REPRODUCTIVE MODULE

Obstetrics

Academic Circle
MFSU Ragama
Contents

1. Introduction to pregnancy

2. Physiological changes at birth

3. Medical disorders in pregnancy

4. Complications of pregnancy

5. Imaging of the fetus

6. Infertility
 Introduction to pregnancy

Physiological changes in pregnancy

Cardiovascular system

• The major hemodynamic changes induced by pregnancy include,

▪ Sodium and water retention leading to blood volume expansion

▪ An increase in cardiac output

▪ Reduction in systemic vascular resistance

▪ Reduction in systemic blood pressure

Plasma volume

o Expansion of the plasma volume

➢ begin as early as the fourth week of pregnancy

➢ peak at 28 to 34 weeks of gestation and then plateau until parturition

➢ 30- 50% increase by 34 weeks

Cardiac output

The cardiac output rises by 30-50% above baseline during normal pregnancy; Maximal
around 20-28 weeks gestation.
 o CO = HR × SV
o Preload is increased due to the associated rise in blood volume
o Afterload is reduced due to the decline in systemic vascular resistance
o Maternal heart rate rises by 15 to 20 beats/min; Maximal around 28-34 wks.; this
compensates for the declining stroke volume towards term
o In early pregnancy – increase in SV
o Late pregnancy- Increase in HR
o CO increase by 15% above pre labour levels in early labour and 25 % during the active
phase
o The additional exertion associated with pushing in the second stage results in a 50% rise
in cardiac output
o Immediately postpartum, cardiac output increases to 80%

Systemic vascular resistance

o Decreased vascular responsiveness to the presser effects of angiotensin II and

norepinephrine
 o Increased concentration of nitric oxide in the circulation

Blood pressure

BP= CO × SVR

o Fall in SVR is manifest by a fall in blood pressure, which begins by the end of the first
trimester and lowest at 22-24 weeks

o Systolic and diastolic blood pressure fall and are about 5 to 10 mmHg below baseline
in the second trimester, declining to a mean of about 105/60 mmHg

o In the third trimester, blood pressure gradually increases and may normalize to non
pregnant values by term

Pulmonary artery pressure

o Pulmonary artery pressure remains unchanged; The increase in pulmonary blood flow
is balanced by a decrease in pulmonary vascular resistance.

o CVP remains unchanged

Anatomical changes in CVS

o The heart is shifted to the left, anterior, and rotated toward a transverse position as
the uterus enlarges.

o The apical impulse is shifted cephalad to the fourth intercostal space and laterally to
the midclavicular line.

Anatomical changes in CVS

o The heart is shifted to the left, anterior, and rotated toward a transverse position as
the uterus enlarges.

o The apical impulse is shifted cephalad to the fourth intercostal space and laterally to
the midclavicular line.
Precordial examination
o A third heart sound is present in most
o Wide splitting of S1
o An ejection systolic murmur (up to grade 2/4) in the pulmonary and tricuspid area is
found in the majority

Cardiac physiology
Left atrial enlargement leads to stretching of the cardiac conduction
pathways and predisposes to alterations in cardiac rhythm.
o Periods of supraventricular tachycardia and ventricular extra systoles are a common
finding.

Normal ECG findings

➢Transient ST segment and T wave changes in lateral leads

➢ Q wave and inverted T waves in lead III

➢ Q wave in lead AVF

➢Inverted T waves in leads V1, V2 and occasionally V3

❖ Respiratory system

Thoracic cavity

➢ Flaring out of lower ribs, increased transverse diam. and elevation of

diaphragm.

➢ Mainly diaphragmatic breathing

Respiratory function

➢ Increased minute ventilation (30-50%) mainly by tidal volume rather than RR

- Stimulated by progesterone; Tidal volume expands into the inspiratory and

expiratory reserve volume.
 ➢ Vital capacity and FEV1 unchanged , FRC reduced., O2
reserves reduced

➢ Increased maternal 2,3 DPG in RBC-shifts oxygen-Hb dissociation curve to the right
Oxygen consumption increase by 20%

➢Rise in arterial oxygen levels from 100 to 110 mmHg.

➢Decrease in PaCo2 from 40 to 27-32 mmHg.

Respiratory alkalosis

➢pH is normal to slightly alkalotic (usually between 7.40 to 7.45)

➢Compensatory renal excretion of bicarbonate.

❖ Renal

Renal size increases by 1-1.5 cm

Pelvicalyceal system dilatation-early as 6 weeks

➢ Hydronephrosis occurs on the right in 90% of cases

Uterine enlargement may cause the ureters to become elongated, tortuous,
and displaced laterally as pregnancy advances.
VU reflux

➢ Bladder flaccidity

➢ Decreased intraureteral pressure

Glomerular function

Increase in GFR is observed within one month of conception and

peaks at approximately 40-50% above baseline levels by the early
second trimester and then declines slightly toward term

➢ Fall in S. creatinine by an average of 0.4 mg/dL

➢ 300 mg/24 hr of urinary protein and 20 mg/24hr of albumin as the upper limit of normal
in pregnancy

➢ Increased natriuresis and Na reabsorption . Serum levels of Na

Decrease

Reductions in reabsorption of glucose, amino acids, and beta microglobulin

➢ Higher rates of urinary excretion with glycosuria and aminoaciduria in the absence of
hyperglycaemia or renal disease

Urinary frequency

➢ Increases in the first trimester; mechanical compression of the bladder by the enlarged
uterus is not likely to be the primary cause

➢ Nocturia is common and increases with advancing gestation

➢ Several studies have described an increase in urgency and urinary incontinence during
pregnancy

❖ Gastrointestinal system

➢Increase in appetite

➢Spongy gums

➢Oesophageal reflux common

➢Gastric secretion and motility reduced

➢Doubling of stomach emptying time

➢Constipation

➢Slower emptying of gall bladder

 ❖ Endocrine system

Human chorionic gonadotrophin(HCG)

➢Syncytiotrophoblast secretes HCG

➢Appears by 8-9 d after ovulation; Maximum levels at 10-12

wks; low levels by 16-20wks

➢Glycoprotein similar to LH, FSH and TSH

➢ Prevents involution of corpus luteum at the end of the monthly

menstrual cycle maintaining the decidual nature of the
endometrium

Placental endocrine functions

Oestrogen

➢ Secreted by CL and placenta

Progesterone

➢ Secreted by CL and placenta

Human placental lactogen (HPL)

Human chorionic somatomammotropin

➢ Lactogenic

➢ Secreted by placenta around 5th wk

➢ Peaks around 30 weeks

➢ Increases progressively throughout gestation

➢ Effects:
-↓ maternal insulin sensitivity leading to an increase in maternal blood
glucose levels.
-↓ maternal glucose utilization, which helps ensure adequate fetal nutrition
-↑ lipolysis with the release of free fatty acids
➢ Structure and function similar to GH

GnRH
There is a decline in circulating gonadotrophin concentrations across
gestation with a progressively diminishing response to GnRH

➢ Inhibitory effect of oestrogen and progesterone

➢Effect of the high maternal serum levels of inhibin A and inhibin

B produced by placenta and fetal membranes

Pituitary gland
The anterior lobe of the pituitary gland enlarges up to threefold
during gestation because of hyperplasia and hypertrophy.
Proliferation of prolactin producing cells
Pituitary growth hormone production is reduced; Placental growth
hormone production is increased.
Net increase in serum growth hormone levels

Pituitary hormones

➢ Increase in serum ACTH concentrations probably in response to

CRH produced by trophoblasts

➢ Its concentration in maternal circulation is high and rises

exponentially throughout pregnancy

➢ The serum prolactin concentration increases throughout pregnancy,

reaching a peak at delivery (10 fold) to prepare the breast for
lactation.

➢ Oxytocin involved in the process of parturition and the "let down"

response during lactation rise continuously across gestation
Cortisol
Increase in cortisol
Total cortisol increase by the end of the first trimester and are 3
times higher than the non pregnant values by the end of
pregnancy
Increase in ACTH and CRH (produced by the placenta)
Diurnal variations in ACTH and cortisol are maintained

Thyroid physiology

Increased production of thyroxine binding globulin from the liver

Total T4 and T3 are increased
Free fraction remains unaltered
Iodine deficiency
Transfer across the placenta
Increased excretion in the urine
WHO recommendation – Iodine intake 150-200 mg/day

The Renin Angiotensin Aldosterone

system
The renin-angiotensin-aldosterone system is stimulated during
pregnancy because of the associated reductions in vascular resistance
and blood pressure

➢ A striking increase in aldosterone levels is observed by the eighth

week of pregnancy and continues to rise
Glucose metabolism
Hyperplasia of pancreatic beta cells, increased insulin secretion, and
an early increase in insulin sensitivity followed by progressive insulin
resistance

➢ Insulin resistance begins in the second trimester and peaks in the

third trimester (doubling of insulin from the end of 1st trimester –

end of third trimester)

It results from increased placental secretion of diabetogenic hormones
including growth hormone, cortisol, HPL, prolactin and progesterone

Insulin resistance and the relative hypoglycaemia of pregnant women

results in increased lipolysis, which allows the mother to:

➢ Preferentially use free fatty acids, triglycerides, ketone bodies for fuel.

➢ Preserve much of the available glucose

Minimize protein catabolism.

Glucose metabolism in pregnancy

First half of pregnancy (Anabolic)

Pancreatic beta cell hyperplasia – hyperinsulinaemia
Increased uptake and storage of glucose
Second half of pregnancy (Catabolic)
Placental hormones block glucose receptors and cause insulin
resistance

Increased lipolysis
Increased gluconeogenesis
 Decreased glycogenesis

Osmoregulation

Systemic arterial vasodilatation

➢stimulates vasopressin release and upregulation of AQP2

➢Stimulates thirst

Plasma osmolality declines below the osmotic thirst threshold, and a new
steady state is achieved

➢There is a decrease in the osmotic thresholds for thirst and arginine

vasopressin (AVP) release

➢Plasma osmolality falls early in gestation to around 280 mOsm/Kg

➢Total body water increases by 6–8 L, most of which is extracellular

Haematology

Red Blood Cells

➢ 3 fold rise in erythropoietin; 50% rise

➢ Physiological haemodilution maximal at 28-32 weeks.

White Blood Cells

➢ WBC peaks at 30 weeks and plateau during the third trimester.

➢ Further increase in labour and may rise to 40.0x109/L in uncomplicated

pregnancy.

➢ The count returns to non pregnant levels by 6 days postpartum

Platelets
➢ Fall progressively

➢ 5-10% mild thrombocytopenia

Clotting factors- Physiological hypercoagulable stage

From T1- 12 weeks postpartum

➢ Factors VII, VIII, IX, X, XII, Von Willebrand factor and plasma fibrinogen

rise.(The latter by 50%)

➢ Antithrombin and protein S decrease slightly.

➢ Plasma fibrinolytic activity is reduced during pregnancy, remains low during

labour and delivery, and returns to normal early after placental delivery.

➢ Invitro APTT, PT and TT remain normal.

➢ Increase in ESR four fold ( increase in globulin and fibrinogen)

DVT and pulmonary embolism

1/3rd of pregnancy related DVT occur postpartum

- Most cases within 1st four weeks
- Elective CS doubles the risk; further doubling with Em LSCS
- Risk remains for 12 weeks postpartum
- Mostly DVT of lower limbs
- L > R – Due to compression of the left iliac vein by the L iliac
artery and ovarian artery
½ of pregnancy related PE occur postpartum.
Half of antenatal VTE occur prior to 15 weeks
Physiological changes at birth
Essential Steps in Transition

• Clearance of foetal lung fluid

• Surfactant secretion, and breathing

• Transition of fetal to neonatal circulation

• Decrease in pulmonary vascular resistance and increased pulmonary blood flow

• Endocrine support of the transition

Foetal Circulation

• Oxygenated blood is preferentially delivered to brain, heart and upper torso

• Lower body and placenta receive blood with low oxygen tension
 • Mediated through 2 parallel circulations via intra and extra-cardiac shunts

• Oxygenated blood from placenta enters IVC via umbilical vein either through liver/
ductus venosus

• This blood is diverted directly to left atrium via foramen ovale and supplies brain and
upper torso

• Deoxygenated blood from superior vena cava and myocardium (via coronary sinus)
enters right ventricle

• This deoxygenated blood is directed via ductus arteriosus to lower body and umbilical
arteries (for re-oxygenation)

• 8-10% of cardiac output passes through high resistance pulmonary circulation

Physiological changes at birth

Umbilical cord clamping

• Low resistance placental vascular bed removed

• Increased systemic vascular resistance
• Reduced blood flow through IVC (hence ductus venosus) leads to spontaneous passive
closure over next 3-7 days

Lung expansion

• Drops pulmonary vascular resistance

• More blood enters left atrium increasing left atrial pressure more than right atrial
pressure
• This leads to spontaneous closure of foramen ovale following first few breaths
Ductus arteriosus

• Rise in SVR and drop in PVR results in reversal of blood flow through ductus
• Reduced blood flow and increased oxygen content in ductus leads to spontaneous
closure 12-24 hours after birth

Lung adaptation

• Most essential adaptation to birth – initiation of breathing

 • Airspaces of the fetal lung are filled with foetal lung fluid

• Lung fluid is essential for normal growth of foetal lung

• Natural birth process and cortisol, thyroid hormones and catecholamine all shut down
secretion of foetal lung fluid in preparation for first breath

First breath

• Clamping of the cord leads to disruption of oxygenated blood supply

• Leading to change in pO2 and pCO2
• Acidotic state stimulates respiratory centre stimulating medullary and carotid artery
chemoreceptors resulting in first breath
• However, new-born will not initiate breathing if hypoxia is severe

Surfactant and lung adaptation

• At term, surfactant is secreted into the fetal lung fluid

• Labor increases surfactant concentration in the fetal lung fluid as fluid decreases

• Catecholamines stimulate pulmonary beta-receptors increasing surfactant secretion

Endocrine adaptation

• Conversion of T4 to T3 increases
• Catecholamine release by adrenal increases
• Glucose metabolic pathways in liver mature
• Gut digestive capacity increases (enzyme induction)
• β-adrenergic receptor density increases in heart and lungs
• Surfactant system in lungs is induced to mature

Cortisol

• Major regulatory hormone for terminal maturation of the fetus

• Cortisol surge around birth facilitate neonatal adaptation

 • Activates sodium pump that clears fetal lung fluid at birth

Catecholamine surge

• Responsible for the increase in blood pressure following birth

• Adaption of energy metabolism – glucose and fatty acids
• Initiation of thermogenesis from brown fat

➢ Increased cortisol and catecholamines increase cardiac output

➢ Provide for increases in basal metabolism, work of breathing, and thermogenesis

Thyroid hormones

• At term, TSH, T4 and T3 increase and rT3 decreases

• At birth, TSH quickly peaks and decreases, and T3 and T4 increase in response to
increased cortisol, cord clamping and cold stimulus
• T3 and cortisol activate Na+, K+, ATPase that helps clear fetal lung fluid after birth

Metabolic adaptation

• Trans-placental transfer of glucose is the main source of energy in fetus

• Fetus has minimal gluconeogenesis
• More glycogen and fat are stored in T3 anticipating delivery
• Following delivery, normal glucose supply falls
• The surge in cortisol and catecholamines activates catabolism of fatty acids and
gluconeogenesis

Thermoregulation

• Although fetus produces heat, heat is effectively dissipated across the placenta and
fetal membranes in-utero
• Towards term, the fetus accumulates brown adipose tissues
• They act as sources of thermogenesis in the term neonate and provide thermo
protection
Medical complications of pregnancy
❖ Renal disease
❖ Diabetes mellitus
❖ Other endocrinology disorders
❖ Heart diseases
❖ Respiratory disease
❖ Neurological disorders
❖ Haematological abnormalities
❖ Gastroenterology disorders
❖ Liver disease
❖ Connective tissue disease
❖ Skin disease

➢ Why medical disorders in pregnancy important?

Most of the medical disorders are responsible for the MATERNAL MORTALITY & MATERNAL
MORBILITY in recent time.

Eg : Heart diseases are the commonest non obstructive cause for the maternal deaths all over
the world.

1. HEART DISEASE

When there is a mother with the heart disease, preconception care is very important (not
only in the heart disease but also in every medical disorder)

Why preconception care is important?

❖ By the time of start of the pregnancy, she would have to optimize the medical
conditions to success & to go through the pregnancy smoothly with the minimal
complications for the mother and the fetus.

Preconception care that related to the heart disease

• Multidisciplinary management – obstetrician, neonatologist, cardiologist/cardiac

surgeon, paediatric cardiac surgeon, Haematologist
• Optimise patient’s cardiac status – By modifying the drugs
• Optimise Haemoglobin – to prevent the heart from the anaemic condition (HF,
Arrhythmias, HPT)
• Risk of heart disease in the fetus – detection can be done through the fetal echo

➢risk higher if mother has congenital heart disease

➢risk higher for outflow tract lesions

➢Marfan and HOCM-AD inheritance

Contraindications to pregnancy (WHO IV)

•Pulmonary hypertension of any cause
•Left ventricular dysfunction LVEF<30% NYHA III/IV
•H/O peripartum cardiomyopathy with residual impairment of cardiac function
•Severe MS/symptomatic severe AS
•Marfan syndrome with marked aortic root dilatation

❖ If there’s a woman who wants to pregnant with the above condition should counsel,
should offer sterilization.
❖ But if these conditions present during the pregnancy - there is a place for the
termination of the pregnancy. The reason is the high mortality rate for mother if these
conditions are continuing during the pregnancy.
Congenital heart disease
•Commonest lesions

➢ASD/VSD/PDA

➢Marfan syndrome

⁻ C/I if aortic root>45mm

⁻ Regular echocardiograms to monitor aortic diameter
⁻ ElecSC if aortic root >45mm

Cyanotic congenital heart disease

•Risk
▪ worsening cyanosis (increased R-L shunting) ->increased thrombophilic risk
▪ increased risk of fetal loss and IUGR (If SaO2<85%)
▪ pulmonary hypertension -> Cyanotic congenital heart disease

Pregnancy outcome improved if

▪ Resting O2 sat >85%
▪ Hb <18g/dl
▪ Haematocrit <55%
▪ Thromboprophylaxis – for better outcomes

Acquired heart disease

•Rheumatic heart disease is the commonest

➢MS - Can deteriorate during pregnancy even though asymptomatic at the beginning of
pregnancy, due to increase load to the heart

⁻ Tachycardia triggers this.

➢Regurgitant valve disease-usually well tolerated in absence of LV dysfunction

Infective endocarditis
•Antibiotic prophylaxis are not routinely indicated
Except if the patient has:

➢H/O IE

➢High risk lesion (artificial heart valves)

Peripartum cardiomyopathy
•Development of heart failure occurs during the last month of pregnancy up to 5 months
postpartum in the absence of a known cause.
•Risk factors

➢Multiple pregnancy

➢Multiparity

➢Gestational HT

➢Advanced maternal age

▪ Normally these patients present with the signs and symptoms of the heart failure.
E.g.: SOB, fever, Chet pain
▪ As it carries high mortality rate, cardiac failure should manage appropriately –
diuretics & other drugs
▪ Not only that, inhibition of prolactin levels also benefited due high level of prolactin
causes PPCM.
E.g.: carbergoline, bromocriptine

Aetiology - Autoimmune
➢myocarditis on endo myocardial biopsy

•Management-
Conventional treatment
•50% -full recovery
•Risk of recurrence in future pregnancies even if fully recovered
•C/I for pregnancy if residual LV dysfunction

Artificial heart valves

Anticoagulation
❖Heparin/warfarin?
➢Risk of maternal thrombosis is higher with heparin
➢Risk of teratogenesis, miscarriage, stillbirth and IC bleed in the fetus is higher with use of
warfarin.

▪ When the pregnant mother with artificial heart valve, there is a risk for the thrombosis
therefore anticoagulants are used. Better one is Warfarin due to the heparin causes the
valvular thrombosis. Here warfarin cannot use in the 1st trimester due its teratogenicity, it has
the ability to cross the placenta and leads to ICH throughout the pregnancy. As the heparin
doesn’t cross the placenta, during this period heparin is used.

Anticoagulation

•3 broad anticoagulation regimes

➢Warfarin throughout pregnancy

➢Heparin between 6-12 weeks followed by warfarin
➢Heparin throughout pregnancy

Thyroid dysfunction in pregnancy

Hypothyroidism in pregnancy
•Autoimmune thyroid dysfunction
•Iodine deficiency

Overt hypothyroidism
•Gestational hypertension
•Placental abruption
•Miscarriage
•Premature birth
•Low birth weight
•Neonatal respiratory distress
•Impaired neurocognitive development in the offspring

Subclinical hypothyroidism
• Shown to be associated with adverse pregnancy outcomes
• Treatment indicated

Management of hypothyroidism

⁻ Levothyroxine replacement
⁻ TFT should be monitored 6 weekly

Hyperthyroidism in pregnancy

• Graves’ disease
• Toxic multinodular
• Toxic adenoma

Overt hyperthyroidism

• Gestational hypertension
• Thyroid storm
• Maternal congestive heart failure
• Miscarriage
• Prematurity
• Low birth weight
• Fetal growth restriction
• Stillbirth
• Neonatal goitre

Hyperthyroidism
• Aim to maintain thyroxin in an upper normal range with the minimum dose of antithyroid
medication

Subclinical hyperthyroidism
• Treatment not indicated

Management of hyperthyroidism
Antithyroid drugs

• Propylthiouracil of pregnancy.
• Carbimazole
Carbimazole contraindicates in first trimester; can continue from 2 nd trimester

KEY LEARNING POINTS

• Woman with medical conditions that adversely affect pregnancy outcome, should be
offered pre pregnancy counselling by appropriately experienced healthcare professionals.
• Woman with medical problems that preclude safe pregnancy, should be offered safe,
effective and appropriate contraception.
• Asthma is the commonest chronic disease encountered in pregnancy.
• Eisenmenger’s syndrome and PH are associated with a risk of maternal mortality of
up to 50% in pregnancy.
• Woman found to be hypertensive in the first half of pregnancy require investigation
for possible underlying causes.
• Women with pre-existing hypertension are at increased risk of superimposed pre-
eclampsia, FGR and placental abruption.
• Women who become pregnant with serum creatinine values above 124 μmol/l, have
an increased risk of accelerated decline in renal function and poor outcome of pregnancy.
• Pre-existing diabetes increases maternal and fetal obstetric morbidity.
• The incidence of fetal macrosomia in diabetes can be reduced through good blood
glucose control.
• The risk of perinatal and maternal morbidity is increased in pregnancies complicated
by sickle cell disease.
• The main issue for pregnant women with epilepsy relates to the teratogenic risk of
anticonvulsant drugs.
 Gestational Diabetes

Hyperglycemia in
pregnancy

Pre existing diabetes Gestational diabetes

Previously Previously
diagnosed undiagnosed

Type 1 DM Type 2 DM
Pre-gestational Diabetes Mellitus
-If the woman already has Type I or II DM before pregnancy
-Universal screening is done at the booking visit using standard criteria used for non-pregnant
adults
-FBS ≥ 126 mg/dL OR PPBS ≥ 200 mg/dL OR HbA1c ≥ 6.5%

Preconceptional Care
• Screening to detect DM before pregnancy
• Optimize HbA1c <6.5%
• Baseline screening for retinopathy, nephropathy (s. creatinine, proteinuria, eGFR) and
cardiac screening (ECG)
• 5mg/day folic acid
• Change over to non-teratogenic drugs (metformin, insulin)
• Self-monitoring is recommended
• General health advice (optimize BMI, stop smoking, minimize alcohol)

Gestational Diabetes Mellitus

• Carbohydrate intolerance the onset or detection that occurs for the first time during
pregnancy
• Universal screening is done in Sri Lanka
• Diagnosed by 75g OGTT done at around 24-28 weeks of gestation (also the best
screening test)
• FPG ≥ 100mg/dL, 1hr PG ≥ 180 mg/dL, 2hr PG ≥ 140 mg/dL

Aetiology

During pregnancy, diabetogenic hormones are secreted maximally at around 24-28 weeks
(hPL, progesterone, GH)
These hormones have an insulin resistance effect that causes GDM
 Complications of DM in Pregnancy

Maternal Foetal Neonatal

UTI Miscarriage Polycythemia
Recurrent vulvovaginal Congenital abnormalities Jaundice
candidiasis
PIH/pre eclampsia Pre term labour Hypoglycemia
Obstructed labour Polyhydroamnios Hypomagnesemia
Operative deliveries Macrosomia Hypocalcemia
Retinopathy IUGR Cardiomegaly
Nephropathy IUD Birth trauma
Cardiac disease RDS

Management of GDM in pregnancy

Following diagnosis Blood glucose monitoring

• Counsel the woman
• Medical nutrition therapy
• Physical activity
• Pharmacotherapy if needed
• Blood glucose monitoring
• Arrange follow up
• Self-monitoring of blood glucose -the best
• 6-point blood sugar series
• 4-point blood sugar series
The 6 points
FBS in the morning
Post breakfast ( 1hr after the start of meal)
½ hr pre lunch
Post lunch

Pharmacotherapy ½ he wore dinner

• Metformin Post dinner

• Insulin
Basal bolus insulin regimen – 3 doses of short acting insulin + long
acting insulin
Mixtard insulin regimen – 2 doses of insulin in the morning and night

Follow up

• Frequent visits in the antenatal clinic (2 weekly) - reviewed by both obstetrician and
endocrinologist/physician
• At every visit, drug and dietary compliance should be asked for and reinforced
• Fetal monitoring for growth - to detect macrosomia
Delivery
• Mode of delivery – decided by obstetric indications
• Timing of delivery
-If no evidence of macrosomia and good metabolic control - Can wait until 40 weeks of
gestation
- If evidence of macrosomia or poor glycemic control - Deliver by term (because there
have been cases of sudden IUD due to cardiomyopathy)
Intrapartum care
• Check FBS on the morning of the delivery - If FBS > 126 mg/dl need to start on an insulin
dextrose infusion and monitor capillary blood sugar hourly during labour

Postpartum care
• Stop the insulin dextrose infusion
• Recheck the FBS or PPBS in the first 24 hours
• Encourage early and frequent breast feeding – due to risk of neonatal Hypoglycemia
• Start hypoglycemic agents only if
• - FBS > 126 mg/dl or - PPBS > 200 mg/dl persistently (non pregnant cut off values since
the placental has been delivered now)
• Review all women with FBS in 6 weeks
• Aim is to stop all Hypoglycemic agents before discharge

Postpartum review
• At the 6-week postpartum review, - FBS < 126 mg/dl
• Can perform OGTT too but not HbA1c as her plasma glucose was under control
during pregnancy
• Reassure that the woman had GDM
• The risk of development of future type 2 DM remains high
• Maintaining ideal BMI, through regular exercise and healthy diet will reduce this
risk
• Advise on yearly FBS assessment
• Assessing for DM prior to planning on a pregnancy

Neonatal Hypoglycemia

• If gestational DM is not properly managed in pregnancy it can lead to development of

neonatal hypoglycemia
• This is because the increased glucose in the mother passes to the fetus and results in
the fetus going into a state of hyperinsulinemia
• After delivery, this hyperinsulinemia state will result in neonatal hypoglycemia
• This hyperglycemia is also the reason for fetal macrosomia
• Mild hypoglycemia – 47mg/dL, severe hypoglycemia – 36mg/dL
• Blood glucose needs to be checked after each feed and monitored for hypoglycemia
Glucose needs to be given to the neonate either orally or via IV access
Neonatal Jaundice

• Hyperbilirubinemia occurs in 25% of neonates born to diabetic mothers (Medscape)

• Prematurity and polycythemia are the primary contributing factors
There is a risk of the neonate developing kernicterus

Treatment is by phototherapy and may even require exchange transfusions

(if the bilirubin levels are markedly high)
 Hypertension in pregnancy

SEQ – Batch 24th Repeat

Batch 23rd Proper
Definitions of hypertensive disorders inpregnancy

• Chronic hypertension – Hypertension that is present before 20 weeks ofpregnancy. It

can be primary or secondary in etiology.

• Gestational hypertension – New hypertension occurring after 20 weeksof pregnancy,

without significant proteinuria.

• Pre-eclampsia – New hypertension occurring after 20 weeks of pregnancy with

significant proteinuria. Excretion of 300 mg in a 24 hr urine collection or albumin more than
2+ in a urine ward test.

• Eclampsia – Occurrence of convulsions in a patient with eclampsia.

• Severe pre-eclampsia – Pre eclampsia with severe hypertension and/or with

symptoms, and/or biochemical, and/or hematological impairment
•considered
HELLP syndrome – Hemolysis, Elevated liver enzymes and lowplatelets count. This is
as severe pre-eclampsia.

• Mild hypertension – Diastolic BP 90-99 mmHg

• Systolic BP 140-149 mmHg

• Moderate hypertension – Diastolic BP 100 – 109 mmHg

• Systolic BP 150 – 159 mmHg

• Severe hypertension – Diastolic BP 110 mmHg or greater

• Systolic BP 160 mmHg or greater

• Transient gestational hypertension – Hypertension develops at any stage that resolves

without treatment. Not a benign disorder. Needextra monitoring throughout the pregnancy.
•BP monitoring
White coat hypertension – Hypertension that occurs exclusively inmedical setting. 24 hr
is needed. Should relieve theanxiety.

•at otherMasked
times.
hypertension – Form of chronic hypertension. BP normal atclinic but Elevated
 High risk factors Moderate risk factors
CKD Age more than 40
Autoimmune disease (SLE, High BMI
antiphospholipid syndrome)
DM type 1 or 2 Multiple pregnancy
HTN in previous pregnancies Primiparity
Chronic HTN after last pregnancy Pregnancy interval more than 10
years

Chronic hypertension inpregnancy

• Before conception patients should be treated and Optimizer organ function.

• Stop- ACE Inhibitors, ARB, Statins, Chlorothiazide as these cause congenital
abnormalities.
• Ask to reduce salt consumption.
• Management – 75 mg aspirin daily from 12 weeks if they have one
high risk factor or more than one moderaterisk factor for development of
pre-eclampsia.
• In Chronic HTN in pregnancy…

risk factors to develop pre eclampsia

• Recommended drugs _ Methyldopa, Nifedipine, Labetolol
• In uncomplicated chronic HTN aim is to keep BP below 150/100 mmHg
• In women with target organ damage 2 ry to chronic HTN BP should be
maintainedbelow 140/90 mmHg.

• Fetal monitoring – USS scan for fetal growth amniotic fluid volume
• Umbilical artery Doppler velocimetry between 28-30 Weeks and 32-34 weeks)
• Tests should be repeated if clinically indicated
• CTG is done if fetal activity is an abnormal
• Delivery best done at 38 weeks
• EARLIEAR DELIVERY IS INDICATED IF… BP 160/110 mmHg or Complications present
• C section done for obstetrics indications, Labour can be induced.
• Postnatally can commence previous antihypertensive drugs.
Gestational hypertension inpregnancy
Gestational hypertension…

• Blood tests that are carried out – Liver function test, Coagulation profile,

• Renal function Test (These tests should be

carried out frequently if resultsImpaired)

• Drugs that can be used – Methyldopa, Nifedipine, Labetolol

• Delivery – If BP is below 160/110 mmHg delivered at 37-38 weeks

• EARLIEAR DELIVERY IS INDICATED IF severe gestational

hypertension which isrefractory for treatment or if maternal or
foetal complications develops.

• Labour can be induced and C SECTION is indicated in severe pre-

eclampsia and forobstetrics reasons only.

• Postnatally Antihypertensive treatment should be continued. Referral to aphysician if

BP is not normal by 6 weeks.
Pre-eclampsia in pregnancy

• Pathophysiology
•uterusand
In normal pregnancy extravillous cytotrophoblasts invade the
spiral arteries transforming them into large vessels of low
resistance.

•spiral arteries
But in pre-eclampsia there is a failure of trophoblast invasion and transformation of
which causes high resistance bloodflow in spiral arteries.

Abnormal placentation in pre-eclampsia

SYMPTOMS AND SIGNS OF PRE ECLAMPSIA

• In preeclampsia Poorly perfused placenta cause IUGR, fetal death and release of pro
inflammatory proteins.

•which leads
These pro inflammatory proteins cause endothelial dysfunction inmaternal circulation
to vasoconstriction giving rise tohypertension.
•severe pre
Local vasospasm in maternal circulation can give rise to varioussymptoms and signs in
eclampsia.
Complications in pre-eclampsia…

• Maternal….
• CNS – Cerebral edema, Corticol blindness, Cerebral
haemorrhage ,Eclampsia
• Renal – Renal tubular necrosis, Renal Corticol necrosis, Acute Renal failure
• RS- Pulmonary edema
• Liver – periportal necrosis, Subscapular haematoma and rupture,
HELLPsyndrome
• Coagulation system – DIC and Microangiopathic heamolysis

Placental abruption and fetal IUGR, hypoxemia and IUD

Edema in pre eclampsia pathophysiology
• Pretein excretion in kidneys cause less amount
of protein invasculature.
HELLP SYNDROME –

• Considered as severe pre eclampsia.

•thrombusPathophysiology – Due to severe hypertension there is endothelial injury and
formation in maternal circulation which give riseto low platelet count , increased
heamolysis and Elevated liver enzymes.
• Investigations done in pre eclampsia
Management of pre eclampsia

• Definitive treatment is delivery

• But aim is to prolong the pregnancy and a safe successful delivery

• For that Control BP, supportive treatment and prevention of eclampsia isessential.

• Antihypertensives should be started if DBP is above 100 mmHg or if othercomplications

exist even in low BP.

• Should start - iv Labetolol and hydralazine in severe pre eclampsia

• Oral – Labetolol, Methyldopa and Nifedipine

• Urine is tested for albumin daily, 24 hr Protein excretion is tested once a week

• Perform FBC, Coagulation profile, Renal function test, Liver function test twice orthrice
weekly.

• Uterine artery doppler studies- Persistent Diastolic notch at 20 weeks has a 20%chance
of pre eclampsia. USS and amniotic fluid volume is done more frequentlyif required.
Timing of delivery-

If there are no maternal or foetal complications and BP can be controlled with

antihypertensives delivery is planned between 34-37weeks depending on risk factors.
Indications for delivery before 34 weeks in pre eclampsia -
•Postnatally Antihypertensives are continued

•Dose is reduced if BP reaches 130/80 MmHg

Referral to a physician is necessary if BP is not normal by 6 weeks.

Eclampsia in pregnancy

•Diagnosed by occurrence of convulsions in association with pre eclampsia.

•Definitive treatment is delivery as soon as possible after stabilising the patient, if foetus is
alive, irrespective of thematurity.

•If the foetus is already dead eclampsia will improve and delivery is delayed until maternal
conditions are stable.

•Maintenance of air way…

•This is the first step.. Turn to lateral side, suck out secretions, insert an oropharygeal airway
and give oxygen

•PREVENTION OF FITS…

•MgSO4 is the therapy of choice for controlling seizures.

•Loading dose of 4 g should be given by infusion pump over 5-10 minutes, followed by a
maintenance dose of 1 g perhour for 24 hrs after the last seizure or delivery whichever the
long.
•Cont… .

•Loss of deep tendon reflex is the first sign of magnesium toxicity. And this is followed by

respiratory depression.

•Treatment is monitored by hourly assessment of the patellarreflex and oxygen saturation.

•Monitoring of serum levels of MgSO4 is needed only whenpatient has oliguria.

•First step in treating MgSO4 toxicity is stop the drug.

•Then give 10 mg of 10% calcium gluconate intravenously.

•Treatment of severe hypertension in eclampsia is managed inthe same way as in pre eclampsia.
But sublingual Nifedipine cannot be given in patients who are unconscious.
MONITOTING OF MOTHER AND FOETUS…

• Admit to ICU
•intake output
Do a Coagulation profile, Liver function test, Renal function test andmaintain a hourly
chart.

• Perform USS scan, Umbilical artery doppler

• Carry out foetal heart rate monitoring continuously.

• Deliver as soon as possible.

Delivery and postnatalcareineclampsia
Usually 1/3 of fits occur during post-partum period.

•Pulmonary
In managing eclampsia and pre-eclampsia managing fluids is very important as
edema is a major cause of morbidity.

• Fluid restriction… 80 ml per hour given, CVP if complicated.

• Prevention of pre eclampsia….

• Low dose aspirin 150 mg for high risk women.

• In the phase of low calcium intake (<600 mg a day) use calcium 1.2 to

2.5 g per day.

•using a combination
Pregnant women should exercise at least 3 days per week for anaverage of 50 minutes
of aerobic exercises,strength and flexibility training ..
Quick recap…
Recap…
HYPEREMESIS GRAVIDARUM
(SEQ – 22nd Repeat Question 02)
• Severe form of nausea and /or vomiting during early pregnancy where there are no
other causes.
• Affects about 0.3-3.6% of pregnant women.
• Thought to be associated with rising levels of beta-HCG hormone levels.
• specially conditions like,
- Gestational trophoblastic diseases
- Multiple pregnancy

Diagnostic criteria

• Characterized by severe protracted nausea and vomiting associated with the triad of;
1) Weight loss of more than 5% of pre-pregnancy weight.
2) Dehydration
3) Electrolyte imbalances such as Hyponatremia, Hypokalemia.

• Measure for the severity of nausea & vomiting by Rhodex Index & PUQE [Pregnancy-
Unique Quantification of Emesis] Index
PUQE score

Clinical presentation
Nausea Sleep disturbances
Vomiting Anxiety & Depression
Ptyalism Fatigue
Weakness
Dizziness
Differential Diagnosis
Peptic ulcers
Gastroenteritis
Hepatitis
Pancreatitis
Metabolic conditions
Neurological conditions
Drug induced nausea and vomiting

Investigations
❖ Urine dipstick (quantify ketonuria as 1+ ketones or more) - HG causes increase ketone
body formation and that leads to weight loss and excess vomiting leads to body fluid volume
depletion
❖ MSU – to exclude UTI
❖ Urea and electrolytes– to identify Hyponatremia, Hypokalemia & Metabolic
hypochloremic alkalosis due to dehydration
❖ Full blood count - due to severe dehydration which increases the
haematocrit levels
❖ Blood glucose monitoring -to exclude DKA if patient is diabetic
❖ USS- to confirm viable IUP, to exclude multiple pregnancy and trophoblastic disease,
identify the fetal risks like IUGR & fetal death in cases with Wernicke ’s encephalopathy.
❖ In refractory cases or Hx of previous admissions, check LFT, TFT, Amylase, ABG
❖ H. pylori antibodies – to exclude the H. pylori infection causes peptic ulcers

Management

1) Manage in community with antiemetics – Mild NVP

2) Ambulatory day care management (which provides parenteral fluids, parenteral vitamins,
antiemetics)
When community or primary care measures have failed and where PUQE score is less than
13.

3) Inpatient management- Should be considered if there is atleast 1 of the followings.

• Continued nausea and vomiting and inabiity to keep down oral antiemetics
• Continued nausea and vomiting associated with ketoneuria and/or weight
loss,despite oral antiemetics.
• Confirmed or suspected co-morbidity.

4) Termination of the pregnancy.

Pharmacological Agents
First line - Antihistamines (H1 receptor antagonist) and Phenothiazines
Second line - Metocloparamide, Ondansetron
Third line - Corticosteroides
• In persistant vomiting IV, rectal, subcutaneous. IM routes can be used.
• If single antiemetic not respond, should use combination of different drugs.

Rehydration is the most important part of the management of HG

▪ The most important intervention is likely to be appropriate intravenous fluid and
electrolyte replacement.
▪ Most women admitted to hospital with HG are hyponatremic, hyperchloremic,
hypokalemic and ketotic, it seems appropriate to use normal saline and potassium chloride.
▪ Dextrose-containing solutions can precipitate Wernicke’s encephalopathy in thiamine-
deficient states hence, each day intravenous dextrose is administered, and high doses of
parenteral thiamine should be given to prevent Wernicke’s encephalopathy.

Monitoring
▪ Urea and serum electrolyte levels should be checked daily in women requiring IV
fluids.
▪ H2 receptor antagonists or proton pump inhibitors may be used for women
developing gastro esophageal reflux, esophagitis or gastritis.
▪ Thiamine supplementation (oral/IV) [polybion] should be given to all women
admitted with prolonged vomiting, specially before administration of dextrose or parenteral
nutrition.
▪ Women admitted with HG should be offered thromboprophylaxis with LMW heparin
unless there are specific contraindications.
▪ Women with previous or current NVP or HG should consider avoiding iron containing
preparations if these exacerbate symptoms.

Adverse effects relate with management

• Drug induced extrapyramidal symptoms
• Oculogyric crisis
• Wernicke’s encephalopathy

Discharge and follow up

▪ Women with continued symptoms into the late second or third trimester – offer serial
scans to monitor fetal growth.
▪ At the discharge - Advise to continue with their antiemetics
- Advice about patient support groups.
▪ Women with previous HG – advice the risk of recurrence in future pregnancies.
(Women with HG are 3 to 6 times more likely than women with nausea and vomiting in
pregnancy to have low quality of life)
▪ Depending upon the clinical and social circumstances – Organize physiological and
social support.
Complications of pregnancy
Early pregnancy problems
1. Miscarriage
2. Ectopic pregnancy
3. Gestational trophoblastic disease
Miscarriage
A pregnancy that ends before 24 weeks of gestation
Causes

• Chromosomal abnormalities
• Medical / endocrine disorders
• Uterine abnormalities
• Infections
• Drugs / chemicals
5 Types of miscarriage

Types of miscarriage USS findings Cervical os in Clinical presentation

speculum
exm
Threatened Intrauterine pregnancy with closed Vaginal bleeding and
miscarriage fetal heart beat abdominal pain
Inevitable miscarriage Intrauterine pregnancy opened Vaginal bleeding and
without fetal heart beat abdominal pain
Incomplete Retained products of opened Vaginal bleeding and
miscarriage conception abdominal pain
Complete miscarriage Empty uterus (repeat hCG to closed No pain, bleeding
exclude ectopic pregnancy) resolved by now
Missed miscarriage Intrauterine pregnancy closed Asymptomatic (often
without fetal heart beat diagnosed at booking
visit)
Normal
pregnancy

Threatened MC

Inevitable MC

Complete MC

Incomplete MC
Missed MC
Management

• Establish the location and the gestation of the pregnancy

• Assess the blood loss and pain
• Blood group and Rhesus status

Expectant management Medical management Surgical management

Good Bad Good Bad Good Bad
1.Don’t 1.Unscheduled 1.Don’t 1.Will 1.Highest 1.Risk of
need need experience success rate surgery and
hospital 2.Take longer hospital pain and (95%) anesthesia
stay stay bleeding
3.Will 2.Can 2.Uterine
2.Avoid experience 2.Avoid 2.May need schedule perforation,
surgery pain andsurgery emergency the event Cervical
bleeding surgery (10%) damage
3.Feels 3.Can 3.Can
closer to 4.May need schedule shorten the 3.Use of
nature emergency the event waiting theatre time
surgery time
4.Can No pain /
shorten the bleeding
waiting
time
Await up to 2 weeks Administration of Under general anesthesia
Review in 2 weeks Misoprostol Cervical dilation and
•Bleeding happened – Is Review after bleeding evacuation of products of
the uterus empty •Has it completely expelled conception
•If no bleeding – Is the
pregnancy still intact

Pregnancy of Unknown Location (PUL)

• A TVS can show a IUGS Intra Uterine Gestational Sac) at around 5 weeks of gestation
• if we don’t see a pregnancy at that time and still hCG positive it’s PUL
• According to hCG can narrow down DDs as below
hCG <1500 hCG >1500
DD DD
Early IUP Ectopic pregnancy
Ongoing Failing IUP
Failing Early multiple pregnancy
Ectopic pregnancy
Management of PUL

• Make sure the woman is hemodynamically stable

• If ectopic is likely (hCG > 1500), inward care.
• Repeat the hCG in 48 hours
✓ >66% rise – likely IUP. Rescan when hCG >1500
✓ >15% drop – failing pregnancy. Review with urine pregnancy test in one week
✓ In-between – likely ectopic pregnancy. Manage accordingly
Ectopic pregnancy

• Implantation of a pregnancy outside the normal uterine cavity

• >98% implanted within the fallopian tubes
• Other rare sites: Interstitium of the tube, ovary, cervix, abdominal cavity

Heterotropic pregnancy:
“Pregnancies within and outside the cavity simultaneously”
(Rare < 1:15000)
Ectopic pregnancies causes

• Abnormal fallopian tube - Unable to transport the embryo

• Damage to the tube - Infection, Tubal surgery, Previous ectopic pregnancy
• Impair the function of the tube - Pelvic disease (endometriosis, PID), Adhesions due to
surgery, IUCD use, Pregnancy during Progesterone use
Presentation

• Mostly of abdominal pain / vaginal bleeding in early pregnancy

• Sometimes with acute presentation after rupture of a tube and haemoperitoneum
• Heamodynamically compromised
• Acute abdomen
• Diaphragmatic irritation
• Shoulder tip pain
Diagnosis
TVS assessment

• Seeing an IUP exclude (except in heterotropic preg)

• An empty uterus with an adnexal mass
• Look for size, FHB
• Free fluid is suggestive of ruptured ectopic.
Serum hCG rise
• In normal IUP hCG nearly doubles every 48 hours (>66% rise)
• In ectopic preg the rise is less
• A falling hCG means a failing pregnancy

Management
In future pregnancies

• The fertility may not be affected if the other tube is normal.

• Higher risk of repeat ectopics
-Even after salpingectomy
• Need to have a scan to locate pregnancy early

Expectant management Medical management Surgical management

Majority of EPs will fail FA antagonist inhibiting DNA Laparoscopy or
synthesis laparotomy
Monitor hCG till it is
undetectable Affect division of trophoblastic cells Salpingostomy or
salpingectomy
Administer IM Methotrexate and
monitor hCG levels (D0,4,7)

Expect a drop between D4-D7

If no adequate drop, may consider a

repeat dose
Avoid surgery
Suitable for Suitable for early gestations Suitable for
• Size haemodynamically not
Asymptomatic – no <3cm stable
bleeding • No
FHB Viable ectopic
Hemodynamically stable • hCG pregnancy (FHB seen)
<3000 IU/L
Early gestations (hCG < High hCG levels (>3000
1000) Need to avoid pregnancy for 3 IU/L)
months
Patient preference

Gestational trophoblastic disease

•A spectrum of interrelated but histological distinct tumours arising from the placenta.

WHO classification
Molar pregnancies Trophoblastic disease
 Hydatidiform mole ❖ Choriocarcinom
❖ Complet a
e ❖ Placental site
❖ Partial trophoplastic tumours
❖ Invasive ❖ Epethelioid
mole trophoblastic tumour

✓ The prognosis of most cases is excellent (nearly 100%)

✓ Incidence 1-2:1000
✓ Higher among Asians
Risk factors

• Extremes of reproductive age

• Previous miscarriage
• Previous GTN
• COCP use

Hydatidiform mole (molar pregnancy)

Feature Complete Partial

Karyotype 46, XX or 46, XY 46, XXX or 46, XXY
Fetus Absent Present
Fetal RBC Absent Can be present
Villous oedema Diffuse Focal
Trophoblastic proliferation Can be marked Focal
Typical diagnosis Molar gestation Missed MC
Post molar malignant sequelae 15% 4-6%

Diagnosis

• hCG level – can be very high

• US appearance
• Histological assessment of missed miscarriages

Treatment

• Suction curettage
• No misoprostol
Follow up

• Risk of neoplasia after evacuation

• Monitor for hCG drop every 2 weeks till it become undetectable
• Monitor monthly up to 6 months. May be shorter
• Avoid pregnancy to aid monitoring
Antepartum haemorrhage
Antepartum haemorrhage is bleeding from the genital tract after 24 weeks of gestation till
the delivery of the baby
Causes
Placental in origin- placenta praevia -nearly 1/3
- Placental abruption- nearly 1/3
Other causes
- Show- blood stained vaginal discharge
- Cervical bleeding – cervicitis, ectropion, post coital, cervical polyp
- Trauma
- Vulval varicocities
- Genital tract trauma
- Genital tract infections
- Vasa previa- some of the blood vessels that connect the umbilical cord to the placenta
lie over or near the entrance of the birth canal

Placental abruption
Premature separation of the normally situated placenta from the uterine wall, before the
birth of the child

Types of abruption
• Revealed abruption
• blood tracking down the cervix, present as bleeding PV
• >2/3 of abruptions
• External bleeding is present
• Concealed abruption
• Though there is a separation of the placenta, bleeding PV is not seen
• presents as uterine, maternal shock, fetal distress or fetal death without or
with minimal bleeding:
(After abruption blood clots form between the placenta and the uterus, with the blood clot
expand the placenta separates more reducing the oxygen supply more to the fetus)

Etiology
Defective trophoblastic invasion- with pre-eclampsia and fetal growth restrictions

Risk factors
• Direct abdominal trauma
• High parity
• Uterine over distention
• Polyhydramnions
• Multiple gestation
• Sudden decompression of the uterus
• After delivery of the first twin or after rupture of the membrane in
polyhydramnions, external cephalic version, abnormalities of placenta like circumvallate
placenta,
• Hypertension
• A direct cause
• Manifestation of poor trophoblastic invasion
• Three fold increased risk in chronic hypertensives
• Smoking
• Evidence of decidual necrosis at the edge of the placenta
• Incidence is 2.46% in smokers
• Cocaine use
• Anti-coagulant therapy
• Fetal Growth Restriction

Clinical presentation- clinical diagnosis

• Classical presentation,
• Clinical spectrum
• Abdominal pain - consistent and continuous pain
• Vaginal bleeding-
• Uterine contractions / irritable uterus
• Due to irritable effect of blood within the uterus
• Generally, ill
• In discomfort / pain

• Pale
• Tachycardia, low BP depending on the degree of blood loss
• Abdominal palpation
• Fundus > dates
• Tender tense uterus – woody hard
• Fetus- difficult to palpate
• Depending upon the Site, size of the abruption
• Couvelaire uterus; Due to large volume of blood within the
myometrium
• Dead/distress/unaffected
• Blood clots in the vagina
• Cervix may be dilating – 50% of mothers are in labour
• Degree of hemodynamic decompensation is more than the blood loss

Investigations
• Ultrasound scan
• Reto-placental blood clot
• Only seen in 30% of acute presentations
• Normal USS does not exclude abruption

Complications of placental abruption

Maternal risks
-Maternal mortality- due to severe haemorrhages
- Recurrence
- Hypovolemic shock- In concealed abruption, if underlying hypertension masks subsequent
hypotension; Central venous pressure monitoring for assessing the degree of the blood loss
and for accurate fluid replacement
- DIC- Secondary phenomenon
- generalized activation of the coagulation system
• Precipitatory triggers for DIC
• Tissue thromboplastin release
• Endothelial damage
• Small vessels
• Pro- coagulant phospholipid production
• Secondary to intra vascular coagulation
• Acute renal failure- Hypovolaemia, hypotension, DIC would contribute
• Poor renal perfusion
• Initially oliguric- may develop acute tubular necrosis
• Long term prognosis for ARF after placental abruption in women will depend on the
resuscitation
• Fetomaternal hemorrhage- Particularly important in rhesus negative mothers
• Quantify the size of the feto-maternal hemorrhage
• Kleihaur test
• Appropriate dose of anti- D immunoglobulin
• Post partum hemorrhage
• Lead to atonic PPH
• Results from coagulation failure or a couvelair uterus
• Severe bleeding occurs into the myometrium impairing the ability to contract

Fetal risks
• -Perinatal mortality- Perinatal mortality rate is influenced by
• Size of the abruption
• Interval to delivery
• Gestational age at which the abruption and delivery occurred
• Other associated factors
• Growth restriction
• Poor placentation
• -Fetal growth restrictions -FGR is reported in chronic or recurrent placental abruptions
• Area of placenta available for nutrient and waste exchange between the mother and
fetus will be lost due to abruptions

• Contributes to FGR or exacerbates pre-existing FGR

Management
• Prepare for PPH
• Dexamethazone if preterm
• Anti D for Rh Negative women.
• Paediatric support
• Expectant management-
• Smaller degrees of abruption with no fetal distress and uncompromised
mother
• Gestational age favours delaying the delivery to allow reach fetal maturity
(before 37 weeks)
• Require close monitoring of fetal well being
• USS of fetal growth
• Amniotic fluid volume
• Umbilical artery Doppler
• Cardiotocography
• Timing of delivery
• Perceived risks of leaving the fetus undelivered >> Risks of premature delivery
• Decision is best taken in conjunction with paediatricians

Placenta previa

Normal placenta -If the placental edge is more than 2cm away from the internal os
Low lying placenta - Pregnancy greater than 16 weeks of gestation, placental edge is less than
20 mm from the internal os
Placenta previa - Placenta lies directly over the internal os

Risk factors

• Previous LSCS
• Multiple pregnancy
• Assisted reproductive technology
• Maternal smoking
• Advanced maternal age

Warning signs

• Low lying placentas at 20-week anomaly scan

• Maternal collapse
• Feeling cold
• Light-headedness
• Restlessness
• Distress and panic
• Painless PV bleeding
Clinical presentation

• Painless or provoked bleeding after 20weeks

• Coexisting abruption (10%)
• High presenting part
• Abnormal lie

Complications
Maternal complications
• Massive obstetric haemorrhage
• Placental abruption
• Preterm delivery
• LSCS
• Complications associated with interventions to placenta acreta spectrum
Neonatal complications- preterm delivery

Diagnosis
Anomaly scan USS 18-21 weeks - Normal, Low lying Placenta, Placenta Previa
32 weeks TVS - Low lying Placenta, Placenta Previa
36 weeks - Low lying Placenta, Placenta Previa
Decide MOD and TOD
(consider symptoms, type, risk factors for PTL-Cervical length and Hx etc)

placental ‘migration’ following the development of the lower uterine segment during the
third trimester of pregnancy results in the resolution of the low-lying placenta in 90% of the
cases before term.

Management of placenta previa

• Screening test of placenta previa – Routine anomaly scan
• Optimization of Haemoglobin level
• Maternal instruction to prevent APH and complications

Antenatal corticosteroids
• A single course of antenatal corticosteroid therapy is recommended between 34+0
and 35+6 weeks of gestation for pregnant women with a low-lying placenta or placenta
praevia
• Prior to 34+0 weeks of gestation in women at higher risk of preterm birth.
Timing of delivery
• Emergency plan –
In case of uncontrolled bleeding – emergency caesarean delivery
• Elective plan –
• 34+0 to 36+6 - delivery for women with placenta praevia or a low-lying placenta and
a history of vaginal bleeding
• Uncomplicated placenta praevia, or low-lying placenta delivery should be considered
between 36+0 and 37+0 weeks of gestation.
Mode of delivery
• Caesarean delivery –
• Placenta previa
• Low lying placenta in the third trimester are more likely to need delivery by caesarean
section when the placental edge is thicker (over 10 mm) and/or contains a sponge-like echo
or marginal ‘sinus’.
• Vaginal delivery –
• Can be considered when placental edge between 10mm and 20 mm from internal os
• Placenta previa care bundle

• Consultant obstetrician and Anaesthetist involved

• Blood and blood products available on site
• Multidisciplinary involvement in preoperative planning
• Discussion and consent include possible interventions / Hysterectomy
• Local availability of critical care bed

Placenta Acreta Spectrum –PAS

abnormally adherent placental tissue to deeply invasive placental tissue

Classification of PAS
• Acreta/adheranta- where the villi adhere superficially to the myometrium without
interposing decidua
• Increta- where the villi penetrate deeply into the uterine myometrium down to the
serosa
• Percreta- where the villous tissue perforates through the entire uterine wall and may
invade the surrounding pelvic organs, such as the bladder
Risk factors
• Previous History of PAS
• Past Caesarean section
• Manual removal
• Submucous myomectomy
• Uterine curettage
• Short CS to conception interval

Diagnosis
• High index of suspicion
• Women with one or more previous caesarean sections and anterior lower lying
placenta/placenta praevia
• Women with a previous scar where imaging of placental localization has found
the placenta to be lying over the previous scar
• Investigations
• Ultrasound
• MRI -Depth of invasion/lateral extension of myometrial invasion (posterior
placenta/? USS parametrial invasion)
Uterine bulge
Dark intraplacental bands on T2-weighted imaging
Heterogenous signal intensity within the placenta
Disorganized vasculature of placenta
Disruption of utero-placental zone

Management
• Elective deliver at 35-37 weeks
• Caesarean Hysterectomy
• Conservative management
• Uterine preserving surgery
• Choice of surgery would depend on the position of placenta, depth of invasion,
parametrial extension
Shoulder dystocia/ cord
prolapse/uterine inversion
• Shoulder dystocia

• Shoulder dystocia define as a vaginal cephalic delivery that requires additional

obstetric manoeuver to deliver the fetus after the head has delivered.

• How can we have diagnosed the shoulder dystocia practically?

The fetys head rotation or restitution is not taken place
Fetal chin is tightly press against the perineum-turtle neck sign
• You must avoid,
• Excessive fraction on fetal head – because if you apply too much traction anterior
shoulder get more and more engaged in pubic symphisis. That can be damage structures
(brachial plexus) beneath it.
Erbs palsy present (hand- waiters tip, damage C5-C6 upper nerve roots. in
majority in case this is transient. But rarely this can be long last.)
• Maternal pushing – because if she pushes harder the shoulder get more and more
refracted.
• Fundal pressure – because shoulder to be more and more infected.

What we want to do

• Get little more space in pelvis, especially in anterior posterior diameter.

• And we want to free the anterior shoulder away from the pubic symphysis
• stay in McRoberts position (patient is brought to edge of the bed and both legs
hyperflexed and extended) but this is not increase antero posterior diameter.
• And also give a gentle traction on fetal head. This called McRoberts manure.

• If the above manure doesn’t work, we go for supra pubic pressure. (use both hands
can do continuously and use stocking movements)
• Anterior shoulder is at pubic symphysis > apply pressure and rotate the fetus shoulder
to oblique diameter of pelvis (more wider)

If it is not effective, we have go for internal manure. Insert one or both hands in vagina
perform certain manure. For that we might do an episiotomy to get some room.
Only episiotomy resolves shoulder dystocia because it is not because of soft tissue problem,
it is because of bony problem.
If we are lucky we get some space anterior to the fetus posterior shoulder. We inset our hand
we use it like bird’s beak.

Internal manure

1. Insert hand and apply slight pressure anterior to posterior.

Try to rotate to an oblique diameter.
Then at the same time supra pubic pressures also apply externally.

2. If it doesn’t work pressure apply posterior to posterior shoulder.

Supra pubic pressure stop. Otherwise both are working in an opposite direction

3. if that also doesn’t work insert hand posterior to posterior shoulder. Then we can move
hand upward and apply pressure to posterior to anterior shoulder. Supra pubic pressure can
be applying. This might be more effective than 1.

4 if that doesn’t also work use both hands to do that. To rotate to an oblique diameter by us
doesn’t working direct pressure on anterior and posterior shoulders.

5. If that also we can rotate shoulders by 180 degrees.

6. If doesn’t work rotation of 180 degrees is attempted by opposite side.

▪ Second line manoeuvres

Other option of internal manoeuvre is delivery of posterior arm.

This is the other way of internal manoeuvre delivery of posterior arm. Traction of axilla
straight away. In the occasions when the baby is too large you can insert two fingers (index
and middle) and apply traction on posterior axilla.
Some people Appling a sling to the posterior shoulders similar to index and middle finger.
Here after deliver the posterior arm and rotation by 180 degrees again combined by two
methods.
That also doesn’t work it seems very sever shoulder dystocia and we have to go for 3 rd line
manoeuvres.

When one manoeuvre doesn’t work we don’t wait for continuing that we must go for another
manoeuvre. At least within 4 mins we should deliver the fetus otherwise we are going to have
a trouble. Because of that after 30 seconds we have to move to the 3 rd line
▪ 3rd line manoeuvre

• If the fetus already dead >>> clavicular fracture / cutting the clavicle.
• Symphysiotomy.
Incision of pubic symphysis. This has been practice mainly in African countries. But this will
cause a lots of damage to mother. In Sri Lanka this is not use at all.

• Rarely fetus in alive there’s a fetus push back in to the vagina delivering by caesarean.
It’s called “Zavanelli manoeuvre”.
How do we prevent shoulder dystocia?

• Control of diabetics to prevent certain extent

• In DM the fetus is larger. even if match for weight in non DM women fetus shoulders
are larger.
• Everybody could be able to do initial manoeuvre.
• Do caesarean delivery if fetus is very large. Fetal macrosomy more than 4 kgs
especially in diabetics and even in non-diabetics.

▪ CORD PROLAPSE

A – Umbilical cord has descended below the presenting part and below the cervix. “Overt
cord prolapse”
B – Umbilical cord is by the side of the presenting part. It is not normally. It is below the cervix
“occult cod prolapse”
C – Umbilical cord is the one which present at the pelvis above the cervix. Membranes might
be intact. “cord presentation”. Cord is above the cervix.
What is the problem??
1. Problem is the umbilical cord is expose to the exterior.
Umbilical cord vessels go in to spasm. That will reduce blood flow to the fetus.

2. The umbilical cord get compress between to the fetal head and pelvis. And that will also
reduce blood supply to the fetus.

• What are the instances of cord prolapsing?

(i)where there is a space fetal presentation and the pelvis

Non engaged head

Poly hydroamnios
Non cephalic presentation
Foot link breech presentation
Some obstetric manoeuvre
Rupture of the membrane when the presenting parts is high
Preterm

• How do we prevent this?

▪ We must educate the mothers seek medical health and get admitted if they rupture
membrane>>> there can be cord prolapse
▪ Foot link presentation >>> we go for caesarean delivery
▪ Must vigilant about complications when doing obstetric manoeuvre
▪ When rupture of membranes >>> always look for cord presentation. When cord
presentation exclude only we can go ahead and perform the rupture of membrane
▪ If there are other methods artificial rupture of membrane to induce labour like
prostaglandin specifics
▪ If we have to do rupture of membrane when presenting part is high
▪ But if we have to rupture of membrane before rupturing we do oxytocin infusion and
hopefully the mother will be having contraction.
▪ When she gets good contraction only we have to rupture the membranes again we
have to exclude the cord presentation and somebody has to stabilize the fetus pelvis or the
maternal pelvis while we perform the rupture of membrane.
▪ Even after rupturing membranes our assistants may have to stabilize the fetus s head
over the pelvis.

In occult cord prolapse (difficult to identify)

▪ The only abnormality may be in CTG. Because if abnormality may be in CTG we must
be aware cord prolapse specially after rupture of membranes.

How do we diagnosis the cord prolapse?

▪ If the cord descended out of vagina we can see the cord

▪ If it is inside the vagina we can palpate in vaginal examination
▪ If present occult cord prolapses, identify only from CTG

Management

▪ There are 2 aims

▪ 1. We have to prevent the further cord getting compressed between the presenting
part and pelvis
▪ 2. We have to prevent vasospasm of cord

(I)Insertion of two fingers

If mother is an oxytocin repro we have to discontinue that because contraction causes more
and more contractions of cord. Insert index and middle finger - digital evaluation of
presenting part.

(ii) Bladder filling method

Full bladder – fetal head automatically disengaged from maternal pelvis.
(iii) Knee chest position
Because of the gravity fetus head disengaged from maternal pelvis. Cord compression
revealed.

(iv) Exaggerated sims position

This is not normal position. Mother has pillow underneath the buttocks which elevate
buttocks against the gravity.

(v) Gently handling the cord and inserting cord into vagina and then preventing it prolapsing
again by inserting a moist gauze pack.
We must to careful not to handle the cord too much. Excessive handling will cause spasms of
cord.
• Above are done until the baby is delivered by C section. Before doing that we must
ensure that fetus is viable. Otherwise if the fetus is already dead there is no point of go ahead
and doing a caesarean section.

How to ensure fetus is viable?

1. Best is USS – just to look at fetal heartbeat.
2. Assessment of heart beat by hand held Doppler.
3. Sometimes we can palpate the cord and look for pulsation
But this is not reliable because even if the baby is alive & there is fetal bradycardia and might
missed it.
Even when fetus is dead, pulse may be felt as cord pulsation. Not reliable

What method we choose?

• If we can do caesarean within minutes we choose two finger method or Knee chest
position above mentioned.
• If caesarean got delayed bladder filling is use. But not practical.
Exaggerated sims position is good because knee chest is tired for mother.
• If we want to transfer the patient from one to another hospital – combination of
bladder filling and exaggerated sims is good
• If mother is not getting many contraction method (v) is good.

Exceptions
If vaginal delivery going to happen soon. The cervix is fully dilated, the criteria to do vaginal
delivery. We can do vacuum delivery.
These incidences are rare.
UTERINE INVERTION

Uterus is turning inside out.

This occurs after delivering baby within 24 hours of delivery.
According to the duration classify as
1. Acute
2. Sub-acute
3. Chronic

A- Fundus is inside the body of uterus. Above the cervix – first degree
B- Fundus is below the cervix but in the vagina – second degree
C- Fundus is outside the vagina third degree
D- Whole of uterus has got inverted – forth degree

Why do usually get it?

1. Appling the traction to placenta when placenta is still attached to uterus. (commonest
cause)
2. Increase intra-abdominal pressure
3. Manual removal placenta still attached to the uterus
How do you prevent this?
This is part of active management of third step.
1. Administration of oxytocin @ the time of the delivering anterior shoulder of fetus
2. Delayed cord clamping.
3. Delivering placenta by controlling cord traction

Arterial forceps are applied and both hands use

Right- handling forceps and traction
Left – placed above pubic symphysis and insert pressure to prevent uterine inversion.

Diagnosis
Above in C, D stage presents whole uterus outside. But in B not see in outside but you can
palpate it. A you can’t even feel. But abdominal dimple in fundus.

Complications
A, B, C, D viscera get pulled. Pulling out these viscera can lead to neurogenic shock.
(bradycardia>hypotension> shock)

And it causes more bleeding.

• If you diagnose and act at the same time you can prevent this
A- You hold the inverted fundus in your hand and replace it in abdominal cavity.
After replacing you have to keep your hand like C otherwise it may invert again.
Also you have to make sure that uterus is contracting nicely. You have to give oxytocin,
ergometrins to contraction.
This is the manual management. If it is not possible it can be done by fluids insert the vagina.
(hydrostatic pressure) but fluid can come out again. Use vacuum cup for it.

When uterus in outside – Laparotomy (in loin David position)

• At laparotomy instruments are applied for traction of rounds ligaments. At the same
time can push the inverted fundus inside. This is called huntinduns techniques.

• Using a vaccum cup from above at laparotomy and creation of vacuum can correct
this.
• Wholetense technique – at laparotomy incision is made posterior side of uterus. And
internal fundus can be corrected.

• Appling gentle pressure to correct inversion at laparotomy.

Post-partum haemorrhage (PPH)
Definition

• Primary PPH blood loss of 500 ml or more from the genital tract within 24 hours of the
birth of a baby

• Blood loss of over 1000ml is defined as major PPH

• Moderate 1000-2000 ml of loss
• Severe> 2000ml

• Iry: excessive bleeding during the first 24hrs of delivery

• 2ry: excessive bleeding after 24hrs to 12 weeks after delivery

Causes of primary PPH

4Ts
1). Tone-Uterine atony
2). Trauma - Trauma to genital tract, haematoma, uterine inversion
3). Tissue Retained tissue, Placenta accrete spectrum disorder
4). Thrombin - Coagulopathy, coagulation disorders

Cause of secondary PPH

1). Infections (Endometritis)
2). Retained products
3). Usually co-exist

Rule of 30'
# If the patient's systolic blood pressure (SBP) falls by 30 mmHg,
# heart rate (HR) rises by 30 beats/min
# Respiratory rate increases to >30 breaths/min
# Haemoglobin or haematocrit drop by 30%
# Urinary output is <30 ml/hour
# Patient is most likely to have lost at least 30% of her blood volume and is in moderate shock
leading to severe shock

Important issues……

• Major cause of maternal deaths

• Mostly preventable
• Sub optimal care-
Too late detection and intervention
Too little done
Too junior staff
• Prolonged hypovolaemic shock leads to coagulation failure

Uterine Atony

Sustained uterine contractions are mandatory for haemostasis after delivery

Due to inadequate contractions of the uterus after delivery

Causes
Fetal causes Leading to over distension of the uterus
Large baby
Multiple pregnancy

Maternal
Multiparity
Multiple pregnancy
Submucous fibroids
Fibroid uterus
Polyhydroamnios
Placenta previa, Abruption
Retained placenta/ placental parts
Labour related
Prolonged labour leading to uterine inertia
Chorioamnionitis

PPH due to genital tract trauma

Cervical-Cervical tear
Vagina -Vaginal wall tears
-paravaginal haematoma
-de-gloving of vagina
Perineum - Perineal tears
-Episiotomy

Uterine-rupture
-inversion

PPH due to coagulopathy

coagulopathy following
⁻ death in utero,
⁻ abruption placentae,
⁻ severe preeclampsia,
⁻ HELLP syndrome,
⁻ sepsis,
⁻ amniotic fluid embolism,
⁻ acute fatty liver
⁻ immune thrombocytopenia, Von Willebrand's disease

Antenatal risk factors for PPH

✓ Previous PPH
✓ Previously retained placenta
✓ Maternal Hb<8.5 g/dl at onset of labour
✓ Increased BMI
 ✓ Multiparity
✓ Antepatum hemorrhage
✓ Overdistention of uterus (Multiple pregnancy or Polyhydroamnios)
✓ Uterine abnormalities
✓ Low lying placenta
✓ Maternal age >35yrs

Intrapatum risk factor for PPH

✓ Induction of labour
✓ Prolonged 1st,2nd and 3rd stage
✓ Use of oxytocin
✓ Precipitate labour
✓ Vaginal Operative delivery
✓ CS

Management of PPH

1.Call for help.

2.Maintain a calm atmosphere.

3.Keep the mother (and labor companion/family) informed and reassure the mother
regularly.
4.Ensure there is intravenous access with two wide (14 16 G) bore cannulaae
5.Assess, monitor and record: general condition, estimated blood los, pulse, blood pressure
and respiratory rate (every 15 minutes)
6.Insert a Foley catheter and monitor urine output hourly.
7.Commence an ongoing chronological record of patient's condition and interventions.
8.Send blood for cross matching (6 units) and baseline full blood count, clotting profile, renal
functions as a baseline.
9.Start Ringer's lactate (Hartmann's) solution.
10. identify the cause of bleeding.
11.Give oxygen via mask
12.Pay attention to the temperature of the room (avoid hypothermia)
13. If deterioration of the patient is greater than expected for the visible blood loss, internal
haemorrhage must be suspected.
14.Check for completeness of the placenta.

Establish the cause for the bleeding

# Palpate the uterine fundus abdominally.
# A poorly contracted uterus usually indicates atonic PPH.
# If the uterus is well contracted, the genital tract must be inspected for trauma

Management of atonic PPH

1.Start uterine massage ('rubbing up the fundus').

2. Clear the cervical canal and vagina of blood clots by vaginal examination.

3.Give ergometrine maleate 0.5 mg slow IV or methyl ergometrine 0.2 mg slow IV (repeated
in 15 mins)
4. Oxytocin 5 IU IV and start an infusion of 40 IU in 500 ml of Hartmann's solution at 125 ml/h
5.lf the bleeding fails to abate completely in 15 minutes administer/repeat ergometrine
0.5mg IV.
6.If the bleeding fails to stop completely ina further 10 minutes administer misoprostol 800ug
per rectally or sublingually.
7. IM Carboprost(PGF2a) 0.25mg, can go up to 2mg
8.Administer tranexamic acid 1 g by slow IV over 10 minutes. This dose may be repeated after
30 minutes if necessary and later if bleeding recommences.
9.If the bleeding fails to stop, uterine balloon tamponade

If fails to control ...

Surgical methods
1.compression sutures
Application of compression sutures /B lynch sutures
2.Devascularisation of the uterus
 Main blood supply to the uterus is from the uterine arteries and the Anastomosing branches
of the ovarian arteries.
3.selective artery embolization
Selected artery embolization using surgical gelatine sponge
4.total abdominal hysterectomy / subtotal hysterectomy
Life saving
Don't leave the uterus until Too late...

Genital tract trauma: Management

1.Initial assessment is similar to above

2.Initial steps in management is the same
3.Simple vaginal wall tear can lead to massive haemorrhage.

4. Suture the tears to achieve haemostasis

⁻ In LR/ Theatre/ good light source/ assistant
⁻ Under anaesthesia
⁻ Absorbable sutures
⁻ Round body needles
5.Diagnosis of cervical tears
⁻ Good light
⁻ lithotomy position
⁻ Sims speculum
⁻ assistant
⁻ Green Armytage forceps

Coagulopathy Management
# due to suboptimal management of the PPH!!
#Early involvement of a haematologist or transfusion medicine specialist
# Transfusion of needed blood components
Packed cells/ FFP/ platelets/ Activated factor x
#Where available, thromboelastometry would be useful in this situation.
Management of secondary PPH
Resuscitation and blood transfusion if bleeding is profuse
Blood and high vaginal swab for culture and ABST if there is sepsis
Iv broad spectrum antibiotics
Ultrasound scanning to exclude retained placental tissue
Evacuation of retained placental tissue if present

MORBIDITY & MORTALITY from PPH

⁻ Shock & DIC
⁻ Renal Failure
⁻ Puerperal sepsis
⁻ Blood transfusion reaction
⁻ Thromboembolism
⁻ Sheehan's syndrome
⁻ 25% Maternal deaths are due to PPH

PREVENTION
⁻ Regular ANC
⁻ Correction of anaemia
⁻ Identification of high risk cases
⁻ Delivery in hospital with facility for Emergency Obstetric Care.
⁻ Otherwise transport to the nearest such hospital at the earliest.
⁻ Keep speedy transport available
⁻ Local Regional anaesthesia
⁻ ACTIVE MANAGEMENT OF 3RD STAGE OF LABOUR
⁻ Good immediate postpartum care Observation, Oxytocin
Imaging of the fetus

➢ Ultrasound in first trimester

The early pregnancy scan (11-14 weeks)

• Usually performed as a trans-abdominal scan

• Principles aims are,
▪ To assess the number of fetuses and confirm the
fetal viability
▪ To determine chorionicity if it is a multiple
pregnancy
▪ To estimate the gestational age
▪ To identify markers of chromosomal
abnormalities
• Eg. Nuchal translucency in Down’s
syndrome
▪ To identify fetal gross structural
abnormalities

Screening and prenatal diagnosis of aneuploidy

• Screening for trisomy 21 can be performed in the

first trimester using the combined test
▪ Nuchal translucency thickness (NT),
▪ Free beta-human chorionic gonadotropin
(β-HCG) level
▪ Pregnancy-associated plasma protein-A (PAPP-A) level).

➢ To determine chorionicity
▪ Best done at 9-11 weeks
▪ λ sign : dichorionic
▪ T sign : monochorionic
▪ Number of placental masses
Determining chorionicity and amnionicity

➢ Ultrasound in second trimester(18-22 weeks)

1. Fetal anatomy to detect any fetal structural abnormalities or markers for

chromosomal abnormalities

➢ Ultrasound in second trimester(18-22 weeks)

 2. Placental location to detect low lying placenta which has a risk of developing into
placenta previa,

➢ Ultrasound in second trimester(18-22 weeks)

3. Amniotic fluid volume can be assessed by calculating Amniotic Fluid Index (AFI) or by
Deepest liquor pool (DP) to assess fetal wellbeing and or any other cause.

Ultrasound in second trimester cont’d

4. Doppler ultrasound examination of maternal uterine arteries to screen for adverse

pregnancy outcome
5. Measurement of cervical length to assess the risk of preterm delivery

➢ Ultrasound in third trimester

-to assess fetal growth and wellbeing
Measurements used to assess fetal growth are,
▪ Biparietal Diameter
 ▪ Head Circumference
▪ Abdominal Circumference
▪ Femur Length
▪ Estimated Fetal Weight
All measurements can be immediately compared with a normal reference range.
In pregnancies at high risk of IUGR, serial measurements are plotted on normal reference
charts.

➢ Biophysical profile
Biophysical variables used are,
1. Fetal breathing movements
2. Gross body movements
3. Fetal tone
4. Reactive fetal heart rate
5. Qualitative amniotic fluid

➢ Waveforms are obtained from both the umbilical and fetal vessels
• Umbilical artery
▪ Information regarding placental health and function is obtained.
• Where there is a constant diastolic flow in normal and in
abnormal a absent or revered diastolic flow and has a strong
correlation with fetal distress and IUD
• A measure of the amount od diastolic flow relative to systolic
flow is provided by several indices such as pulsatility index or
resistant index.
• When these indices are high it indicates high resistant flow

➢ Fetal vessels
▪ Middle crebral artery Doppler
• Useful in detecting late onset FGR with cerebral redistribution
of blood
• An indicator of fetal anemia
• In anaemia the peak systolic velocity increases
• Useful in assessing severity of Rhesus disease and twin-to-twin
transfusion syndrome which results in anaemia in donor twin
Fetal growth and wellbeing
 • by above risk factors mothers divided as high risk and low risk mothers
• Fetal size can be assessed antenatally in two ways, either externally by (symphysis–fundal
height [SFH] measurement) or using ultrasound.
• High risk mothers- USS
• Low risk mothers- SFH
IU death, postdates and post maturity
Definitions

•Stillbirth=Death in utero after a viability

•Perinatal death=Stillbirth + Early neonatal death(END)
•Perinatal mortality rate = No of perinatal deaths *1000
Total number of births

•Still birth rate = No of stillbirths * 1000

Total number of births

•Prospective risk of stillbirth = No of stillbirths *1000

Total no of ongoing pregnancies

•Post-term pregnancy: pregnancy going beyond 42 weeks

Main causes for stillbirths

•Delivery complications
•Maternal infections in pregnancy
•Maternal disorders specially hypertension and diabetes
•Fetal growth restriction

Interventions that can prevent still birth

1.Emergency obstetric care

2.Identification and induction for pregnant women with >41 weeks of gestation.

3.Detection and management of fetal growth restriction.

4.Detection and management of diabetes in pregnancy.

5.Detection and management of hypertensive disease in pregnancy.

6.Preconceptionalfolic acid and fortification.

7.Syphillisdetection and treatment.

Interventions that can prevent still birth

1) Comprehensive emergency obstetric care

•700,000 stillbirths could be prevented worldwide.

•Partogram
•Access to electric fetal monitoring (CTG) during labour
•Safe use of oxytocin
•Mandatory training in obstetric emergencies (breech delivery, shoulder dystocia)
2)Identification and induction for pregnant women with >41 weeks of gestation.

•Menstrual history based dating is not reliable.

•Ultrasound dating could prevent post-term pregnancies up to 60%.

-Between 8 and 13+6 fetal crown rump length(CRL)

3)Detection and management of fetal growth restriction.

•40% of antepartum stillbirths due to FGR.

•Up to 70% of unexplained stillbirths are due to undiagnosed FGR.

•Prevention of FGR related stillbirths.

-Accurate pregnancy dating
-Customized fetal growth charts.
-Use of latest fetal wellbeing techniques (Doppler, computerized CTG)
-Timely intervention.
4)Detection and management of diabetes in pregnancy.

•All pregnant women should be screened for diabetes at the first visit.

•One stage, non-fasting 75g OGGT as described by the Diabetes in Pregnancy Study Group of
India(DIPSI) is recommended for screening at the first visit and at 28 weeks. A 2-hour blood
glucose of more than 140mg/dl confirms gestational diabetes.

5)Detection and management of hypertensive disease in pregnancy.

•Screening for preeclampsia.

•Regular blood pressure check-ups.

6)Preconceptional folic acid and fortification

•Reduction in fetal malformation.

Post term/ post maturity pregnancy

•Stillbirth risk increases with gestation

•It increases significantly after 42 weeks

•Induction of labour is indicated after 41 weeks.

Multiple pregnancy
The presence of more than one fetuses in the gravid uterus is called multiple pregnancy.

2 fetuses (twins)
3 fetuses (triplets)
4 fetuses (quadruplets)
5 fetuses (quintuplets)
• Multiple pregnancy represents 2%- 3% of all pregnancies. But present day due to the
in vitro fertilization or assisted reproductive Technologies there are many mothers
with multiple pregnancies.

Risk factors for multiple pregnancy

1) Race- most common in black Africans. The reason is black Africans they used to
consume lot of legumes which contain anti estrogens and can promote multiple
ovulation that can lead to dizygotic twins.
2) Increased maternal age - with increased age, circulating FSH Increased in the blood
and it can promote multiple eggs to develop.
3) Parity- more common in multipara exact reason is not known
4) Hereditary - family history of multifetal gestation
5) Maternal nutritional status - multiple follicular development can be seen in well-
nourished women.
6) Use of assisted reproductive technologies with clomiphene citrate, gonadotrophins
and IVF.

Embryology of multiple pregnancy

• In dizygotic twins there are always two sperm and to eggs fertilized separately which
will give rise to dichorionic pregnancy. Therefore, all dizygotic twins are dichorionic.
That will represent two third of multiple pregnancies.
• Whereas in monozygotic twins if it divides in first 3 days they will end up as dichorionic
diamniotic twins.
• If they divide between 3rd and 9th days, there will be only one placenta and will called
monochorionic diamniotic pregnancy.
• If they divide between 9th and 13th days there will be single sac and a single placenta
what we call monochorionic monoamniotic twins.
• If they divide after 13th day they will share body parts what we call conjoined twins.
• Monozygotic twins are one third of all twins.
 • Lambda sign - where are you can see triangular shaped tissue projection in between
fetal membranes.
• T sign - membrane straightly go and bind with placenta there is no tissue projection
like in Lambda sign. Therefore, it can be recognized as T sign.

Maternal physiological changes associated with multiple pregnancy

1) Increased blood volume and cardiac output

2) Increased demand for Iron and Folic acid.
3) Maternal respiratory difficulty
4) Excess fluid retention and edema
5) Increased episodes of supine hypertension
6) Because the gravid uterus disturbs the venous return.
7) Hyperemesis gravidarum due to increased HCG levels
8) Cardiorespiratory embarrassment- palpitations or shortness of breath
9) Tendency of swelling of the legs
10) Varicose veins
11) Hemorrhoids

Diagnosis and management of multiple pregnancy

History
1) History of ovulation inducing drugs specially gonadotropins
2) Family history of Twin pregnancies
3) Exaggerated pregnancy symptoms

Examination
1) Presence of anemia is more than in singleton pregnancy.
2) Unusual weight gain, not explained by preeclampsia or obesity.
3) Normally there can be around 12 KG of weight gain in entire pregnancy period.
4) Fundal height more than the period of gestation (Measurement of symphysis fundal
height is not recommended for twin pregnancies.)
5) Palpation of too many fetal parts
6) Two distinct fetal heart sounds

Investigations

• Ultrasound in multifetal pregnancy first trimester scan (11-14 weeks) is done to obtain
the following information.

1) Confirmation of diagnosis
2) Viability of fetuses- multiple pregnancies can be complicated with vanishing twins in
early pregnancy where one baby is growing well and the other baby stops growing.
Common in first trimester.
3) Chronicity determination
4) Pregnancy dating
5) Labelling (orientation) - whether babies are lying left or right or top or bottom
 • There are two complications in monochorionic diamniotic (MCDA) pregnancies. They
are twin to twin transfusion syndrome (TTTS) and selective fetal growth restriction
(sFGR).
• This begin to appear after 15 to 16 weeks. So mothers with MCDA pregnancies should
be offered first trimester scans early and more frequently.

Aims of antenatal care

1) Prolongation of gestation age increase fetal weight

2) Improve perinatal mortality and morbidity
3) Decrease incidence of maternal complications
• In singleton pregnancies the risk of stillbirth increases beyond 40 weeks. It will become
statistically significant beyond 42 weeks.
• According to the present understanding, singleton pregnancies can be prolonged up
to 41 weeks. But if the mother doesn't deliver after 41st week, induction of labour has
to be done before 42 weeks.
• But when we consider twin pregnancies, stillbirth rate goes up beyond 37 weeks and
it becomes very high levels at 40 weeks.
• Therefore, the present understanding is all MCDA twins should be plan to deliver after
36 weeks and all DCDA twins should be plan to deliver after 37 weeks unless there is
an indication to deliver early.

• The cumulative loss rate of monochorionic twins is very high specially Between 16
weeks to 26 weeks. Beyond 26th week up to 40 weeks it is somewhat static. But in
dichorionics it is same throughout.
• The huge gap between monochorionic and dichorionic perinatal loss around 16 weeks
to 26 weeks is due to the two main pregnancy complications but before mentioned.
(TTTS & sFGR).
 • The left figure shows cumulative loss rate before introduction of laser therapy. Right
figure shows rate after introduction of laser therapy. Therefore, the death rate is low
nowadays when compared to early, but still the gap is there.

Method of delivery

• Vertex- vertex (50%)

Vaginal delivery, interval between twins not to exceed 30 minutes.

• Vertex- breech (20%)

Vaginal delivery by senior obstetrician.

• Breech-vertex (20%)
Safer to deliver by cesarean section to avoid the rare interlocking twins (1:1000 twins)

• Breech-breech (10%)
Usually by cesarean section.

Potential maternal and fetal complications associated with multiple pregnancy

1) Twin to twin transfusion syndrome (TTTS)

• Up to about 10 to 15% of monochorionic twin pregnancies are complicated by twin to

twin transfusion syndrome (TTTS) due to abnormal placental vascular anastomosis.
(Due to unequal vascular sharing)
• In normal circumstances there are vascular connections between two babies in all
monochorionic twins via the placenta. But their perfusion from one baby two other is
well balanced.
• Suppose if one baby gets 100, he will give back 100 to the other baby. So there is no
net shunting of blood from one baby to other.
• But when there is an imbalance between vascular anastomosis, for an example one
baby will give 100 but other baby will give only 80. So there will be a net mismatch
that will lead to TTTS.

Placental anastomosis in monochorionic placenta.

Quintero staging of TTTS

• Most importantly TTTS has to be identified early stage because we offer Laser
treatment beyond stage 2.
• Most of the times stage 1 we don’t need to give any treatment because it can
spontaneously resolve with time.
• But if it goes beyond stage 3 or 4 the management is going to be difficult even with
laser treatment.
• So ideally they have to be identified at stage 1 and at stage 2 laser therapy should be
provided.
• In that we put a scope across the maternal tummy to the uterus and identify the
crossing vessels between fetuses and they are ablated. By doing so we make
monochorionic placenta artificially into dichorionic placenta.

Laser ablation treatment in TTTS

2) Selective fetal growth restriction (sFGR)

• Another 8 to 12% of monochorionic twins can be complicated with selective fetal

growth restriction (sFGR) due to unequal placental sharing.
• One baby will get bigger proportion of placental mass while other baby gets small
proportion. So one baby will be growth restricted while other baby will be normal.

3) Twin revered arterial perfusion – TRAP

• During early part of the pregnancy one baby is not getting enough blood. So their
upper part of the body is not properly formed.
• They have no heart and no head, but rest of the body gets blood from the other twin.
Therefore, this baby is called “acardiac monster”.
 4) Conjoined twins

Monitoring for intrauterine growth restriction

• Growth discordance = (Larger twin's Weight-Small twins weight)/ Larger twin's weight
× 100%
• If the growth discordance >25% in twins or triplets it is considered as a severe growth
discordance and clinically important indicator of intrauterine growth restriction.
• So offer referral to a tertiary level care. Has a poor prognosis.

Maternal complications

1) Hypertension
• Women with twin pregnancy have a two to three time’s higher risk of developing
hypertension during pregnancy than women with singleton pregnancies.
• Advice women with twin and triplet pregnancies that they should take 75 mg of
Aspirin daily from 12 weeks until the birth of the babies if they have one or more of
the following risk factors for hypertension;

❖ First pregnancy
❖ Age 40 years or older
❖ Pregnancy interval of more than 10 years
❖ BMI of 35 kg/m2 or more at first visit
❖ Family history of pre-eclampsia

• Even though it is said 75 mg of aspirin the present understandings if you give 150mg
of aspirin at night we can reduce risk of pre-eclampsia.

2) Preterm birth

• More than 50% of twins and almost all triplets are born before 37 weeks of gestation.
• Very high risk when the number of fetuses are growing up.
• The methods that are used to prevent preterm birth in singleton pregnancies are not
useful in twin pregnancies.

1) Bed rest (at home or in hospital)

2) Progesterone (intramuscular or vaginal administration)
3) Cervical cerclage
4) Tocolytics (oral betamimetics)
Normal Labour and Management
Normal Labour

• Diagnosed by
▪ Symptoms – colicky lower abdominal pain (increase in frequency, intensity and
duration with the passage of time and not relieved by common analgesics)
▪ Signs – presence of painful uterine contractions with progressive effacement and
dilatation of the cervix

Stages of Labour

First stage Second stage Third stage

• From 0 to 10cm • Full dilatation of the • From delivery of the
dilatation of the cervix to the delivery of baby to the delivery
cervix the baby of the placenta and
• 2 phases • 2 phases membranes
▪ Latent phase ▪ Passive phase (Descent
From 0 to 4cm phase)
dilatation of the
Descend of the fetal head
cervix
with aid of uterine
Slow rate contractions
▪ Active phase ▪ Active phase (Expulsive
From 4cm till full phase)
dilatation of the Fetal head reaches the
cervix pelvic floor
Rapid rate Mother feels the urge to
bear down
Mother is encouraged to
bear with contractions
 3P s in labour

Power Passage Passenger In addition

From uterine Bony pelvis which Fetus Patient factors

contractions in 1st the fetus has to
Changes occurs • Preferences
and 2nd stages negotiate
• Anxiety
▪ Flexion of the
And from maternal
fetal head Provider factors
pushing
▪ Moulding
• Doctors
▪ Asynclitism
,nurses
• Labour
companions

Flexion of the fetal head Moulding Asynclitism

A. Well flexed fetus
B. Deflexion of fetal head
C. Extension of fetal head
D. Hyperextension of fetal head

- Fetal skull bones which are

slightly apart comes together
or slightly overlap in the birth
canal
- Various degrees of
moulding (+1, +2, +3)
- +1- skull bones come
together but don’t overlap
- +2 – one bone overlaps the
other
- up to +2 normal
- Position of a fetus in the
uterus
- Because of the sacral
hollow in the pelvis (not
because of gravity) baby’s
head tilts to one side
- Later on in the mid cavity
during the phase of
engagement of the head it
is corrected by itself with
contractions
Types of labour

Modern labour curve

1. Prolonged labour
Labour is considered to be prolonged if it lasts for more than 12 hours in a primipara and
more than 8 hours in a multipara.
2. Primary Dysfunctional Labour
Labour is slow from the start due to inadequate contractions.
3. Secondary Arrest
The progress is normal at first, but stops later in the presence of strong uterine contractions,
due to some form of obstruction, which could be fetal or maternal in origin.

❖ Modern labour curve

Cervix dilates at a slow rate up to 6cm.
Then in P1, P2+ mothers cervix dilates more rapidly than P0 (primi) mothers.

Management of first stage

Management of normal labour
Management of second stage
• Established labour
Management of third stage

• Avoiding fecal soiling

• Shaving of perineal hair
• Oral fluids Identify risk factors by,
• IV access Review antenatal records
• Light snacks Detailed clinical history
• Mobilize- transfer to the labour suite Examination Urine for
• Maternal position- left lateral protein
recombinant position
• Routine intravenous cannulation and intravenous fluids not necessary.
• Routine amniotomy is not advised
• Routine oxytocin is not needed

Management of first stage

Monitoring by Partogram Assessments at vaginal examination

• Fetal condition • Cervical dilatation
▪ Intermittent auscultation of fetal
• Station of presenting part
heart by pinard
▪ Liquor volume • Fetal position
▪ Meconeum in liquor
• Colour of liquor
• Maternal condition
▪ Pulse, BP, Temperature & hydration • Signs of cephalo-pelvic disproportion
▪ Evaluation of drugs(oxytocin,
▪ Significant caput
antibiotics, Anti hypertensives,
▪ Moulding
Analgesics
▪ Undistended bladder-catheterize if
indicated
• Progress of labour
▪ Cervical dilatation
▪ Decent of the presenting part
▪ Uterine contractions

Pain relief

Assessment of station of presenting part

Vaginal Ex: middle finger palpating the
ischial spine and index finger palpating the
leading part of fetal skull.

Leading part at ischial spine- 0

Above ischial spine- -1,-2,-3
Below ischial spine – +1, +2
Management of second stage

Second stage

Positioning Diagnosis
Descent phase
▪ Most comfortable ▪ Vaginal
position Not to bear down examination for full
▪ Supine position- dilatation
Fetal heart assessed
avoided due to ▪ Perineal distention
every 15 mints
compression of IVC ▪ Anal dilatation

Perineal protection Expulsive phase

Episiotomy
Encourage to bear
down ▪ Medio-lateral Episiotomy
▪ At the time of crowning
Fetal heart assessed
after each contraction

To prevent perineal trauma

Delivery
Right hand – thumb and index
finger support perineum and
3rd, 4th, 5th fingers guard the
perineum
▪ Not all needed, majority
Left hand – control the delivery
done in primigravida
of the fetal head
mothers
Perineal massage

Just before delivery- might

reduce perineal trauma
Management of third stage
Not a standard practice
 1. Oxytocic agents
At the time of delivery of
anterior shoulder
Oxytocin is the drug of
choice (5 units IV)
However, in PPH -
ergometrine is the drug of
choice (0.5mg)
3. Controlled cord traction
To deliver the placenta
Before applying make sure that
Active management the uterus is well contracted
From right hand held the artery
forceps which clamp the cord and
pull it while left hand keeping
above the pubic symphysis to
push the fundus of uterus upward
to prevent inversion of uterus

2. Cord clamp
4. Examine the
Delayed for 2 minutes placenta
Reduce the incidence Placenta and
of neonatal anemia membranes should be
and growth problems inspected after
delivery to confirm
that they are complete
Pain relief in labour
⁻ Pain in labour causes physiological effects in the mother
⁻ Could be harmful
⁻ These changes may affect the foetus
⁻ Therefore, labour pains are harmful to both the mother and the foetus

Pain pathway

• Afferents from the uterus, cervix and vagina

⁻ T6 to T12 - Uterus
⁻ S2- S4 – Cervix and vagina
• Ascends via the spinothalamic tract to the pain areas in the cortex
• Have to block these spinal segments to relief pain

Physiological changes

With pain;
1. Changes in cardiac system
⁻ Activation of the sympathetic system
⁻ Increase HR, SVR, CO, BP
⁻ Can cause heart failure or myocardial ischemic event in mothers with cardiac
problems (valvular heart disease or IHD)
⁻ Can cause heart failure or pulmonary oedema in mothers with PIH

2. Changes in respiratory system

⁻ Pain will stimulate respiration and cause hyperventilation
⁻ CO2 will get washed off and cause respiratory alkalosis
⁻ Alkalosis shifts oxygen dissociation curve towards the left and increase O2 binding to
Hb

3. Foetal changes
⁻ Increase O2 binding to Hb reduce O2 unloading at the placenta
⁻ Reduce the amount of oxygen reaching the fetus
⁻ Foetal metabolic acidosis and distress

Psychological effects
⁻ Distressed
⁻ Poor cooperation and straining
⁻ May delay the progress of labour
 “Pain should be treated to minimise the harmful effects to both the mother and the
foetus”

Methods to relieve pain

▪ Should be effective
▪ Should not be harmful to the mother and the foetus
▪ Should not interfere with the progress of labour
Two methods;
➢ Pharmacological methods – most commonly used and most effective methods
➢ Non Pharmacological methods

Non pharmacological methods

▪ Psychotherapy – talking with mother to relief stress and anxiety
▪ Breathing exercises – mothers are told to breath in a rhythmic fashion during labour
▪ Hydrotherapy – mother is in a warm water bath and deliver the baby into warm water
bath
▪ Acupuncture, TENS – blocks the afferent fibers

Pharmacological methods

• Opioid analgesic agents

• Epidural analgesia
• Entonox (O2: N2O) inhalation
• Nerve blocks-pudendal

Opioids
⁻ Most popular- pethidine IM
⁻ Safer, easy to administer and monitor
⁻ Can be given by nursing staff as well
⁻ Should be used if delivery is anticipated within 4 hours
⁻ Can cause maternal and foetal respiratory depression
⁻ Naxalon should be available to reverse the effects of pethidine on the new born
⁻ Can cause nausea, vomiting, drowsiness, pruritus
⁻ Pethidine is given with IM promethazine or metoclopramide to prevent nausea and
vomiting
⁻ Not very effective
⁻ With high doses can affect to the progression of the labour
Epidural analgesia
⁻ Bupivacaine (local analgesic) and fentanyl (opioid) is administered to the epidural
space via an epidural catheter
⁻ The best form of pain relief during the first and second stages of labour
⁻ Blocks the spinal nerves
⁻ Very effective
⁻ Can cause hypotension, bradycardia, respiratory depression, because it causes the
blockage of motor and sympathetic fibers as well
⁻ Delay the progress of labour
⁻ Contraindications
o Antepartum haemorrhage
o Coagulopathy
o Hypervolemia
o Sepsis
o Heart disease with gross reduction of the ejection fraction
o Breech presentation (relatively contraindicate due to impairment of maternal
bearing down effects during second stage)
o Spinal deformities
⁻ Needs expertise to administer and needs close monitoring

Entonox
⁻ Mixture of 50% Oxygen and 50% Nitrous Oxide is inhaled
⁻ A special mask (demand mask) used
⁻ Inhale the gas only during labour contractions
⁻ Effective only in the first stage to patients who are not on epidural analgesia
⁻ Vomiting, confusion, sedation

Nerve blocks
⁻ Pudendal and Cervical nerve blocks
⁻ Effective only in the second stage
⁻ Not cause the delay in the labour
⁻ Not very popular; nowadays only use with forceps/vacuum deliveries and for
episiotomy
Malpositions and Malpresentations
Malpositions
❖ Normal position
▪ Left or right occipito-anterior position
▪ The fetal head is well flexed
▪ Presenting diameter is suboccipito-bregmatic and is around 9.5 cm
▪ Posterior fronatanalle can be felt
▪ Anterior frontanalle can’t be felt

❖ Malpositions
Any position other than occipitoanterior position
▪ Occipito-posterior position
▪ Occipito-lateral position
Occipito-posterior position

• The presenting diameter is occipito-frontal, and is around 10.5 cm

• Head is not that flexed

• AF can be easily palpated
• May increase the risk of delayed
labour, perineal trauma, fetal
distress

A. Right occipito-posterior
Posterior frontanalle (PF) at 7 O’clock
B. Left occipito-posterior
PF at 5 O’ clock
C. Direct occipito-posterior
PF at 6 O’ clock
 1. Fetal head rotate to 90- 180
degrees
Delivered in direct occipito-
anterior position
2. Rotate only up to 90 degrees
Fetal head arrested at that point
(deep transverse arrest)
PF at 9 O’clock
AF at 3 O’clock
3. Will not rotate at all
Arrested as right occipito-
posterior
4. Fetal head rotate, occiput from 7
O’clock to 6 O’clock position

Management options in occipito-posterior position

• Await spontaneous rotation

• Await face to pubes delivery

Has a risk of perineal trauma as the head is deflexed and

risk of PPH

• Vacuum delivery

Vacuum is created in the cup and

it is placed on the fetal face
Occipito-posteriorly positioned
head rotate to occipito-anterior
position

• Application of forceps in occipito-posterior position

Forceps got a pelvic curve. Non rotational forceps.
 • Manual rotation to occipitoanterior position and forceps delivery

Fetal head is rotated from occipito-

posterior to occipito-anterior
Done with the aid of 3 fingers

• Rotational forceps delivery

Rotational forceps have no pelvic

curve

• Caesarean delivery
Occipitolateral (occipitotransverse position)
Malpresentations
❖ Normal presentation
• Vertex
• Area between 2 parietal eminence, posterior frontanalle and anterior frontanalle

❖ Malpresentations
• Any presentation other than vertex
▪ Breech
▪ Brow
▪ Face
▪ Shoulder, Dorsal
▪ Compound

Breech presentation
Types of breech

A. At the knees
extended –
commonest
Flank / extended
type
B. At the knees leg is
flexed
Feet are above the
level of buttocks
Flexed type
C. One leg flexed and
one leg extended at
both hip and knee
Foot limb type
As there is lot of
space between
pelvis and fetal
buttocks cord
prolapse can occur
Management of breech
Look for predisposing factors for
a breech presentation
▪ Multiple pregnancy
▪ Placenta praevia
▪ Uterine malformations
▪ Fibroids in the lower
segment of uterus
▪ Polyhydramnios /
Delivery options oligohydramnios
▪ Fetal abnormalities
▪ External cephalic version at
36 (primi) / 37 (multiparty)
weeks
▪ Elective caesarean delivery
▪ Assisted vaginal breech
delivery

External cephalic version (ECV)

ECV prevent the mortality and
morbidity of vaginal breech
delivery and the need for
caesarean section
Procedure for ECV
▪ Performed after 36 weeks in primi-
parous women and after 37 weeks in
multiparous women
▪ A CTG is performed before and after the
procedure.
▪ The patient should be well relaxed.
▪ No need for fasting, intravenous
cannulation or group and save
▪ Intravenous tocolytics are not routinely
indicated but may be used in selected
cases where the uterine tone is high
▪ A maximum of three attempts are
carried out.
▪ Careful assessment should be carried
out by a consultant before selection for
vaginal breech birth.
▪ Most common complication – transient
fetal bradycardia
▪ Anti D if the woman’s blood group is Rh
negative
Absolute Contraindications for ECV
▪ Contraindication for vaginal delivery of a
cephalic presentation
▪ Antepartum hemorrhage within the last 7
days
▪ Abnormal cardiotocograph
▪ Major uterine abnormality
▪ Prelabour rupture of membranes
▪ Multiple pregnancy (except during delivery of
the second twin)
Relative Contraindications for ECV
▪ Small-for-gestational age fetus with abnormal
umbilical artery Doppler parameters
▪ Pre-eclampsia
▪ Oligohydramnios
▪ Major fetal anomalies
▪ Scarred uterus
▪ Unstable lie

Brow presentation

▪ Appears as a cephalic presentation with a non-

engaged head before the onset of labour
▪ The anterior fontanelle, frontal suture, frontal
bones, supraorbital ridges and the bridge of the
nose can be palpated
▪ The diagnosis is confirmed by palpation of the
supraorbital ridges and the bridge of the nose
▪ The presenting diameter is the mento-vertical
diameter, which is 13.5 cm and is too large for
vaginal delivery
▪ Spontaneous rotation will not occur
▪ Manual rotation is not possible
▪ Caesarean section is the only method of delivery
 Face presentation

▪ Appears as a cephalic presentation before the onset of

labour
▪ A soft presenting part with orbital ridges, mouth, nose and
malar bones is felt. If the chin is posterior mento-posterior
face presentation results. Vaginal delivery is not possible.
Caesarean section is the safest route of delivery.
▪ If the chin is anterior mento-anterior face presentation
results. Vaginal delivery is possible because the presenting
diameter is 9.5 cm (submento-bregmatic).

Mento-anterior position Mento-posterior position

Shoulder presentation with arm prolapse

▪ Fetus is in transverse lie

▪ Arm prolapse can occur
▪ Management is caesarean section

Compound presentation

▪ Combination of
Head + hand
Breech + hand
▪ As labour progresses hand move away.
Then normal vaginal delivery progresses.
▪ If hand persists pushed away manually
Infertility
Infertility and its management
What is infertility?

A couple’s inability to conceive after 1 year of unprotected intercourse

Define when to investigate and treat

Earlier investigations for

• Advanced age
• Features suggestive of abnormality
• Conditions affecting fertility
• Social / personal reasons

I. Requirements for fertility

1. Ovulation
2. Normal semen parameters

3. Normal sexual functions

4. Patent and functional fallopian tubes

• Normal pelvis

5. Normal uterus and endometrium

II. What are the causes for infertility?

1. Anovulation or ovulatory dysfunction

• Hypogonadotropic hypogonadism
• Hypergonadotropic hypogonadism
• Normogonadotropic hypogonadism

2. Seminal fluid abnormalities

• Anejaculation
• Abnormal Volume, count, motility, morphology, viability
• Azoospermia
3. Sexual dysfunction
• Frequency
• Regularity
• Penetration
• Ejaculation

4. Fallopian tube abnormalities

• Blocked tubes
• Scarred tubes
• Peritubal adhesions
 • Pelvic disease
• Endometriosis
• PID
5. Uterine abnormalities
• Congenital abnormalities
Septate uterus
Uterine agenesis

• Fibroids
• Polyps
• Abnormal endometrium
TB, infection, Asherman’s syndrome

III. How to investigate for aetiology

1. Anovulation
• Midluteal progesterone level
• USS follicle tracking
• BBT
• LH surge
2. Seminal fluid abnormalities
• Seminal fluid analysis
• Sperm functional tests

3. Sexual dysfunction
• Mainly by history
• Low frequency
✓ Lack of libido
• Irregular intercourse
✓ Work commitments
• Non-Penetrative sex
✓ ED
• Ejaculatory problems
✓ Premature, retrograde
✓
4. Tubal disease

✓ Hysterosalpingogram (HSG)
• LOOK AT THE OUTLINE OF UTERUS AND TUBES
• PATENCY OF TUBES CAN BE DEMONSTRATED

✓ Laparoscopy and dye test

• Assess tubes and pelvis
• When pelvic disease is suspected
• Corrective surgery also at the same time.
 5. Uterine abnormalities
✓ Ultrasound scan
• Growths and indentations
• Fibroids, Polyps, Adenomyosis

✓ 3D scan to assess cavity

✓ Hysteroscopy

IV. How to treat infertility

• Specific treatment
• Myomectomy
• Polypectomy
• Ovulation induction

• Empirical treatment
• Augmentation of ovulation
• Intrauterine insemination
• In vitro fertilisation

o Ovulation induction / Augmentation

• Induction - In the presence of anovulation
▪ Find the underlying cause
▪ Treat if a treatable cause present
✓ Augment / Induce ovulation by hormonal
manipulation
 • Clomifene / tamoxifene
• Letrozole
• Gonadotropins
• Laparoscopic ovarian drilling (only in
PCOS)
o Intrauterine insemination
• Include various steps
• Ovulation induction / augmentation
• Timing of ovulation with hCG injection
• Sperm processing
• Insemination in the uterine cavity

o IN Vitro fertilisation
• Include the following steps
• Superovulation (10-15 oocytes)

• Oocyte retrieval
• Sperm processing
• Fertilisation outside body
• Embryo replacement
• Luteal support
• ICSI (intracytoplasmic sperm injection)

o Other treatment modalities

• Gamete donation
• Sperm – IUI
• Oocyte – IVF
• Embryo donation
• Surrogacy
MALE INFERTILITY

Causes of male Infertility

Pre testicular
◦ Environment / lifestyle factors
◦ Endocrine causes
◦ Chromosomal or Genetic
causes

Testicular
◦ Infection
◦ Varicoceles
◦ Antisperm antibodies (ASA)
◦ Testicular cancer

Post testicular
◦ Ejaculatory failure
◦ Erectile dysfunction

Envt. / lifestyle factors

Recreational drugs low testosterone

 Certain medications (anabolic steroid)
Industrial chemicals, gases, heavy metals
Stress – increased prolactin
level
Overweight – low T levels
Varicoceles
-Palpably dilated veins of the pampaniform plexus
-Prevalence is around 25% of men with subnormal semen
Majority are left sided (90%)
Pathophysiology
◦Increase in testicular T (poor heat exchange)
◦Reflux of renal and adrenal metabolites
◦Formation of ASA
◦Oxidative stress (formation of free radicals)

◦Minor changes in hypothalamo- pituitary axis (Inhibin Testosterone reduces

)
◦Testicular atrophy / germ cell apoptosis
◦Hypoxia ?
Laboratory findings

◦ Increase in immature germ cells

◦ Reduced sperm count, motility, viability and morphology
◦ Plasma membrane damage due to lipid peroxidation by Reactive Oxygen Species
(ROS)
◦ Sperm DNA damage
Anti-Sperm Antibodies (ASA)
Immunoglobulins and immunocompetent cell are not allowed to enter the lumen of
seminiferous tubules by blood testes barrier

Intra epithelial lymphocytes, macrophages, immunomodulatory factors in

semen (Prostaglandins, Cytokines, Polyamines, Zn) provide further protection

Loss of barrier function leads to formation of ASA

ASA secrete in to the fluids of accessory sex glands

Prevalence 9-35% in subfertile men
Found in serum and cervical mucus of women
Three classes of immunoglobulins are implicated in male infertility
IgM – not secrete in to the genital tract , Large molecular size / found in serum
 IgG – enters in to the GT , Attach to sperm
IgA – Produce locally in the GT , Not present in serum
Causes
Obstruction of the epididymis or vas
Trauma to the BTB
Infection / inflammation
Cryptorchidism
Varicocele
Malignancy
Anal sex
Surgical interventions
Spinal cord injury
Effects on semen
◦ Reduction of ability to penetrate cervical mucus
◦ Destruction of sperm in the uterus by phagocytosis action
◦ Prevent sperm capacitation and acrosome reaction

Laboratory findings - Sperm agglutination

Endocrine disorders
Endocrinopathy present in up to 20%
5-10% of males the etiology is purely endocrine
Classified in to
◦ Hypogonadotropic hypogonadism
◦ Hypergonadotropic hypogonadism
◦ Hyperprolactinaemia
Hyperprolactinaemia

◦ Modulation of action of dopamine and TRH

◦ Infiltrative diseases (Tuberculosis)
◦ Micro/ macroadenomatous PRL secreting tumor
◦ Hypothyrodism
◦ Drug induced
◦ Acromegaly (excess GH)
◦ Chronic renal failure
◦ Stress

Effects
◦ Decreased libido / impotence
◦ Disrupt GnRH release
◦ Oligozoospermia
Hypogonadotropic hypogonadism
Kallmans syndrome
Isolated LH/FSH deficiency
Pituitary tumor
Prolactin excess
Panhypopituitarism
E2 (obesity, adrenal cortex or sertoli cell tumor)
Liver diseases
Haemochromatosis

Hypergonadotropic hypogonadism
Klinefelters syndrome
Anorchia (vanishing testes syndrome)
Sertoli cells only syndrome (germ cell aplasia)
Cryptorchidism
Androgen receptor defects (testicular feminization)
Auto-immune disorders
Orchitis (Mumps/Tuberculosis)
Varicocele
Radiation/chemotherapy/torsion
Laboratory findings
FSH LH Testosterone

Hypogonadotropic Low Low Low

Hypogonadism

Hypergonadotropic High / Normal High / Normal Low / marginal

Hypogonadism

Infection
Prevalence is around 6 – 10 % among infertile men
Majority of infections / inflammations are asymptomatic
Caused by
Sexually transmitted pathogens -Eg. Chlamydia trachomatis
 Uropathogens - Eg. Escherichia coli
Damage is done by
◦Direct action of microorganisms
◦Secretory components
◦Inflammatory cells &
◦Their mediators (IL6, 8)
Compartment specific classification
Urethritis
Prostatitis -affect on pH, motility,viability, volume, viscosity
prostato-vesiculitis -affect on pH, motility, viability, volume, viscosity
Epididymitis - affect of motility, viability
epididymo-orchitis - affect of motility, viability
Orchitis- affect on sperm production, morphology
Effects on semen
◦ Reduction of volume
◦ Increase ROS and DNA damage
◦ Changes in biochemical composition
◦ Production of ASA
◦ Low sperm maturity
◦ OAT with reduced viability
Laboratory findings
Suspect with the presence of high round cells in semen

peroxidase positive leucocytes should be differentiated

Genetics causes

Spermatogenesis is regulated by about 2000 genes

Majority are present on the autosomes
Around 30 genes identified on Y chromosome
Genetic factors manifest as
◦ Chromosoamal disorders
◦ Endocrine disorders
◦ Multifactorial disorders
Chromosoaml abnormalities
 Numerical
Klinefelter syndrome (47 XXY -Azoospermia) /(47XXY /46XY – Oligo-
Azopspermia)
Structural

Ring / dicentric Y chromosome

Translocations (XX males)
Gene mutation

• Y micro deletions (AZF region)

• DAZ gene
• Kallmann’s syndrome (X linked)
• AR receptor gene (androgen resistance)
• 5 alpha reductase gene
• primary ciliary dyskinesia- chromosome1)
• CFTR mutation (chromosome 7)
• Congenital bilateral absence of vas deferens (CBAVD)

Testicular cancer
Rare (6 per 100,000 men in USA)
Types
Germ cell tumor
◦ Seminoma
◦ Non- seminomatous germ cell
tumors

Stromal tumors

◦ Leydig cell tumors

◦ Sertoli cell tumors

Laboratory findings
Oligo/astheno/azoospemia

Ejaculatory disorders
Anejaculation – No ejaculate (aspermia)
Retarded ejaculation
Retrograde ejaculation
Complete – Azoospermia with very low volume
Partial – Oligozoospermia with low volume

Obstructions

-Epididymal level – Azoopermia with normal volume

-Ejaculatory duct level – Oligo/Azoos. with low volume

Causes of Anejaculation
◦ Spinal cord injury
◦ Diabetic neuropathy
◦ open bladder neck (RE)
◦ Multiple sclerosis
◦ Psychological factors
◦ Traumatic (Surgery)
◦ Drugs (eg. alpha blockers)
◦ Androgen deficiency (lack of puberty)
Retarded ejaculation
◦ Cannot ejaculate during sex
◦ Nocturnal emission possible

Psychological
Drug induced (eg. antiadregergic

Causes of Retrograde ejaculation

◦ Congenital wider bladder neck
◦ Diabetics
◦ Paraplegics
◦ Bladder neck operation
◦ Drugs (eg. antihypertensives)
Obstructions
◦ Mullerian duct cyst (Low volume / oligo/azoospermia)
◦ CFTR gene mutation (Low volume / azoospermia)
◦ Infections (severe oligo-azoos, low volume)
◦ Nephrolithiasis (Haemospermia possible)