucose
(American diabetes
association criteria)
75 g glucose
(WHO criteria)
Fasting 95 mg/dl 5.3 mmol/L 95 mg/dl 5.3mmol/L
1-h 180mg/dl 10mmol/L 180mg/dl 10mmol/L
2-h 155mg/dl 8.6mmol/L 155mg/dl 8.6mmol/L
3-h 140mg/dl 7.8mmol/L - -
19. Maternal risks
• Birth trauma
• Operative delivery
• Polyhydraminos
• 50% lifetime risk in developing Type II DM
• Recurrence risk of GDM is 30-50%
20. Fetal risks
• No increase in congenital anomalies
• Increased risk of stillbirth if fasting+ PP hyperglycemia
• Macrosomia, BW >4000gm occurs in 17-29% of
pregnancies
• Birth trauma-shoulder dystocia and related complications
• Neonatal hypoglycemia
21. Fetal macrosomia
• Defined as fetal weight > 4000gm
• Brain not effected, shoulder dystocia 3%
Maternal hyperglycemia
Fetal hyperinsulinemia
Excessive somatic growth
• Diagnosis and management is important
• USG should begin at 20wks; to be done at every 4 wks
• Also due to IGF-1 and IGF-2
• Maternal obesity is important confounding factor
24. Management of GDM
• Diet : general principles
• 55% CHO 25% Protein 20% fat
• Normal weight gain 10-12 kg
• Avoid ketosis
• Liberal exercise program to optimize BG control
• Daily self BG monitoring
• Breakfast should provide 25%, Lunch 30% and dinner
30%. Obese women may be managed with lower
caloric intake.
25. Management of GDM
• If persistent hyperglycemia after one week of
diet control proceed to insulin
• 6-14 weeks 0.5u/kg/day
• 14-26 weeks 0.7u/kg/day
• 26-36 weeks 0.9u/kg/day
• 36-40weeks 1 u /kg/day
26. Oral hypoglycaemic agents
• Traditionally not recommended in pregnancy
because of teratogenic effects
• Glyburide and Metformin
27. Glyburide
• Sulfonylureas
• MOA- release of insulin
• Hypoglycemia and weight gain are the main
side effects
• Non-teratogenic, classified as category B drug
28. Glyburide treatment regimen
who fail Diet therapy
1. Glucometer BG measurment fasting and 1 or 2 hrs
following breakfast, lunch and dinner
2. Glucose level goals (mg/dl): fasting < 100, 1-h < 155
and 2hrs < 130
3. Glyburide starting dose 2.5mg orally with morning
meals
4. Increased daily glyburide dose by 2.5mg/wk,
increment until 10mg/day, then switch to twice
daily dosing until max of 20mg/day, then switch to
insulin if 20mg/day does not achieve glucose goal.
29. Obstetrical management
• Cesarean delivery should be considered in women
with sonographical estimated weight > 4500gm
• Elective cesarean delivery has no significant effect on
incidence of brachial plexus injury
• Fetal monitoring
30. Postpartum evaluation
• Women diagnosed with GDM to be evaluated with 75gm
OGTT at 6-12wks postpartum
• Metabolic assessment recommended after preg with GDM
• Contraception: low dose hormonal contraceptives
Time Test purpose
Postdelivery (1-3 d) Fasting or random plasma
glucose
Detect persistent, overt
diabetes
Early postpartum (6-12wk) 75g 2h OGTT PP classification of Glu met
1yr Postpartum 75g 2h OGTT Assess Glu metabolism
Annually Fasting plasma glucose Assess Glu metabolism
Tri- annually 75g 2h OGTT Assess Glu metabolism
Prepregnancy 75g 2h OGTT Classify glu metabolism
31. Pregestational diabetes/ overt diabetes
• Patients with symptoms of DM and plasma Glucose
concentration 200mg/dl or more
• The condition may be preexisting or detected during
present pregnancy
32. Criteria for diagnosis of impaired Glucose
tolerance and diabetes with 75g oral
glucose
Time Normal
tolerance
Impaired glucose
tolerance
diabetes
Fasting < 110 mg/dl ≥ 110 and <126 ≥ 126 mg/dl
2 hr Post glucose <140 mg/dl ≥ 140 and <200 ≥ 200 mg/dl
34. Maternal effects
• During labor:
– Prolongation of labour due to big baby
– Shoulder dystocia
– Perineal injury
– Postpartum hemorrhage
– Operative interventions
• During Puerperium:
– Puerperal sepsis
– Lactation failure
37. Preconceptional counselling
• Preconception Counselling
• Risk of NTD ~1-2%
• Folic Acid 400µg/day
• Preconceptional glucose control using insulin.
• Fasting < 70-100 mg/dl, and PP <140mg/dl at the
end of 1 hr and <120mg/dl at the end of 2hr.
38. Preconceptional counselling
• Normoglycemia prior to conception
• Ideally HBA1C 6% or less
• Team approach
• Glucose monitoring qid
• ACE inhibitors contraindicated
• Baseline HbA1C, 24h urine for protein Cr Cl ,
ophthalmology review
• Switch from OHA to insulin
39. Pregestational /Overt Diabetes
• Assess for end organ disease
– assess for nephropathy - inc risk of PIH
– Assess and treat retinopathy - may progress
– assess for neuropathy
• generally remains stable during pregnancy
– assess and treat vasculopathy
• CAD is a relative C/I for pregnancy
40. Maternal Surveillance
- Blood pressure monitoring
– renal function every trimester
– urine culture monthly
– thyroid function
– BG control HB A1C every trimester
41. Fetal Surveillance
– USG for dating/viability ~ 8 weeks
– Transvaginal USG examination at 10-14 weeks
– Fetal anomaly detection
• nuchal translucency 11-14weeks
• maternal serum screen- free β HCG and PAPA-A
• MSAFP at 16w to screen for open Neural tube
defect
• anatomy survey 18-20 weeks
• Fetal echo 22weeks
– Weekly biophysical profile, NST
42. Trimestric approach
• 1st Trimester:
– Careful monitoring of glucose control is essential
– OHA to Insulin therapy
• 2nd trimester:
– Maternal serum alpha fetoprotein at 16-20wks
– Targeted sonographic examination at 18-20wks
– Euglycemia with self monitoring is the goal
– Increased insulin requirement after 24wks
• 3rd Trimester:
– Cesarean delivery to avoid traumatic birth
43. Admissions
– At 34-36 weeks in uncomplicated cases
– It facilitates
i. Stabilisation of diabetes
ii. Less incidence of Preeclampsia, Polyhydramnios
and Preterm labour
iii. Selecting time and mode of termination
44. Insulin therapy
• OHA not currently recommended for overt diabetes
• Maternal glycemic control with multiple daily insulin
inj and adjustment of dietary intake
• S/C insulin infusion by calibrated pumps
• Self monitoring using glucometer recommended
46. Management of diabetes in pregnancy
insulin therapy
• Insulin Pump
– Allows insulin release close to physiologic levels
– Use short acting insulin
– 50-60% of total dose is basal rate
– 40-50% given as boluses
– Potential complications
• Pump failure
• Infection
• Increased risk of DKA
48. Insulin therapy
• Regular and NPH are the most commonly used
preparations
• Regular insulin/NPH combination-
– Slow absorption, administered 30min before
meals
– Midmorning & midafternoon snacks necessary
– Rapidly acting insulin like Lispro prevent
hypoglycemia
49. Insulin therapy
• Lispro and aspartate–
– should be taken immediately before meals
– Lispro and aspartate used for prandial insulin and
insulin pump therapy
50. Insulin therapy
• Glargine-
– Longest acting
– Less episodes of nocturnal hypoglycemia
– Given in morning hours
• Detemir
51. Timing of Delivery
• Diet controlled
– Same as non diabetic
– Offer induction at 41 weeks if undelivered
• On Insulin/Type II/Type I
– If suboptimal control deliver following confirmation of lung
maturity if <39 weeks
– Otherwise deliver by 40 weeks
– Generally do not allow to go post term
• DOC for initial tocolysis: Nifedipine
52. Mode of Delivery
• Macrosomic infants of diabetic mothers have
higher rates of shoulder dystocia
• Cord is to be clamped immediately
• Reasonable to recommend C/S delivery if EFW
is >4500g
53. Insulin requirement in labor
Insulin requirements
During induction of labor During elective caesarean section
•Usual insulin dose and meal on evening before surgery
•Overnight fast from 12 midnight
Day before IOL
•Normal diet
•Normal insulin dose
evening before IOL
•No overnight fast
Day of IOL
•give half the morning dose of insulin before
light breakfast
•Insert prostaglandin gel as early as possible
•Continuous CTG
•Start IV insulin infusion once labor establishes
54. Insulin therapy intrapartum
CG Level Management
• 60-90 mg/dl 5%-10% DNS at 100 ml/hr
• 90-120mg/dl 0.9% NS or RL at 100ml/hr
• 120-140 mg/dl 5Uin 500ml 5% dex at 100ml/hr
• If >140 mg% then plain insulin sc by sliding scale:
• 140-180 mg/dl 4U
• 180 -250 mg/dl 8U
• 250-400 mg/dl 12U
• >400 mg% 16U
• CG and urinary ketone level should be measured every
2 hourly.
55. Contraception in DM
• Barrier methods are safe, inexpensive with fewer side effects
• OCPs cause insulin resistance due to progesterone component
and there is high risk of thromboembolism, MI and CVA.
• IUCDs cause infection, glucose precipitates with Copper and
thus reduction of efficacy.
• Permanent method are used in couples with complete family
56. Diabetic Ketoacidosis
• 5-10% of pregnant Type 1 patients
• Serious medical emergency
• Risk factors
– New onset DM
– Infection
– Insulin pump failure
– Steroids
• Fetal mortality 10%
58. Diabetic Ketoacidosis
• Management
– ABC’s and ABG
• Assess BG, ketones electrolytes
– Insulin
• 0.2-0.4U/Kg loading and 2-10U/h maintenance
– Begin 5% dextrose when BG is 250 mg%
– When potassium is N range begin 20mEq/h
– Rehydration isotonic NaCl
• 1L in 1st hour
• 0.5-1L/h over 2-4h
• 6-8 L over 1st 24 hours.
• 250cc/h until 80% replaced
• Replace Bicarb and phosphate as needed
60. Metabolic syndrome
• Definition (NCEPATP III)
– At least 3 of the following:
• Fasting plasma glucose > 110mg/dl
• Abdominal obesity (waist circumference> 35 in.)
• Triglycerides >150 mg/dl; HDL < 50mg/dl
• BP ≥ 130/85 mmHg
61. Indian experience
• Incidence of GDM is 3-5%
• Numbers are increasing
• 90% diagnosed cases are of GDM
• Fetal macrosomia 32%
• PIH 48%
• Hydramnios 4%
• IUD 12%
• Fetal malpresentation 16%
• Cesarean section 44%
• Maternal mortality 10 times
62. Medicolegal Pitfalls
• Congenital anomalies in infant-
– Explained to the mother
– Preventability by good glycemic control should be
mentioned and recorded
• Birth injuries and Perinatal asphyxia
– USG should be done 2-3wks prior to delivery
– Offer cesarean section if EFW >4500gm
63. Take Home Message
• Preventing congenital anomalies is a challenge
• Maintaining euglycemia is the key
• Educating community is the cornerstone
