Before we discuss about the main topic for today, I'll be talking briefly about pregnancy dating.
Pregnancy is dated based on the last menstrual period, LMP (1st day of menstruation) and NOT the date of conception.
The mean period of gestation is around 280 days or 40 weeks, and hence the estimated date of delivery (EDD) can be calculated, by bringing forwards the LMP for 9 months and 7 days. This rule assumes that :
The Aims of antenatal care :
1) To detect, prevent, and manage the risk factors which adversely affects both mothers and fetus
2) To provide advice, reassurance, education and support to both mothers and family members
3) To deal with minor ailments encountered by mothers during pregnancy
4) To provide a general health screening
Normal antepartum fetal CTG :
Baseline rate : 110-150 bpm
Baseline variability : 10-25 bpm
2 accelerations in 20 min
Absence of deccelerations
Nause and Vomiting in pregnancy is common, usually occurs upto 16 weeks of pregnancy. Such problems are usually dealt conservatively by :
a) Eating small meals in frequent intervals
b) Avoid food that precipitates/aggravates symptoms
However, when it's prolonged, severe, frequent, intractable, not responding towards conservative management as mentioned above, and it's severe to the extent of causing dehydration, alkalosis and hypokalemia, it is known as Hyperemesis Gravidarum.
Nowadays, neurological complications of Hyperemesis Gravidarum is rare, more common complications are : Mallory-Weiss Tear and Esophageal rupture
It is more common in :
1) Multiple pregnancy
2) Molar pregnancy
3) Presence of UTI
Investigations
FBC, BUSE, Daily urinary ketones, MSU culture, if recurrent - TSH and T4 evaluation, and USG - to rule out multiple and molar pregnancy
How do you manage it?
For moderate symptoms and signs (without dehydration) -> reassurance, reduce fear of pregnancy, adequate rest
For severe cases (with dehydration) :
a) Admit the patient
b) I/O chart
c) Administer IV Prochloperazine 12.5 mg tds
d) Give vitamin B complex and folic acid
e) IV fluid regime :
Calculate the percentage dehydration
Give 2 pints of Hartmann's + 2 pints of dextrose 10% + 2 pints of normal saline over 24 hours
Strict I/O chart
Allow oral intake as tolerable
f) If oral intake is non-tolerable, parental vitamins can be given in selected patients
g) If problem persist even with optimal treatment -> refer medical/psychiatric
Maternal steroid
Current recommendation of :
12mg Betamethasone 2 doses, 24 hrs apart OR
6mg Dexamethasone 4 doses, 6 hrs apart
Given during 28-34th week of pregnancy, within 7 days of delivery is said to improve the outcome. Betamethasone is actually more superior than dexamethasone since it more readily crosses the placental barrier as compared to dexamethasone.
There are two definitions of post-term pregnancy :
a) From WHO and FIGO : pregnancy which has complete a total of 42 weeks or 294 days, starting from the first day of LMP
b) From American O&G Association : period of gestation of 2 weeks beyond estimated date of delivery
Definition
The umbilical cord, upon rupture of membranes, lies either within the vagina or protruding out of the introitus.
There's 5 components in it's definition :
a) Blood pressure of >140/90, two readings, 4 hours apart
b) With significant proteinuria
c) Occurs de novo after 20th week of pregnancy
d) In previously normotensive mothers
e) And subsides completely after 6 weeks of delivery
Defined as bleeding from genital tract after 22nd week of gestation.
Ectopic pregnancy
H/O suggestive of ectopic pregnancy :
Abdominal pain
PV bleeding
Amenorrhoea
Previous ectopic pregnancy
IUD in situ
Previous abdominal/pelvic surgery
Previous h/o of PID
Endocrinal changes :
a) Placental hormones
During pregnancy, two important hormones are produced from syncytiotrophoblast.
Stages of labour
First stage of labour is divided into 2 phases, latent and active.
Latent phase : onset of true labour pain -> cervical dilatation of 3cm and full effacement.
What is CTG?
It's a method of fetal well-being assessment, to monitor the fetal heart rate in relation to the uterine contraction.
Definition
Onset of uterine contraction with frequency and intensity sufficient to cause progressive cervical dilatation and effacement prior to term gestation (22 – 37 weeks)
Definition
Gestational diabetes mellitus
A state of carbohydrate intolerance, first identified during pregnancy, usually the latter half (hence no effect over organogenesis), and resolves after delivery.
Pre-gestational diabetes mellitus
Pregnancy in an overt diabetic, can be either type I or II.
Changes in carbohydrate metabolism
The carbohydrate metabolism is altered in such a way that more glucose is made available to the fetus.
Increased levels of placental hormones and cortisol increases the FFA mobilisation, causing maternal hyperglycemia. These hormones have counter-regulatory effects over the action of insulin.
Hence, GDM occurs when despite insulin secretion from pancreas is increased, but was unable to overcome the counter regulatory effects of these hormones.
Screening test
Two screening test is used worldwide.
1) Universal screening
Screening test is offered to all pregnant women.
At 24-28 weeks of gestation, glucose challenge test is done, where 50gm of glucose in solution is taken.
Blood is then taken 1 hour later to determine the glucose level and if it's 7.8 mmol/L or more, diagnostic test (OGTT) is done.
2) Selective screening
Screening test is only offered to mothers with risk factors of developing GDM.
Age > 30 years
Previous h/o of GDM
Family h/o of Diabetes mellitus
BMI > 30 (Obesity)
Previous big baby >4.5 kg
Previous fetal anomalies
Bad obstetric history
Once these risk factors are identified, a modified glucose tolerance test (MGTT) is done. Instructions given :
3 days of unrestricted diet
Fast for at least 8 hours (overnight) before the test (Best 10-12 hours)
Blood is withdrawn first -> fasting sample
Given 75gm of glucose in solution, and blood is again taken 2 hours later
If the fasting sample is 5.6 mmol/L or more and/or 2-hours post-prandial is 7.8 mmol/L or more -> GDM is confirmed
Complications of GDM and Pre-gestational diabetes
1) GDM
Maternal
Polyhydramnios
Pre-term labour
Pre-eclampsia
Pyelonephritis
Operative delivery
Monilial vaginitis
Fetus
Shoulder dystocia
Macrosommia
Intrauterine death (IUD)
2) Pregestational diabetes
Maternal
Ketosis
Hypoglycemic attacks
Diabetic vasculopathy
Difficult sugar control
Fetus
Miscarriage
Congenital anomalies
Antenatal management
Aims in antenatal management :
Good glycemic control
Antepartum surveillance
Appropriate time of delivery
Optimal neonatal support
Frequency of antenatal visits need to be increased, that is :
Every 2 weeks until 32-34 weeks of gestation
Beyond 34 weeks, weekly antenatal visits
For those with pre-gestational diabetes, during 34 weeks or more should be hospitalised for better management
Overall period of gestation shouldn't be > than 38 weeks
Blood sugar profile
If MGTT has confirmed a mother to have GDM, the first thing to do is to admit the mother to the hospital for blood sugar profile.
This is done to determine, whether dietary therapy alone or with addition of subcutaneous insulin is required.
If BSP values are normal -> only dietary therapy
If BSP values are abnormal -> Dietary therapy + SC insulin
For mothers under dietary therapy, BSP should be done every 4 weeks.
For mothers under dietary and SC insulin therapy, BSP should be done every 2 weeks.
In Muar Hospital, BSP is done following the pre-meal protocol :
Pre-breakfast, pre-lunch, pre-dinner and before sleep -> blood glucose level is assessed by glucometer.
And glucose level need to be maintained within 4-6 mmol/L
In Melaka GH, they have start using the post-meal protocol :
Post-breakfast, post-lunch, post-dinner and before sleep
Glucose level to be maintain < 7mmol/L
Dietary therapy
For those with lean body mass, intake of 30 kcal/day of calories is permitted
For those mothers who are obese, intake of only 24 kcal/day is allowed.
These calories are equally distributed in 3 meals and 3 snacks
Diet to be planned by a dietitian.
Insulin therapy
No oral hypoglycemic agents should be used during pregnancy, reasons :
a) ORH crosses the placental barrier, causing fetal hypoglycemia
b) Difficult to monitor it's level
SC insulin is usually given 20-30 min before breakfast and dinner, 2 doses.
2/3 of total dose can be given before breakfast, 1/3 of it given before dinner.
Antenatal investigations
1) Urine microscopy and culture at 28, 32 and 36 weeks of gestation
2) Urine dipstick at each visit
3) For those with pre-gestational diabetes :
Ketonuria and proteinuria -> each visit
BUSE, Creatinine, fundoscopy and HbA1c in every trimester
4) Starting from 16-20 week -> maternal alpha-fetoprotein
5) Ultrasound at 18-22 weeks of gestation -> fetal anomalies scan
6) Fetal echocardiography at 22-24 weeks of gestation -> Cardiac defects
7) Ultrasound at 3rd trimester
Amniotic fluid assessment (polyhydramnios), fetal biometry (macrosommia)
8) For those with bad obstetric history/poor glycemic control -> twice weekly NST and Biophysical profile
9) Especially for mothers with pre-gestational diabetes -> Umbilical artery doppler
Intrapartum management
MO/Specialist to decide the mode of delivery, and :
Entire labour process should not exceed 12 hours
Glucose level during labour should be maintained within 4-6 mmol/L
During active phase of labour :
Start one IV drip
2 hourly glucometer
CTG monitoring
Maintain blood glucose at 4-6 mmol/L
If it goes up to 6-8 mmol/L -> 2 IU SC insulin
If it goes up to 8-12 mmol/L -> 4 IU SC insulin
If the mother is hypoglycemic -> 5% dextrose IV infusion
WATCH OUT FOR SHOULDER DYSTOCIA
All babies born from GDM mother should be referred to a Paediatrician for further observation to be done.
For LSCS :
Skip the morning dose of insulin
Infuse 5% dextrose and 5 IU insulin in 500ml of normal saline
Infusion rate for insulin -> 1.0 IU/hr
To maintain blood glucose level within 4-6 mmol/L
Definition
One or more fetus developing in-utero.
Monozygotic
Twin resulted from fertilisation of a single ovum by one sperm.
The time when the separation of the zygote occurs decides the no. of placenta and amniotic sac.
A pregnant mother came to you with eclamptic fits :
First, guard the mother against cardiorespiratory compromise and secondary injury due to seizure activity,
a) Give supplementary oxygen
b) Place the mother in left lateral position
This is to relieve compression of gravid uterus against Inferior vena cavae
And also to prevent aspiration during convulsions
c) Raised guardrails and padding to prevent maternal injury
d) Use padded tongue blade in between teeth and perform oral suction as required
Classifications of Hypertensive disorders in pregnancy
1. Gestational hypertension
2. Pre-eclampsia / Eclampsia
3. Chronic hypertension
4. Superimposed pre-eclampsia
- The foetus requires an increasing oxygen supply as it grows. How are these increased oxygen needs met?
The factors involved are:
- Increased maternal blood supply to the placenta (Uterine flow increases 20 fold during pregnancy)
- Increased foetal blood supply to the placenta
- Presence of foetal haemoglobin which has a higher oxygen affinity than maternal HbA
- Higher [Hb] concentration in the foetus (40% higher than in adult)
- The Double Bohr Effect.
- What is the uterine blood flow at term?
About 500-750 mls/min and 85% of this goes to the placenta. Note that the uterine supply to the placenta is not autoregulated and flow is pressure dependent.
- What vessels supply foetal deoxygenated blood to the placenta?
Umbilical arteries.
- What is the umbilical artery flow at term?
The foetal cardiac output at term is about 1,000 mls/min: from 25 to 55 percent of this goes
to the placenta.
- What is the special feature of foetal haemoglobin? How does it assist the foetus?
It has a lower P50 (18 to 20 mmHg) than adult Hb (26.6 mmHg). This means foetal
haemoglobin has a higher oxygen affinity and this assists it to load oxygen in the placenta
while maternal haemoglobin is unloading oxygen. It has a higher saturation at a given pO2
than adult haemoglobin eg foetal Hb has a saturation of 80% at a pO2 of 30 mmHg.
- Why does foetal haemoglobin have such a low P50?
- The higher P50 of adult haemoglobin in red cells is due to the right shift that occurs in the presence of high levels of 2,3 DPG in the red cell.
- The 2,3 DPG binds to the β-chains of HbA (especially deoxy HbA) to cause this effect.
- Several amino acids are involved in the binding and each tetramer of adult haemoglobin binds one molecule of 2,3 DPG.
- Foetal Hb is a tetramer: α2γ2.
- There are no β-chains so HbF is insensitive to a shift due to 2,3 DPG binding.
- How long does foetal haemoglobin persist after birth?
At birth about 80% of the neonate’s haemoglobin is HbF. This decreases rapidly so that by the age of 6 months less than 5% of the baby’s haemoglobin is HbF. Only very small amounts of HbF are normally present in adults (<1% style="text-align: left;">
- What is the ‘double Bohr effect’? How does this affect oxygen uptake by the foetus?
- The term double Bohr effect refers to the situation in the placenta where the Bohr effect is operative in both the maternal and foetal circulations.
- The increase in pCO2 in the maternal intervillous sinuses assists oxygen unloading.
- The decrease in pCO2 on the foetal side of the circulation assists oxygen loading.
- The Bohr effect facilitates the reciprocal exchange of oxygen for carbon dioxide.
- The double Bohr effect means that the oxygen dissociation curves for maternal HbA and foetal HbF move apart (ie in opposite directions).
- What are the special factors which assist carbon dioxide transfer across the placenta?
The important factors relevant to the placenta are:
• Maternal hyperventilation results in a low maternal pCO2 which increases the gradient favouring CO2 transfer
• A double Haldane effect occurs and this is unique to the placenta.
- What is the [Hb] at birth?
This is typically high: about 17 to 18 g/dl.
- In what ways does the haemoglobin change in the first year after birth?
The major changes are:
- Decrease in [Hb] (physiological anaemia of infancy)
- Rapid decrease then elimination of HbF (as discussed above)
- Increased production of adult haemoglobin (HbA) to replace HbF.
- After birth, the arterial pO2 (and Hb saturation) in the neonate is much higher and erythropoietin levels consequently drop to undetectable levels.
- Red cell production is markedly decreased and [Hb] falls.
- The decrease in oxygen delivery is partially compensated by a shift of the haemoglobin oxygen dissociation curve to the right as HbF is replaced by HbA and red cell 2,3 DPG levels rise.
- Finally, [Hb] levels fall far enough to cause increased levels of erythropoietin and red cell production increases.
- The physiological anaemia of infancy lasts for about 6 months.
- Can you tell me what are the pO2, SO2 and pCO2 values in the uterine vessels and in the umbilical vessels?
Typical values are:
Maternal circulation
• Uterine artery: pO2 100mmHg (SO2 98%); pCO2 32mmHg
• Uterine vein: pO2 40mmHg (SO2 75%); pCO2 45mmHg
Foetal circulation
• Umbilical artery: pO2 18mmHg (SO2 45%); pCO2 55mmHg
• Umbilical vein: pO2 28mmHg (SO2 70%); pCO2 40mmHg
Gas exchange in the placenta is much less efficient than in a lung. This is because the minimum diffusion distance is much larger (eg 3.5 μm vs 0.5 μm in the lung) and the permeability of the blood-blood barrier is much lower then the permeability of the blood-gas barrier in the lung.
The total surface area of the placenta at term is about 16 m2 as compared to 50 to 60 m2 in the adult lung. The surface area is about a quarter of the size but it transfers only one-tenth of the oxygen. The inefficiency of the gas exchange is compensated for by a relatively much larger surface area.
In summary, as compared to the adult lung, the placenta is inefficient at gas exchange because of larger diffusion distance and lower gas permeability.