Obstetrics Flashcards
Internal Genital Development
Develop from the Paramesonephric (Müllerian) System, becoming the uterus and fallopian tubes. Undifferentiated testes become ovaries, and the urogenital sinus becomes the vagina.
Histology of the vagina
Squamous stratified epithelium until the external os
Histology of the cervix
Simple columnar epithelium, beginning at the squamocolumnar junction at the external os. Lined with small, irregular crypts.
Ligaments of the Uterus/Ovaries (7)
- Round ligament (NOT SUSPENSORY, helps keep it anteverted) - attaches to proximal fallopian tubes, go around inguinal canal, end up in labia majora
- Uterosacral ligament (Suspensory, has PNS/SNS innervation) - begins at sacrum, inserts into posterior uterus at isthmus
- Cardinal Ligaments (Suspensory) - lateral uterus to lateral pelvic wall
- Pubocervical Ligaments - pass anteriorly around the bladder to the posterior pubic symphysis
- Broad Ligament - sheet of peritoneum covering ovaries and uterus
- Infundibulopelvic Ligament (NOT SUSPENSORY, contains ovarian aa, vv, nerve plexus and lymphatics) - from ovaries to the pelvic wall, part of the broad ligament
- Ovarian Ligament (Suspensory) - attaches ovary to the base of the fallopian tubes.
Peritoneal folds around the Uterus/Ovaries (5)
- Vesicouterine fold (between bladder and uterus)
- Pouch of Douglas (rectouterine fold, behind uterus)
- Mesometrium (Common stalk of peritoneum going up)
- Mesosalpinx (Fold off the mesometrium covering the fallopian tube)
- Mesovarium (fold off the mesosalpinx covering the ovary)
Histology of the Fallopian Tubes
Lined with ciliated, folded columnar epithelium
Blood supply of the ovary
Ovarian arteries come off the abdominal aorta, just underneath the renal aa, come through the infundibulopelvic ligaments to the ovary
Ovarian veins - L drains into the L renal vein, R goes into the IVC
Blood supply of the Fallopain tubes, uterus, and vaginal canal
Ovarian artery supplies part of the fallopian tube
Internal iliac –> Uterine artery –> Ascending and descending uterine arteries –> Uterus and fallopian tubes (Anastomosis with ovarian aa)
Uterine aa –> Vaginal branch of uterine aa –> Superior vaginal canal (anastomosis with uterine aa)
Inferior pudendal aa –> Inferior vaginal canal
Venous drainage follows arterial supply
Most commonly used surgical incisions in Gynaecological Surgery
Pfannenstiel Incision (Horizontal incision just above the pubic symphysis) - cosmetically appealing
Maylard (transverse) Incision (Horizontal incision between both ASIS) - bigger access, decent cosmesis
Median or Paramedian incision (Vertical down linea alba or just beside it) - for extensive procedures that may require abdominal exploration (e.g. ovarian cancer)
Phases of the Female Reproductive Cycle
The Follicular Phase (from menses to ovulation, consists of menstrual phase and proliferative phase)
The Luteal Phase (from LH spike/ovulation until just before menses)
Hormonal Changes during the Follicular Phase
Dropping levels of oestrodiol and progesterone lead to menses (as the lining is not maintained/arteries constrict), and a rise in FSH (mainly) and LH levels. Stimulates theca cells and granulosa cells in the ovary to produce E1 and E2, which have negative feedback loop on hypothalamus
Hormonal Changes during Ovulation
As oestrodiol levels rise to a critical level (>200 picograms over 50 hours), this switches it to a positive feedback loop, boosting LH and FSH levels. 36-44 hours later, ovulation occurs.
Hormonal Changes during the Luteal Phase
The Corpus Luteum (CL) produces oestrodiol and progesterone, promoting endometrial growth and development, as well as inhibiting the hypothalamus and pituitary gland. If pregnancy occurs, the CL is “rescued” by hCG released from the placenta, promoting further progesterone release - otherwise, the CL dies, and the cycle begins again, with dropping progesterone levels leading to artery constriction in the endometrium and menses begins.
Steroid Hormone Pathways
Cholesterol
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Pregnenolone –> Progesterone – … –> Aldosterone
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17-OH Pregnen. –> 17-OH Progesterone –…–> Cortisol
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DHEA –> Androstenedione –> Estrone (E1)
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Androstenediol –> Testosterone –> Estradiol (E2)
Early Development of Oocytes/Follices (before Puberty)
Peak numbers of oocytes at 20 weeks (6-7 mill), drops to 1-2 million at birth. Granulosa cells surround the oocytes to form the primordial follicle with a zona pellucida. These oocytes are arrested in Meiosis I at birth.
Development of Oocytes/Follicles from Puberty to Ovulation
At puberty, these follicles grow and develop, forming primary follicles.
Each cycle, these develop rapidly, forming a corona radiata and antrum (space), stimulated by high FSH levels. “The dominant follicle” is usually oestrogen-dependent, and becomes more and more sensitive to FSH, developing LH receptors on the granulosa cells just before ovulation.
The oocyte finish Meiosis I just before ovulation, producing the first polar body, and are then arrested at Meiosis II each month.
Oocytes/Follicles from Ovulation to Fertilization and Implantation
LH surge at ovulation causes proteolytic enzyme release, leading to dissolution of the follicle wall and release of the oocyte, zona pellucida and corona radiata onto the surface of the ovary. Here, it is picked up by the fallopian tube’s muscular movements and ciliary action, where it travels down into the tube, and is fertilized.
Just before fusion of male and female pronuclei, Meiosis II is completed, and the second polar body forms, giving the egg 23 single chromosomes.
Histophysiology of the Endometrium - layers and phases (3)
Divided into two layers - the funcitonalis (outer portion, has spiral arteries, sloughed off at menstration) and the basalis (has basal arteries and stem cells, minimal changes during the cycle)
Proliferative phase - endometrial proliferation from oestrogen, endometrial glands lined with pseudostratified columnar cells grow, and spiral arteries develop.
Secretory Phase - progesterone stimulates the glandular cells to secrete mucous, glycogen, and other substances - makes them tortuous and dilated. Stroma is oedematous.
Menstrual Phase - drop in oestrogen and progesterone (if no pregnancy) leads to constriction of arteries and tissue involution - becomes necrotic and WBC infiltrated, with RBC extravasation and sloughing off.
Spermatogenesis
Primordial Germ Cell
(Mitosis)
Primary Spermatocyte (Diploid) x1
(Meiosis I)
Secondary Spermatocyte (Haploid) x2
(Meiosis II)
Spermatid (Haploid) x4
(Develops to)
Sperm Cell (Haploid) x4
Sperm Capacitation
A process that allows the sperm to be able to fertilize in vivo.
Involves disinhibiting the acrosome of the sperm by it swimming free of seminal fluid.
Sperm Acrosome
A modified lysosome lying over the sperm head that allows penetration of the layers of the egg (ZP, CR) and moving the nucleus into the oocyte.
Timeline from fertilization to implantation
Immediately - once the sperm nucleus enters the oocyte, cortical granules inside the oocyte cause changes in the ZP to make it impenetrable to other sperm.
Day 1 - Pronuclear migration
Day 3 - Fusion of the pronuclei to form a zygote, begins divisions
Day 3-4 - Formation of a 16+ cell morula, and compaction of the morula (formation of desmosomes and tight junctions). Blastula forms.
Day 5 - Blastula cells migrate into cavity, forming a trophoblast, and the whole thing becomes a blastocyst. “Hatching” of the blastocyst from the ZP.
Day 7 - Implantation of the blastocyst into the endometrial wall.
Events after implantation
Blastocyst embeds into the endometrial wall, becoming surrounded by endometrial tissue.
Day 8 - Trophoblast begins to differentiate into the syncytiotrophoblast (conjoined, multi-nucleated cell) and the cytotrophoblast (reminant of the trophoblast), with the former beginning to invade into tissue, absorbing endometrial cells that have swelled from glycogen and lipids, and producing hCG. The embryonic disk differentiates into a hypoblast and an epiblast, with an amniotic sac developing in the epiblast.
Day 10 - continued development of the bilaminar disk, producing a amnionic sac and a yolk sac. Syncitiotrophoblast continues to invade, developing lacunae that fill up with maternal blood
Day 12 - primary chorionic villi form, and foetal circulation begins to become established.
The decidual reaction
The process that endometrial cells undergo to prepare for foetal implantation - swelling as they fill up with glycogen and lipids for foetal nutrition.
The Foetal adrenal gland (anatomy and function)
Consists of:
- Outer (Definitive) Zone - Secretes glucocortioids and mineralocorticoids, later becomes the 3 zones seen in adults (fasciculata, glomerula, and reticularis)
- Inner (Foetal) Zone - Comprises 80% of the gland, primarily secreting androgens, losing function at delivery and disappears after first year of life.
- Adrenal medulla - Synthesizes and stores catecholamines
Endocrine role of the placenta
- Releases corticotrophin releasing hormone (CRH)
- Produces progesterone and cortisol (takes over from the corpus luteum)
- Produces oestrogens - lacks 17α-hydroxylase, so cannot synthesize them from progesterone, instead using foetal androgens
hCG
Human Chorionic Gonadotrophin (hCG) is secreted by trophoblastic cells of the placenta, maintains the corpus luteum for first 6-8 weeks, also suppressing maternal immune system (increasing T-regulatory cells)
Rises after 8th day of pregnancy, peaks at week 6-12, should double every 2 days in the first few weeks of pregnancy.
CRH
Corticotrophin-Releasing Hormone (CRH) is produced by the placenta to stimulate release of foetal ACTH, leading to placental production of oestrogen from DHEA-S.
Plays a role in activation and progression of labour, and is suppressed by progesterone.
Oestriol (E3)
Most abundant oestrogen found in pregnancy
Cortisol
Promotes differentiation of Type II alveolar cells, bioproduction of surfactant into alveoli, and helps release CRH and prostaglandins before labour.
Oxytocin
Originates from the supraoptic and paraventricular nuclei in the maternal hypothalamus, released from the posterior pituitary in response to mammary stimulation and birth canal stretch. Results in uterine contractions.
Short half life of 3-5 minutes.
Prostaglandins and Leukotrines
Produced locally in the uterus, placenta and foetal membranes - help decidualization, cervical ripening before labour, and contraction of the uterus. This is why local infection (UTI, endocervical, etc) can induce premature labour.
PGE2 also helps keep the ductus arteriosus open, and so NSAID use during pregnancy can result in DA closure, foetal pulmonary hypertension and death.
Stages of Parturition
1 - Activation
Trigger comes from uterine stretch from foetal growth, as well as a surge of cortisol coming from the foetal HPA axis. Cortisol also triggers SP-A (lung surfactant) release from the lungs into the amniotic fluid, signalling that the lungs are mature (last organ to do so)
2 - Stimulation
Positive feedback loop set up between placental CRH release and foetal cortisol. This promotes prostaglandin production. In the myometrium, ratio of progesterone receptors shifts towards PRA (progesterone insensitive) and away from PRB, reducing progesterone’s inhibitory effects, and promoting oestrogen receptor ERα. Oestrogen’s effects include increasing oxytocin receptors, increasing prostaglandin receptors, promoting the actions of phospholipase C (producing inositol triphosphate –> calcium release from SR) and COX-2, and promoting gap junction production.
3 - Involution
As the foetus leaves the uterus, there is a massive surge of oxytocin (thought to be from foetal head compression), promoting uterine contraction to stem bleeding.
Weak contractions before parturition (name and mechanism)
Braxton-Hicks contractions are weak and not co-ordinated, occur 4-8 weeks before labour, and are due to a lack of gap junctions between muscle cells, and inadequate disinhibition of progesterone and stimulation by prostaglandins and oxytocin. DO NOT AFFECT CERVICAL EFFACEMENT AND DILATATION.
Supine Hypotensive Syndrome
Occurs in 10% of women, caused by drop in blood pressure when supine, as the uterus compresses the IVC, without any compensatory increase in peripheral vascular resistance. Leads to dizziness, nausea, and syncope. Managed by rolling patient to left side.
Poseiro Effect
Foetal distress that may occur when the mother is supine in late pregnancy - the heavy uterus compresses the aorta. Clinically, there is an absence of femoral pulses.
Metabolic Changes during pregnancy (halves)
First half = potentiated anabolic effects of insulin = glycogen storage and synthesis, reduced fasting glucose levels
Second half = insulin resistance = reduced glucose tolerance, increased FFA levels in blood, risk of ketoacidosis rises.
Summary of Maternal changes during pregnancy
Respiratory (5) Cardiovascular (6) Musculoskeletal (2) Endocrine (3) Dermatological (3) Gynaecological (3) Urological (2) Gastrointestinal (3)
Respiratory
- Diaphragm pushed up 4cm
- Increased Tidal Volume
- Increased O2 consumption
- Increased minute ventilation
- Respiratory alkalosis (7.40-7.45)
Cardiovascular
- Increased CO (higher HR and stroke volume)
- Water retention and increased blood volume
- Increased RBC, lower Hb
- Blood pressure lower
- Lower peripheral resistance
- Increased clotting factors
Musculoskeletal
- increased BMI
- Back pain, sciatica, calf cramps
Endocrinological
- Increased thyroid function (hCG)
- Cortisol levels rise
- Human Placental Lactogen
Dermatological
- Increased skin pigmentation
- Distension and proliferation of blood vessels
- stretch marks
Gynaecological
- Breast enlargement and pigmentation
- Uterine hypertrophy/stretch
- Lactobacilli proliferaction in vagina - low pH
Urological
- Increased GFR
- Ureter/collecting system dilatation (progesterone)
Gastrointestinal
- Oesophageal relaxation - Reflux
- Increased intra-abdominal pressure (haemorrhoids, reflux)
- Reduced motility (constipation)
Why does foetal blood have higher affinity for O2 than mother? (2)
- Prescence of HbF
- Higher concentration of Hb
Uterine/Placental flow diagram
Umbilical Artery
- PO2 = 18mmHg
- PCO2 = 55mmHg
- SaO2 = 40%
FLOW = 300-500mL/min, 50% shunt
Umbilical Vein - PO2 = 28mmHg - PCO2 = 45mmHg - SaO2 = 70% \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Uterine Artery
- PO2 = 100mmHg
- PCO2 = 32mmHg
- SaO2 = 95%
FLOW = 700-1200mL/min, 20% shunt
Uterine Vein
- PO2 = 33mmHg
- PCO2 = 40mmHg
- SaO2 = 60%
Foetal Cardiovascular Structure, their courses, and their adult reminants (5)
Umbilical Vein
- From placenta to ductus venosus
- Becomes ligamentum teres hepatis
Ductus Venosus
- From Umbilical vein to IVC
- Becomes Ligamentum venosum
Ductus Arteriosus
- From Pulmonary Artery to descending aorta
- Becomes ligamentum arteriosum
Foramen Ovale
- From right to left atrium
- Becomes intraventricular septum (closure)
Umbilical Artery x2
- From common iliac arteries
- Becomes the superior vesical arteries
Cardiovascular changes at birth (5) (in order)
1 - Elimination of placental circulation
2 - Vasodilation and reduced resistance of pulmonary vessels –> due to breathing
3 - Closure of foramen ovale –> right pressures < left pressures
4 - Closure of ductus arteriosus –> dropping PGE2, high O2 saturation
5 - Closure of ductus venosus
Immunology of Pregnancy (5 + what isn’t affected)
Uterus decidua
- Absence of B cells
- Increased numbers of T-suppressor cells
Placenta
- Absence of classic MHC I/II molecules on syncytiotrophoblast, only MHC I molecules on trophoblast to help with infection response
- HLA-G suppresses immune system
Vitamin D essential for these functions
Phagocytosis and maternal adaptive immune systems not significantly altered by pregnancy
Timing of Antenatal Visits
1 - week 8-12 (for risk assessment and health optimisation) 2 - week 17-19 3 - 24 4 - 28 5 - 32 6 - 36 7 - 38 8 - 40
The first antenatal visit - Components (4)
- Complete History (inc reproductive, genetic, family, social, nutritional)
- Physical examination (including BP, maternal weight)
- Labs (see other flash card)
- Estimating gestational age and date of confinement (due date)
The first antenatal visit - Labs (13)
- Complete blood count, including Hb (for baseline)
- Blood type and Rhesus factor
- Rhesus Antibody screen
- Pap smear screening (if indicated)
- Glucose tolerance test (if indicated)
- Ultrasound (if indicated)
- Urine dipstick screen - protein, glucose, leukocytes
- Urine culture
- Rubella serology
- Syphilis serology
- Chlamydial culture (if indicated)
- Hep B/C serology
- HIV Serology
Signs of Pregnancy (3 categories)
- Cardiovascular
>Physiological systolic murmur
>S3 (due to hypervolaemia) - Dermatological
>Linea nigra (down from the umbilicus)
>Spider naevi
>Palmar erythema
>Dark discolouration of the vulva and vaginal canal (Chadwick’s sign) - Gynaecological Signs
>Asymmetric enlargement (Piskacek’s Sign)
>Softer uterus (palpate uterus above cervix = Hegar’s sign)
Which vaccines are contraindicated in pregnancy? (5)
- BCG
- Measles
- Mumps
- Rubella
- Varicella
(all are live, attenuated vaccines)
Management of Rh negative pregnant women
RH0 (D) immunoglobulin should be given at 28 weeks, postpartum, and at any point where sensitization may occur (e.g. during a procedure)
Implantation bleeding
Abnormal vaginal bleeding caused by implantation, experienced in 30-40% of normal pregnancies.
Spontaneous Abortion rate
10-15% of recognised pregnancies, however may be as high as 50% of all conceptions, the majority in the first 14 days.
Drops to 3% by the 8th week.
Threatened abortion
Pregnancy complicated by vaginal bleeding before 20 weeks, sometimes with abdominal ache. 25-50% progress to spontaneous abortion. Best managed with US examination - determine viability of foetus, and later to manage the higher risk of preterm birth.
Types of spontaneous abortion (5)
- Threatened abortion
- Inevitable abortion (cramps, bleeding, cervical dilatation)
- Incomplete abortion (above + some products have come down, BEWARE OF SEPSIS AND HAEMORRHAGE)
- Complete abortion
- Missed abortion (When the foetus has died, but is retained, usually for over 6 weeks. Beware of coagulation problems, check fibrinogen until all tissue comes)
- Recurrent abortion (3+ clinically confirmed spontaneous abortions)
Domestic Violence risks to pregnancy
- Spontaneous abortion
- Preterm birth
- Low birth weight
Recurrent Abortion - Definition, Risk Factors (8) and Mangement
Defined as 3+ clinically confirmed spontaneous abortions.
Risk factors include:
- Infection (Mycoplasma, Listeria, Toxoplasma)
- Smoking and Alcohol
- Psychosocial stress - especially domestic violence!
- Medial conditions (e.g. DM, Hypothyroidism, SLE)
- Maternal Age
- Local Factors
> Uterine Abnormalities
> Cervical Incompetence
> Uterine Submucous Fibroids
> Intrauterine Adhesions
- Foetal Factors - significant genetic/chromosomal abnormalities
- Placental factors
Managed by screening for all the risk factors, uterine US, and chromosome testing, as well as Vitamin D levels. Over 50% of cases will be normal.
Estimating Gestational age and Date of Confinement (due date)
Should be done in the first visit, done by either using the date of last menstration (add 9 months and 1 week = 38 weeks) or US to determine crown-rump length in week 6-11 (accurate to within 7 days)
Indications for genetic screening (9)
Should be offered to all, however there are some indications for testing:
1) Maternal age >38
2) Previous child affected by genetic disorder or mental retardation
3) Previous child who died in neonatal period
4) Multiple foetal losses
5) Abnormal serum marker results
6) Consanguinity
7) Maternal/Paternal conditions/carrier status predisposing the foetus to congenital abnormality/genetic disorder
8) A current pregnancy that has been exposed to teratogens (e.g. antiepileptics)
9) A foetus with abnormal US findings.
10) Women/Couples in difficult life situations where they won’t cope with a disabled child
Most common chromosomal abnormalities (3)
- Sex chromosomal aneuploidies (e.g. Turner’s, Kleinfelter)
- Balanced robertsonian translocations
- Autosomal trisomies (e.g. Tri-21)
Incidence of Down Syndrome vs Age, and main mechanism
<35 = 1/800 35-39 = 1/300 40-45 = 1/80
Most from meiotic nondisjunction (95%)
Fragile X Syndrome Pathophysiology
X-linked disorder that is the second most common cause of developmental delay after Down’s Syndrome. Caused by CGG triplet repeat in the Fragile X mental retardation 1 gene (FMR1), leading to inhibited expression of FMR protein, required for neural development.
First and Second Trimester Screening (5 and 3)
First trimester screening looks at:
- Maternal age
- Foetal nucial translucency (US) = between 10-14 weeks
- Maternal serum β-hCG
- Pregnancy associated plasma protein A (PAPP-A)
- US nasal bone assessment
= down syndrome detection rate of 93%
Second trimester screening is a serum triple screen:
- α-fetoprotein (AFP) –> helps detect neural tube defects, false positive in multiple gestation, foetal demise, or inaccurate gestational age.
- Maternal serum β-hCG
- Unconjugated estratriol (UE3) - at 16-20 weeks
Time of maximum haemodilution
Week 28 - need Hb to compare with first antenatal visit
SF-height measurement
Used to assess foetal growth, between week 20 and 34 - correlates closely with gestational age.
Measured from pubic symphysis to top of the fundus, BLADDER MUST BE EMPTIED. Foetus should be in longitudinal lie, and there cannot be multiple gestations or any other uteral masses (e.g. fibroid)
Foetal heart rate measurement and normal value
110-160 bpm
Doppler US can be used from week 12.
Pinard’s stethoscope can be used in most from week 16, all by week 22. Can help confirm lie of the foetus.
Leopold’s Manouvers, 6 characteristics and method
Start at week 36, helps determine a few characteristics:
- Situs = longitudinal vs transverse?
- Presentation = cephalic/breech/shoulder?
- Position = 1st (back to left) or 2nd (back to right)
- Altitude/Station = how far the leading part has descended
- Habitus = Foetal head in relation to body (deflexed/flexed)
- Engagement = foetal head is descended and locked in the pelvis
Involves 4 manouvers:
1) Hands on top, determine presentation (breech or cephalic?)
2) Lateral palpation - position? Lie?
3) Single handed palpation of presenting part - presentation? Station/engagement? (i.e. ballottable?)
4) From behind, similar to first except away from fundus - presentation? Confirm ballot.
Indications for antenatal OGTT testing (5)
- Age >38
- Type 1 or 2 diabetes in family history
- BMI > 27
- Gestational diabetes in previous pregnancy
- Immigrants from Indian subcontinent or North Africa
Period of organogenesis
weeks 4-10
Role of routine US in antenatal visit (when and why?)
Performed in week 17-19 (visit 2) - referred in visit 1.
The following is checked:
- Length of gestation/due date estimation
- Number of offspring
- Placental position
- Foetal anatomy
Biophysical Profile Testing - 3 components
Used to assess foetal wellbeing, especially indicated in higher risk pregnancies with:
- Intrauterine Growth Restriction
- Diabetes Mellitus
Consists of:
- Maternal assessment –> 10 kicks per hour is normal
- Non-stress testing –> measuring for rises in heart rate every time the baby moves
- Ultrasound assessment –> several components, including measuring amniotic fluid problems (oligohydramnios/polyhydramnios), foetal breathing and stretching movements (30 breaths/3 movements every 10 mins is normal), and doppler assessment of umbilical artery vascular resistance.
Definition of normal labour
Normal labour is defined as progressive cervical effacement and dilation as a result of regular uterine contractions, occurring at least every 3 minutes, and lasting 30-60 seconds each.
Closure of the fontanelles
Posterior fontanelle - 6-8 weeks of life
Anterior fontanelle - 18-24 months of life
Foetal head dimensions (6)
From top:
- Biparietal diameter: 9.5cm
- Bitemporal diameter: 8cm
From side:
- Suboccipitobregmatic (if flexed presentation, from base of skull to ant. fontanelle) - 9.5cm
- Occipitofrontal (if anteflexed presentation, from occipital bone to glabella) - 11cm
- Supraoccipitomental (if brow presentation, from parietal bone to chin) - 13.5cm
- Submentobregmatic (if face presentation, from jaw to ant. fontanelle) - 9.5cm
Pelvis dimensions (5)
AP lengths
- Inlet = 11cm
- Middle = 12cm
- Outlet = 13.5cm
Transverse lengths
- Inlet = 13.5cm
- Outlet = 11cm
Shapes of pelvis (4)
Gynecoid - Found in 50%
- Round inlet
- Curved sacrum
- Straight sides
- Spaceous pubic arch
- Average size spines
- PROMOTES OCCIPUT ANTERIOR
Android - Found in 30%
- Triangular inlet
- Straight sacrum
- Converging sides
- Narrow arch
- Prominent spines
- PROMOTES OCCIPUT POSTERIOR
Arthropod - Found in 20%
- Oval inlet (larger AP)
- Posteriorly inclined sacrum
- Straight sides
- Narrow arch, curved outwards
- Prominent spines (because of diameter)
- PROMOTES OCCIPUT POSTERIOR
Platypelloid - Found in 3%
- Oval inlet (larger transverse)
- Flat sacrum
- Straight sides
- Wide arch
- Large distance between spines (because of diameter)
- PROMOTES TRANSVERSE ENGAGEMENT
Synclitic engagement definition
When the biparietal diameter of the foetal head is parallel to the pelvic plane (when the head lines up nicely with the pelvic plane)
Asynclitic engagement may help reduce the diameter in some situations.
Indications for clinical pelvimetry (2)
1) Clinical evidence/obstetric history suggestive of pelvic abnormality
2) History of pelvic trauma
Lightening
2+ weeks before labour, the baby’s head drops snugly into the pelvic canal.
Induction vs Augmentation of labour
Induction = starting labour artificially Augmentation = stimulating labour artificially after it started naturally.
Cervical ripening
Occurs before labour, often including effacement. Softening of the cervix as a result of prostaglandins and enzyme action
Indications for Induction (3 and 7)
MATERNAL INDICATIONS
> Diabetes Mellitus
> Pre-eclampsia
> Heart Disease
FOETOPLACENTAL INDICATIONS > Prolonged pregnancy > 42 weeks > IUGR > Abnormal foetal testing > Rh Incompatibility > Foetal abnormality > Premature membrane rupture > Chorioamnionitis
Absolute and Relative Contraindications for Induction (1 and 7)
ABSOLUTE
> Contracted pelvis
RELATIVE > Previous uterine surgery > Classic caesarian > Transected uterus (e.g. myomectomy) > Overdistended uterus > Premature baby with immature lungs > Abnormal presentation > Acute foetal distress
Bishop Score
Used to assess likelihood of successful induction.
Uses four cervical indicators and the station of the foetal head.
High score is between 9 and 13.
Induction process (6 pre-induction steps and 5 principles)
There are several things to consider before starting induction:
> Cervical ripening –> promote using PGE2 applied vaginally
> Assess likelihood of successful induction with Bishop score
> Draw blood and perform Rh screen, as well as type and Hb.
> Ensure patient is on continuous Cardiotocography (CTG)
> Check urine for protein/glucose
> Know Hep B status of the mother
Oxytocin infusion is given, keeping in mind several principles
> Give oxytocin IV, to allow fast discontinuation
> Infusion to be “piggybacked” onto saline IV
> Best infused with an infusion pump
> Should not exceed 72 hours
> Reduce dosage if adequate labour established, to avoid complications
Complications of Induction (3)
HYPERSTIMULATION
- occurs from excess infusion, can lead to foetal distress and uterine rupture (rare)
ANTIDIURESIS
- ADH-like effect means water is retained
- If infused for >24 hours, risk of severe water intoxication, leading to convulsions and coma
UTERINE FATIGUE
- Muscular non-responsiveness and post-delivery hypotonus increases the risk of post-partum haemorrhage.
The stages of labour (4)
1) From the onset of true labour contractions until the completed dilation and effacement of the cervix
2) From cervical dilation and effacement until the baby is delivered
3) From the delivery of the baby until the placenta is delivered
4) From the placental delivery until the patient stabilizes
The first stage of labour - phases, rate, and management steps (7)
The two phases are latent and active.
LATENT PHASE
Effacement and early dilation occurs, highly variable in length.
ACTIVE PHASE
Begins when the cervix is dilated between 4 and 6cm, and uses active uterine contractions to dilate the cervix. Occurs at a rate of 1cm/hour in primiparous women and 1.2cm/hour in multiparous women.
Management of the first stage involves:
> Positioning - the mother may be mobile, or lying down on side (to promote blood flow)
> Maternal Monitoring - Mother’s vitals should be checked every 1-2 hours
> Foetal Monitoring - Foetal HR should be recorded every 30 mins in uncomplicated delivery
> Uterine Monitoring - Uterine contractions should be palpated every 30 minutes to assess strength, duration, and frequency
> Hydration - the mother may drink small amounts of high-calorie fluids/solids, however gastric motility is depressed. IV dextrose/fluids preferred.
> Analgesia
> Vaginal examination - should be performed every 2 hours during the active phase (avoid in latent phase to prevent infection)
Gravidity vs Parity
Gravidity = how many pregnancies the woman has had Parity = how many deliveries the woman has had
The second stage of labour - movements and management (5)
Commences when the cervix is fully dilated at 10cm, and ends when the baby is delivered. Should take 30 mins to 3 hours in the primiparous woman, and 5-30 mins in the multiparous woman.
4 cardinal movements:
1) FLEXION - the baby’s head is flexed if occiput anterior, to allow for the shorter, suboccipitobregmal diameter. The baby begins in a transverse orientation here.
2) INTERNAL ROTATION - the baby’s head rotates 90 degrees, to bring the occiput anteriorly. Usually completed by the time it reaches station 0 (at the spines)
3) EXTENSION - in order to be delivered through the opening, the neck needs to extend - crowning occurs here.
4) EXTERNAL ROTATION - once the head is through the opening, the baby rotates another 90 degrees to align the shoulders with the rest of the opening.
Management should include:
> Positioning - any position acceptible, all fours common
> Valsalva - encourage valsalva during contractions
> Foetal monitoring - continuously
> Vaginal examination - every 30 minutes to determine status
> Baby delivery - another flashcard, mother is in the lithotomy position and Ritgen’s manouvers used.
Delivery of the baby
The mother adopts the lithotomy position, and the perineum is supported using one hand. Ritgen’s manouvers are used to deliver the baby.
1) Support the perineum with one hand, while pushing on the head with a few fingers, to stop sudden slippage in or out of the canal.
2) When the head is delivered, gently grasp both sides of the head, and gently assist external rotation, still supporting the perineum with one hand.
3) Gently pull downwards to expose the anterior shoulder, and then upwards for the posterior shoulder. NOT TOO HARD, risk of damage to brachial plexus
4) Support as the rest of the baby is delivered, grasping the chest and the feet as they come out.
5) Place the baby on the mother’s chest, and allow 1-2 minutes before cutting the chord (especially important in premature babies)
The Three P’s of obstetrics
POWER
> the uterus, regular contractions
PASSAGE
> the bony pelvis - inlets and outlets
> the muscular pelvis - the pelvic floor
PASSENGER
> the foetal head and moulding
> presentation and position of the skull
The third stage of labour - management (5)
Lasts from the birth of the baby until the placenta is delivered, usually about 2-10 minutes.
Management involves:
> Examination - any heavily bleeding tears of the cervix and vagina should be inspected and attended to, especially since there is little blood flowing from the placenta at this point.
> Placental delivery - DO NOT PULL until the following four are observed: the cord begins to lengthen, there is fresh bleeding, the fundus rises, and the uterus contracts and firms (signs that the placenta has separated). Then, gentle traction and pressure on the uterus. INFUSE OXYTOCIN BOLUS.
> Massage - to help uterus contraction
> Inspection - inspect the placenta to see if it is intact and 100% has been delivered. Estimate the amount of blood lost, and check the maternal vitals to ensure stability.
> Repair - any episiotomy cuts or other tears.
The fourth stage of labour
Lasts 5-6 hours after delivery of the placenta, until the patient is stable. Requires close monitoring for postpartum haemorrhage, keep checking the vitals for signs of hypovolaemia. May bleed for up to 10 days afterwards, due to unrepaired tears, placenta fragments, or uterine relaxation.
Puerperium (4 components)
The period of 6-8 weeks following delivery, in which several physiological changes occur to revert the body back to it’s pre-pregnancy state.
UTERUS AND VAGINA
> Uterus undergoes involution, where tissue undergoes catabolism to shrink the uterus from about 1000g to 100-200g. The patient may experience lochia rubra, lochia serosa, and lochia alba as this occurs.
> The cervix stiffens again
> The vagina may never regain it’s previous tone
> Pelvic floor regains tone, should be assisted with Kegels
CARDIOVASCULAR CHANGES
> Rapid increase in peripheral vascular resistance, due to loss of uteroplacental shunt
> CO and blood volume return to normal levels within 2 weeks
PSYCHOSOCIAL CHANGES
> Due to hormone and emotional changes, may experience postpartum blues. Should be screened with Edinburgh Postnatal Depression Score.
RETURN OF MENSTRATION AND OVULATION
> Menses return usually within 6-8 weeks
> Ovulation may take several months to return
> Delayed by nursing
> Contraception should be considered to avoid unwanted pregnancy
Benefits of Breastfeeding (4)
- Breast milk is ideal for the newborn, relatively cheap and in good supply
- Ideal for release of oxytocin, which helps uterine involution and pregnancy weight loss
- Release of IgA into the breast milk confers passive immunity to the newborn
- Gut microbiome established in the newborn via breastmilk.
Lactation physiology
Initiated as oestrogen levels drop when the placenta is removed, and prolactin/oxytocin levels soar when suckling begins. Oxytocin initiates contraction of myoepithelial cells in alveoli and breast ducts.
Colostrum first secreted, mostly protein, fat, mineral and IgA, this changes to mature milk after 3-6 days, mainly composed of protein, fat, water and lactose, as well as casein and omega-3 FA’s.
Complications of Breastfeeding (4)
- Cracked nipples - best managed by stopping breastfeeding, risk of infection
- Mastitis (uncommon)
- Breast abscess (following mastitis)
- Drug passage to newborn - notably for antibiotics (including penicillin, tetracycline), heroin, methadone (death), and anticonvulsants.
Mastitis - pathophysiology, presentation, and management
Uncommon, develops usually after 2-4 weeks of breastfeeding, caused by s.aureus infection.
Presents first with fever and chills, followed by red, swelling and acutely painful breast.
Managed by swabbing for culture, and treatment with dicloxacillin/flucloxacillin for 7-10 days. Consider stopping breastfeeding.
Obstetric Pain Pathways (2 nerves, which roots?)
Uterus = afferent nerves via the inferior hypogastric plexus to T10-L1 (4 nerve roots)
Vagina and Pelvic floor = L1 - S4
External Genitalia = via pudendal nerve to S2-S4
Adverse effects of pain during labour (2)
1) Hyperventilation = Alkalosis = increased maternal affinity for O2 = reduced O2 offloading to foetus
2) increased catecholamine release = reduced uterine blood flow and contraction
Non-Pharmacological pain relief during labour (6)
- Education and psychoprophylaxis
- Emotional support
- Back massage
- Hydrotherapy
- Acupuncture => evidence supporting
- Transcutaneous electrical nerve stimulation (TENS) => little evidence
Pharmacological pain relief during labour (2 categories, 5 in one category)
PARAENTERAL NARCOTICS
> very limited efficacy, may cause neonatal respiratory and HR depression. Fentanyl most commonly used.
NEUROAXIAL ANALGESIA
> Lumbar epidural - most common, allows pain block to T10 while preserving motor function.
> Combined spinal/epidural - advantage of rapid spinal block with lasting epidural analgesia
> Pudendal block - local infiltration around the vagina just before delivery, does not stop contraction pain.
> Caudal block - very similar to epidural, same effect
> Paracervical block - blocks pain from contractions by affecting uterus nerves to T10-L1, lasts 40-60 minutes, may affect foetal HR, breathing, and CNS.
Epidural procedure and considerations
Before initiating:
> Administer 500-1000mL bolus of fluid
> Patient/foetus monitoring continuously
Insert needle into L3/4 space, placing epidural catheter. Trial small dose of bupivacaine, then begin continuous infusion. Should start with loss of cold/pinprick sensation.
EPIDURAL CAN BE INITIATED WHENEVER, will have no effect on any stage of labour.
Epidural complications
> Systemic toxicity (if hits a vessel) - dizziness, tinnitis, numbness, seizures, loss of consciousness > Cardiovascular toxicity - hypotension, tachycardia, arrhythmia/arrest > Infection > Block failure > Nausea and vomiting > Respiratory depression > Epidural abscess > Epidural haematoma
Epidural vs Spinal
EPIDURAL
- Slow-onset
- Predictable spread/effect
- May spread to body/foetus
- No motor block
- Reduced risk of hypotension
- Can be continuous
SPINAL
- rapid onset
- Large, predictable dense block
- No foetal spread/systemic toxicity risk
- Motor block
- Hypotension
- Defined, single-dose duration
Absolute and relative contraindications to regional anesthesia (4 and 3)
ABSOLUTE > Patient refusal > Coagulopathy > Infection over the needle site > Severe and ongoing hypovolaemia
RELATIVE
> Previous back surgery
> Heart condition (especially aortic stenosis)
> Increased ICP
Process to give Anaesthesia for Caesarian (5)
> Give antacid (sodium citrate)
Put on monitoring and give supplemental oxygen, as well as fluids
Pre-oxygenation with at least 4 vital capacity breaths
Rapid sequence induction (propofol) and intubation (succinylcholine)
Confirmation of intubation by end-tidal CO2 and auscultation
Factors suggesting difficult intubation
- Obesity/short neck
- Neck flexion/extension issues
- Receeded chin
- Poor dentition
- Large tongue/excess oropharyngeal tissues
Anaesthesia related complications in obstetrics (7)
> Arrest > Abscess/meningitis > Epidural hematoma > Neurological injury > Respiratory arrest > Failed intubation > Death
Circumstances when GA should be used (3)
> Extreme emergency when the patient does not have epidural cathether
Regional anaesthesia contraindicated
Regional anaesthesia failure (1.7% of cases)
Effects of epidural on labour
> Slightly prolonged second stage - hormone release
Impaired ability/reduced maternal urge to push
Slight fever (0.5 degrees)
Headache (1% incidence)
Facilitating Neonatal Adaptation - what to do when the baby comes out (5)
1) CLEAR THE AIRWAY
A towel or suction should be used to remove the secretions on the face and mouth. If meconium is present, this should be intensified, and intubation considered for tracheal suction.
2) DRY THE NEWBORN
Prone to evaporative cooling.
3) CLAMP THE CORD
Arteries should close within 40-60 seconds, but the vein may take up to 5 mins. Delaying is known to confer benefits.
4) ENSURE RESPIRATION
The baby should start breathing within 30 seconds of birth - if not, or if the HR <100, should be given to the resus team for stimulation and positive pressure ventilation.
O2 supplimentation should begin at room air levels, and titrated up according to baby vitals - excess O2 associated with retinopathy and bronchopulmonary displasia.
5) CORRECT SURFACTANT DEFICIENCY
Deficiency associated with respiratory distress, so should be corrected with tracheal injection of synthetic or natural surfactant.
APGAR SCORE
Normal values are >7 at 1 minute, and >9 at 10 minutes. Uses: 1) Heart Rate 2) Respiratory Effort 3) Muscle Tone 4) Reflex Irritability 5) Colour
Resuscitation of an Asphyxiated Infant (5, ABCDE)
1) AIRWAY
Establish airway, suction any secretions/meconium from airway, consider endotracheal tube.
2) BREATHING
Positive Pressure Ventilation indicated in apnoea, gasping, or HR <100. Give through either bag ventilation or endotracheal tube, start breathing at rate of 40-60 breaths/minute, should help HR.
3) CIRCULATION
If HR still <60, begin cardiac massage at rate of 90/minute (once every half second). Give adrenaline if not successful.
4) DRUGS
Correct any other biochemical abnormalities:
> Acidosis - checked using umbilical blood gases, give sodium bicarbonate
> Anaemia - from blood loss, give blood transfusion
> Narcotic Depression - rare, give naloxone as antidote
> Hypoglycaemia - if IUGR or diabetes, give low concentration (10%) glucose - high concentrations can cause lactic acidosis and brain swelling.
5) EXTREME MEASURES
If still not resuscitating, consider ECMO
Normal Neonatal Vitals
HR = 110-160 BPM
BP 75-100/50-70
RR = 30-60
Temp = 36.5-37
Contraindication to Internal Foetal scalp electrode
If the mother has HIV or Hep B, or other infection which might be transmitted.
Methods of measuring uterine contractions (3)
> Manual palpation (gives intensity)
Tocodynamometer - external electrode, does not give intensity
Internal uterine catheter - measures pressure changes, gives intensity
Periodic FHR change patterns (3 categories, 3 subcategories in 1)
Response of FHR to uterine contractions, several response patterns
1) NO CHANGE
2) ACCELERATION - normal response, reassuring
3) DECELERATION
> Early Deceleration - co-incides with the contraction, seen when the foetal head is engaged (Cushings reflex and increased vagal tone to head compression)
> Late Deceleration - Occurs due to foetoplacental insufficiency and hypoxia
> Variable Deceleration - Occurs due to cord compression, may be non-repetitive. Rapid changes.
Three-tiered FHR interpretation system & Intervention
CATEGORY I (normal) Characterised by: > Normal baseline > Moderate variability > Abscence of abnormal decelerations
CATEGORY II (Intermediate) Characterised by changes in: > Baseline rate > Baseline variability > Accelerations > Decelerations that are not early Should be approached by trying to find the underlying cause. Generally helped by changing the mother to a lateral position, giving fluids, and reducing oxytocin infusion.
CATEGORY III (Abnormal)
Characterised by either:
> Absent baseline variability with deceleration or bradycardia
> Sinusoidal pattern
Indicates the baby should be delivered in the next 30 minutes, either vaginally or via caesarian.
Bleeding after 20 weeks (late second trimester and third trimester) - Differential Diagnosis (7)
COMMON
> Placenta Previa
> Preterm Labour (marginal separation of placenta)
UNCOMMON > Uterine rupture > Chorionic vessel rupture > Cervical/vaginal lacerations or lesions (e.g. cancer) > Congenital bleeding disorder > Unknown (via exclusion)
Placenta Previa - Risk Factors (5) and Classification (3)
RISK FACTORS > Multiparity > Multiple gestation > Previous placenta previa > Caesarian > Maternal Age
CLASSIFICATION
> Complete Placenta Previa - where the placenta completely overlies the internal os
> Partial Placental Previa - where the placenta covers only a part of the internal os
> Marginal Placenta Previa - where the edge of the placenta is at the edge of the internal os
Placenta Previa - Presentation, Investigation/Diagnosis, and Management
Presents with painless vaginal bleeding in an otherwise normal pregnancy - usually after 30 weeks. More common in early pregnancy, however 90% of cases resolve due to development of the lower uterine segment.
Best diagnosed with transvaginal ultrasound.
Management of all cases requires admitting and bed rest. Further management depends on gestational age and severity of bleeding - if maternal health compromised, needs caesarian no matter the age. If mild, wait until lung development at week 36 (confirm with amniocentesis), then elective caesarian.
Placenta Accreta
Abnormal placental attachment, where the defective decidua formation leads to deep attachment to the myometrium. May also be deeper (increta) or through the uterus (percreta).
Predisposed to by uterine surgery, including caesarian.
60% will require hysterectomy after placental removal, as the bleeding is too severe. Elective hysterectomy must be considered after caesarian.
Abruptio Placentae - Risk Factors (9)
> Maternal HTN (Most common risk factor) > Previous placental abruption > IVF pregnancy > Trauma > Polyhydramnios with rapid decompression > Short umbilical cord > Premature membrane rupture > Folate Deficiency > Substance abuse - heroin, cocaine, tobacco
Abruptio Placentae - Presentation, Diagnosis and Management
Presents as painful vaginal bleeding with uterine tenderness and hypertonia/hyperactivity. May also present with foetal distress.
A clinical diagnosis, however requires US to rule out coinciding placenta previa.
Management involves close monitoring, establishing IV access, and typing/cross-matching blood to prepare for emergency caesarian (can deliver vaginally if foetus deceased and mother stable enough). May require hysterectomy to stop the bleeding.
Abruptio Placentae - Complications (5)
> DIC - most common cause in pregnancy > Hypovolaemia > Acute renal failure (due to hypovolaemia) > Foetal/Maternal death > Sheehan syndrome
Sheehan Syndrome
Necrosis of the pituitary gland, as a result of perfusion insufficiency or clots. Pituitary becomes swollen in pregnancy, and so is very sensitive to reduced blood flow, as may occur in massive postpartum haemorrhage, or other causes of hypovolaemia.
Presents with lactation difficulty (early), amenorrhea, adrenal insufficiency, and adrenal crisis during infection or surgery.
Requires hydrocortisone, thyroid, and oestrogen/progesterone replacement
Uterine Rupture
Complete separation of the uterine wall, occurs in about 0.5%.
May be spontaneous, traumatic, or associated with previous scar (40%), and can occur before or during labour.
Typically presents with sudden, intense abdominal pain, with or without vaginal bleeding. Foetal HR is abnormal, and the presenting part may have retracted on examination. Foetal distress common, death or long-term neurological sequalae may occur. Foetal death seen in 30%.
Requires urgent laparotomy, decision to do hysterectomy based on severity and location of tear, and the desire of the patient to have more children.
Foetal Bleeding
Rupture of umbilical vessel complicates about 0.5% of pregnancies, usually due to a velamentous insertion - inserting between the amnion and chorion (seen in 1% of single pregnancies and 10% of twins)
Diagnosis via Apt test, mangement = immediate caesarian.
Different insertions of the umbilical vessels (4)
Can insert: > Normally (centrally) > Eccentric (off to the side) > Marginal (at the edge of the placenta) > Velamentous (off the placenta)
Apt Test
Helps determine if a blood sample (usually from the vagina) is from the mother or the foetus.
1) Add sample to a test tube, and add water to lyse the RBC and free the Hb.
2) Add KOH
3) If the solution turns brown, it is maternal blood, as the Hb becomes denatured, however if it stays red, it is foetal (HbF not denatured by KOH)
Postpartum Haemorrhage - Causes (8)
> Uterine Atony (75-80%) > Vaginal/Perineal lacerations > Retained placental tissue > Trauma > Low placental implantation > Coagulation disorder > Amniotic fluid embolism > Abruptio Placentae > Uterine Inversion
Uterine Atony - Risk Factors (7)
> History of PPH > Prolonged labour > Parity of 5+ > Uterus overdistension (due to multiple gestation, polyhydramnios, etc) > Oxytocin augmentation > Vitamin D deficiency > Genetic factors
Obstetric Shock - definition and differential (5)
Hypotension without significant external bleeding
Differentials include:
> Concealed haemorrhage within the uterus
> Uterine inversion
> Amniotic fluid embolism
> Concealed haemorrhage under repaired episiotomy
> Uterine rupture
Management of High-Risk PPH patients (5)
> Perform labs before labour - Hb, blood typing and cross match, and antibody screen
Oxytocin infusion as soon as baby is delivered, continue for 6h
Inspect vagina/perineum for lacerations
Assess placenta, ensure entirety removed
Frequent uterus assessment afterwards
PPH Management (5)
1) Assess and monitor vitals closely
2) Estimate blood lost, consider blood coag panel
3) Rapid oxytocin infusion
- if failure, give methylergonovine
- if failure, give misoprostol
4) Bimanual uterus compression and massage, consider packing/catheter
5) Consider uterine artery ligation, embolization, or hysterectomy if very severe
Amniotic Fluid Embolism
Uncommon, caused by amniotic fluid escaping into the maternal circulation, with the thromboplastin leading to consumption coagulopathy, intense bronchospasm, and vasomotor collapse. 80% mortality rate.
Managed by respiratory support (usually mechanical), CPR, positive cardiac ionotrope, rapid vascular volume expansion to help shock, and reversal of coagulopathy with platelets, fibrinogen, and blood products.
Dystocia of the Latent phase of Labour - upper limit, differential, and management
Normal upper limit is 18 hours for nulliparous women and 10 hours for multiparous women.
Differential includes: > False labour/prelabour (common) > Excess sedation/analgesia > Foetal malposition > Large foetal size
Usually has favourable outcomes, if caused by medication, allow this to wear off. Oxytocin augmentation if this is not the case.
The active phase of labour - minimum rates and definition of “Adequate labour”
Dilation should continue at a rate of 1.2cm/h (nulliparous) or 1.5cm/h (multiparous)
Descent should occur at a rate of 1cm/h (nulliparous) or 2cm/h (multiparous)
Active labour = 200 Montevideo Units, where MU are measured as the added amplitude (in mmHg) of each contraction in 10 mins.
Transverse Arrest
When the head does not rotate through the pelvis, instead stopping in a transverse position in the pelvis for more than 1 hour.
Managed through either manual rotation, vacuum extraction, or caesarian if required.
Occiput Posterior Delivery
Results in prolongation (>2 hours) of the active phase, plus increased discomfort for the mother, however there is no reason to be alarmed if the baby’s descent is progressive, and the FHR is normal.
Macrosomia - Definition, risk factors (8), and consequences (5)
Defined as a foetus weighting >4500g, equal to >90% percentile of gestational weight.
Associated with: > Genetic Predisposition > Maternal Diabetes > Pre-pregnancy BMI > Pregnancy weight gain > Male foetus > Multiparity > Over 40 weeks gestational age > Maternal age
Can result in: > Labour dystocia > Shoulder dystocia > Genital trauma > PPH > Post-delivery infection
Shoulder Dystocia - Definition and significant risk factors (2)
Difficult delivery of the shoulder, either requiring use of special procedures, or a head-body delivery interval of more than 60 seconds. May present with “turtle sign” of baby’s head retracting between contractions.
Significant risk factors include
> Maternal diabetes
> Macrosomia
Complications of Shoulder Dystocia (5)
> ERB Palsy - Palsy of C5-C6, but only of the ANTERIOR shoulder (posterior = scapular injury during delivery). Limp shoulder in neonate, and asymmetrical Moro reflex. > Klumpke Palsy - Deficit in C8-T1 > Clavicular fracture > Humerus fracture > Hypoxia, brain injury, and death
Shoulder Dystocia Management manoeuvers (5)
In order:
> SUPRAPUBIC PRESSURE - Guides the shoulder under the symphysis
> McROBERT’S MANEUVER - “knees to ears”, reduces sacrospinous angle and helps guide the baby under
> GASKIN MANEUVER - “on all fours”, helps deliver posterior shoulder. May be combined with WOOD MANEUVER of turning baby around
> Forceful posterior shoulder delivery - may result in fractured humerus, heals quickly
> Fracture of one/both clavicles for delivery
High-risk pregnancy factors (8)
> Family hx of prematurity > Personal hx of obstetric complications > Maternal medical conditions - HTN, Obesity, diabetes > Under 36 weeks > Multiple gestation > Malpresentation > Foetal distress > Meconium staining
Causes of Preterm Labour (8)
> Late Preterm Birth (50-70%) (between 34 and 37 weeks)
Spontaneous preterm labour
Multiple gestations
Pregnancy-associated HTN
Premature preterm rupture of membranes
IUGR
Cervical incompetence/uterine abnormality
Antepartum haemorrhage
Smoking
Pathways to Preterm Labour (4)
> INFECTION - especially bacterial vaginosis, leads to shorter cervix and distruption of membranes
PLACENTAL/VASCULAR - failure of trophoblasts to invade spiral arteries
STRESS - elevated cortisol and catecholamines, promoting uterine contractility
UTERINE STRETCH - progesterone and parathyroid-related hormone overcome by uterine stretch (e.g. macrosomia, twins)
Diagnosis and Management of Preterm Labour (3 and 5)
Diagnosis based on:
> Labour between 20-37 weeks
> Documented uterine contractions
> Cervical changes - effacement of 80% or dilation more than 2cm
Management involves:
1) Fast assessment and identification of any causes - includes routine bloods
2) Patient should be started on fluids and dextrose, and admitted for bed rest - resolves 20% of cases
3) Culture should be taken for group B strep, investigate for bacterial vaginosis, and begin ampicillin and erythromycin for 7 days
4) Initiate Tocolytic Therapy with glucocorticoids
5) If all fails, deliver if after 24 weeks.
Tocolytic therapy - Methods (3)
> MAGNESIUM SULPHATE
Competes with calcium for cellular entry, lowers intracellular levels - should give a loading dose and continuous infusion for at least 12 hours.
Side effects = warm, flushed feeling, resp depression, cardiac conduction defects (overdose), reduced APGAR
NIFEDIPINE
Slow calcium channel antagonist.
Side effects include = headache, hypotension/tachycardia, cutaneous flushing
PROSTAGLANDIN SYNTHASE INHIBITORS
Includes indomethacin, used short-term only. Risks include premature DA closure, reduced foetal renal function, and increased risk of NEC and ICH.
Tocolytic Therapy - Contraindications (5)
> Severe pre-eclampsia > Severe antenatal bleeding > Chorioamnionitis > IUGR > Foetal demise/incompatibility with life
Premature Rupture of Membranes (PRM) - definition and diagnostic testing
Defined as amniorrhexis before onset of labour, at any gestational age. Predisposed to by infection, abnormal membrane physiology, and nutritional deficit.
Diagnosis should involve STERILE speculum examination (risk of infection), rule out urinary incontinence or mucous plug loss. Take cultures, and test amniotic fluid for pulmonary maturity.
Testing if a fluid is amniotic fluid can be done via:
> NITRAZINE PAPER TEST - tests alkaline pH of amniotic fluid
> FERN TEST - leaving the fluid to dry will make ferns
> AmniSure TEST - gold standard, measures PAMG-1
Premature Rupture of Membranes - Managament
Decisions based on gestational age/pulmonary maturity of the foetus, and the risk of infection/chorioamnionitis
Conservative management involves keeping the pregnancy until the lungs mature, including:
> Careful surveillance for infection
> Antibiotic therapy - ampicillin and erythromycin
> Glucocorticoids
> Tocolytic therapy controversiala
Testing for Lung Maturity
Amniotic fluid is tested for three products of lung maturity, and one control:
- Lecithin (increased levels after week 35)
- PI and PG (phospholipids in the surfactant)
- Sphyngomyelin (baseline, doesn’t change)
Lecithin:Sphyngomyelin ratio can be affected by blood or meconium in the amniotic fluid, but PI and PG levels are not.
Intrauterine Growth Restriction (IUGR) - Definition and Aetiology (3 categories - 9, 2, 2)
IUGR occurs when foetal weight falls below the 10th percentile for that gestational age.
Causes grouped into: MATERNAL > Poor nutrition > Smoking > Drug use > Alcohol > Diabetes > Hypertension > Obesity > Heart disease > Antiphospholipid syndrome PLACENTAL INSUFFICIENCY > HTN > Chronic renal disease FOETAL > Intrauterine infection (Listerosis or TORCH) > Congenital Abnormality
IUGR - Types
Symmetric - when the head and body are restricted together, seen in infection and congenital abnormality
Asymmetric - when the head grows at the cost of the abdomen, liver and pancreas most severely affected.
IUGR - Diagnosis (5, 6 in last)
Involves:
> Establishing correct last menstrual date
> Evaluating uterine size
> Foetal heart rate auscultation date (between week 12 and 14)
> Quickening date - between week 16-20
> US assessment
- Foetal crown-rump length
- Head circumference
- Abdo circumference (MOST VALUABLE)
- Femur length
- Amniotic fluid volume
- Calculated foetal weight
- Doppler US of umbilical vessels
IUGR - Management (3) and Complications (5)
MANAGEMENT
> Pre-pregnancy involves lifestyle changes and medical management
> During pregnancy, goal is to deliver once lungs are developed. If not sure, bed rest and surveillance with regular measurements required.
> After birth, watch baby for hypoglycaemia, hypothermia, and respiratory distress.
COMPLICATIONS > Hypoglycaemia > Asphyxia > Meconium aspiration > Mental retardation > Adult-onset disease - HTN, Obesity
Post-Term Pregnancy
Defined as lasting beyond 42 weeks, increased risk of perinatal mortality. Biggest risk from Foetal Dysmaturity Syndrome (FDS), from the aged and infarcted placenta, leading to insufficiency and hypoxia. May result in macrosomia and associated risks. Unknown aetiology in most instances.
Management involves identifying higher risk foetuses with FDS, and initiating labour if the head is engaged, especially in the presence of oligohydramnios or FHR decelerations.
Types of twins (plus timing of split)
DIZYGOTIC (Fraternal) TWINS
Come from two different eggs that were fertilized simultaneously, have separate amnions, chorions and placentae. Incidence depends on maternal factors, including family hx, ethnicity, and age, overall twice as often as monozygotic.
MONOZYGOTIC (identical) TWINS
Come from splitting of the same egg, what they share depends on the timing of the split:
> 0-72h = diamniotic, dichorionic (30%)
> 4-8 days = diamniotic, monochorionic (thin septum) (69%)
> 9-12 days = monoamniotic, monochorionic (no septum, same sac) (1%)
Constant incidence of about 1/250
Abnormalities of Twinning (6)
> CONJOINED TWINS
If division occurs after 13 days, cleavage will be inadequate, resulting in conjoined twins. Classified according to location - Thoracopagus (anterior, most common), Pyopagus (posterior), Craniopagus (cephalic), Ischiopagus (caudal).
INTERPLACENTAL VASCULAR ANASTAMOSES - most commonly AA, can be AV or VV. Predisposes to TTTS, hydramnios, and malformations.
TWIN-TWIN TRANSFUSION SYNDROME - when there is an asymmetric distribution of blood flow via the placenta. In the donor twin, can lead to hypotension and growth restriction, and HTN, hyperviscositiy, thrombosis, oedema, and CHF in the recipient. 50% survival, needs photocoagulation of the vessels responsible.
FOETAL MALFORMATIONS
UMBILICAL CORD ABNORMALITIES
RETAINED DEAD FOETUS SYNDROME - can lead to DIC in the mother.
Complications of Twinning (7 and 8)
MATERNAL > Anaemia > Hypertension > Hydramnios > Preeclampsia > PPH > Premature labour > Caesarian FOETAL > Malpresentation > Congenital abnormality > IUGR > Umbilical cord prolapse > Placenta Previa > Abruptio Placentae > Prematurity > Death
Management and Delivery of Twins
ANTENATAL
> Intense follow-up
> US every 2 weeks
> Monitor diet and weight gain closely
> Bed rest, hospitalization, and vaginal progesterone
> Monitor for pre-eclampsia
> Tocolytic therapy if before 34 weeks
DELIVERY
> If Vertex-vertex delivery (50%), can be delivered vaginally, just need to watch second birth for uterine cord prolapse, abruptio placentae, and malpresentation, and mother is at higher risk of PPH and atony.
> Any breech presentation requires caesarian.
Malpresentation - Predisposing Factors (6)
> Prematurity > Structural Abnormalities (e.g. hydrocephalus) > Multipule gestation > Placenta previa > Pelvic tumors > Hydramnios
Breech Presentation - Classification and Diagnosis
CLASSIFICATION
> Frank - both legs curled up (65%)
> Complete - legs both extended straight up
> Incomplete/Footling - One foot extended down, one leg curled up
DIAGNOSIS
> Via leopold’s maneuver’s
> Confirmed via US
Breech Presentation - Management and Delivery
MANAGEMENT
> Exclude foetal/maternal abnormalities (e.g. congenital abnormality, myomas)
> External Cephalic Version (ECV) - obstetric rotation of the foetus, carried out after 36-37 weeks gestation. Small risk of placental abruption and cord compression.
DELIVERY
> Standard is to deliver via caesarian
> If vaginal delivery unavoidable:
- DONT TOUCH UNTIL UMBILICUS OUT
- Gentle traction until scapulae
- Deliver arms by sweeping them down
- Head is delivered by flexion of neck and traction of maxilla
Face Presentation - Make sure to rule this out!
Anencephaly
Pre-eclampsia - Pathophysiology and Pathology (3)
PATHOPHYSIOLOGY
Thought to be caused by inadequate uteroplacental perfusion, from failure of cytotrophoblast to invade spiral arteries, leading to placental ischaemia, and immune vascular damage.
PATHOLOGICAL LESIONS
> Lack of Decidualization of the myometrium
> Glomerular capillary endotheliosis
> Ischaemia, haemorrhage, and necrosis of the liver, placenta, and brain, as well as the retina (ominous)
Pre-eclampsia - Clinical Presentation (7)
Normally presents in young, nulliparous women with:
> HYPERTENSION - from generalized vasospasm
> WEIGHT GAIN AND OEDEMA - from vascular endothelial damage, leading to fluid leakage into the extravascular space
> PROTEINUREA - From damage to glomerular membrane
> LIVER - RUQ pain and elevated LFT’s from liver necrosis
> COAGULOPATHY - Most commonly thrombocytopenia, however DIC can develop.
> PLACENTA - Insufficiency can lead to IUGR and oligohydramnios, as well as abruption. Resistance seen on doppler.
> CNS - Increased cerebral vascular resistance leads to visual disturbance (retinal vasospasm), headache and hyperreflexia are worrying. Seizures if severe.
Pre-eclampsia - Diagnostic Criteria (2 main and 6 minor)
FOR DIAGNOSIS
> HYPERTENSION - Systolic >140 or Diastolic >90 in two measurements, 4 hours apart in previously normotensive patient.
> PROTEINUREA - via either:
- >0.3g protein over 24 hour urine sample
- Protein:creatine ratio >0.3
- Urine dipstick result >1+
FOR SEVERE PREECLAMPSIA DIAGNOSIS, ADD ONE:
> Severe HTN - Systolic >160 or diastolic >110 in two measurements, 4 hours apart
> Reduced hepatic function
> Impaired renal function
> Pulmonary oedema
> Visual/Cranial disturbances
> Thrombocytopenia (<100,000/uL)
HELLP Syndrome
A form of severe pre-eclampsia, characterised by
> Haemolysis
> Elevated Liver enzymes
> Low Platelets (thrombocytopenia)
Seen in elderly, multiparous women mainly, may occur without HTN.
Evaluation of Pre-eclampsia (3 questions)
3 questions to keep in mind when evaluating:
> Is it severe?
> Is there foetal compromise? (IUGR, Oligohydramnios, or FHR abnormality)
> Is the foetus mature enough to be delivered?
Should include thorough hx and ex, as well as:
> CBC + coags + smear
> Renal function testing
> LFT's
> US evaluation of:
- Fluid index
- Congenital abnormality
- Foetal growth
- Doppler resistance index
> Non-stress testing of foetus
Management principles of Pre-eclampsia
Balance maternal health with foetal maturation:
> If MILD, deliver at 37 weeks
> If SEVERE, deliver at 34 weeks (if possible)
Hospitalize and monitor every case
If the disease is sever, but the foetus is still immature, the patient may need stabilization with:
> CLOSE MONITORING
> SEIZURE PROPHYLAXIS - Patients should recieve Magnesium Sulfate, watch closely for signs of CNS irritability - hyperreflexia, headaches, visual changes, and Chvostek’s sign. Watch urine output closely, as toxicity may occur - flushing, paralysis, cardiac arrest
> ANTIHYPERTENSIVE THERAPY - Will reduce risk of CNS haemorrhage, however does NOT change disease course. Labetalol, hydralazine or nifedipine all used for this, just beware of hypotension, as placental perfusion is vulnerable.
> GLUCOCORTICOID THERAPY - for lung maturity
Risk Factors for Pre-eclampsia
> Nulliparity (biggest risk factor) > Maternal age >40 (second biggest risk factor) > Previous history of pre-eclampsia > Chronic HTN > Renal disease > Ethnicity > Diabetes > Obesity > Family History
Risk Factors for Pre-eclampsia (9)
> Nulliparity (biggest risk factor) > Maternal age >40 (second biggest risk factor) > Previous history of pre-eclampsia > Chronic HTN > Renal disease > Ethnicity > Diabetes > Obesity > Family History
Chronic HTN in Pregnancy - Definition and Management
Defined as Systolic >140 or diastolic >90 that was present before pregnancy - usually essential, however may be secondary from renal disease or endocrine disorders - needs to be investigated if appears very early in pregnancy.
The primary management goals include HTN management and detection of pre-eclampsia and IUGR.
Pharmacotherapy recommended if systolic >160 or diastolic >105, safest meds to use include:
> Methyldopa
> Labetalol
> Hydralazine
Goal is to keep pressure under 160/100
Foetal growth should be monitored every 2-3 weeks, and NST/Doppler studies may be indicated.
Antihypertensives to AVOID during pregnancy (3)
> ACEI - e.g. perindopril
ARB’s - e.g. Irbesartan
Mineralocortiocoid blockers - e..g. Spirinolactone
Superimposed Preeclampsia - what to look for
Look for sudden HTN spikes and proteinurea, follow management of preeclampsia
Gestational HTN - Definition and Management
Development of HTN (systolic >140, or diastolic>90) after 20 weeks pregnancy, resolves within 12 weeks after delivery. RETROSPECTIVE DIAGNOSIS.
Managed similarly to Chronic HTN.
Rhesus Alloimmunization - Pathophysiology
An immunological disorder occurring only in Rh- women with Rh+ babies. 15% of Caucasians are Rh-, whereas 8% of African Americans and 1-2% of Asians are Rh-.
The Rh complex is made of various antigens (C, D, E, c, d, e), with 90% of cases occurring as a result of sensitization to the RhD antigen.
Requires leakage of foetal cells into maternal circulation, leading to sensitization and production of RhD antibodies –> most likely to occur during delivery, thus this becomes the sensitization event, with the following pregnancy being at risk of hydrops foetalis
Initially, IgM antibodies are produced, which cannot cross the placenta, however these are replaced by IgG antibodies which can, leading to foetal RBC haemolysis.
If mild, haemolysis can be compensated for by increased erythropoiesis, however, if severe, can lead to hydrops foetalis - extramedullary haematopoiesis, portal HTN, hypoalbuminaemia, hyperbilirubinaemia, and heart failure.
Testing for Rhesus Alloimmunization - Parents
Blood should be taken from every pregnant woman and tested for blood grouping, Rh type, and antibody screening.
If the mother is Rh-, the father should also be screened:
> if Rh-, no risk
> If Rh+, need genetic testing. Homozygous = foetus will be Rh+. Heterozygous = 50% chance of Rh+.
Testing for Rhesus Alloimmunization - Foetus
Indicated after parents come back as “at risk”
Initial testing involves:
> FOETAL ANTIBODY TESTING - cell-free foetal DNA in the maternal plasma can be tested at the end of the first trimester
> MATERNAL ANTI-D TITRES - used to estimate severity of foetal haemolysis - if under 1:16, the first pregnancy is safe, however requires repeating every 2-4 weeks, and needs US investigation if comes back higher.
Ultrasound testing involves:
> MCA Peak Systolic Velocity - serial measurements for detecting anaemia, should be repeated every 1-2 weeks from week 18-35 (after this, false positives)
> Foetal Anatomy Assessment - look for changes of hydrops foetalis.
If US testing comes back positive:
> PERCUTANEOUS UMBILICAL BLOOD TESTING (PUBT) - May be done if the foetus is under 35 weeks, allows testing for Hb, haematocrit, blood gases/pH, and bilirubin levels. Risk of foetal exsanguination, mortality risk of 1-2%.
Hydrops Foetalis - Diagnostic Criteria + associated features (2)
Done via US assessment of baby, requires two or more of:
> Ascites
> Pleural effusion
> Pericardial effusion
> Skin oedema
> Polyhydramnios
May also see two associated features of hydrops foetalis - liver and placental enlargement.
Rhesus Alloimmunization - Management (3)
INTRAUTERINE TRANSFUSION
Goal of transfusing fresh Group O, Rh- PRBC after 18-20 weeks of age (due to size of vessels), repeating every 1-3 weeks until just before delivery at around week 37. Survival rate of 90%
Given intravascularly via the umbilical cord in US-guided procedure (used to be intraperitoneal infusion, RBC delivered via lymphatics)
MATERNAL PLASMAPHORESIS
Researched at the moment, reserved for special severe cases
DELIVERY
Balance of risk of intrauterine demise vs neonatal mortality risk - usually at week 37.
Rhesus Alloimmunization - Prevention (2)
1) Avoid maternal exposure (e.g. procedures)
2) Rh immunoglobulin given at:
> Any possible sensitization event
> At 28 weeks
> Within 72 hours of delivery
Gestational Diabetes - Pathophysiology
80-90% of diabetes in pregnancy will be gestational, promoted by the actions of human placental lactogen, progesterone, prolactin, and cortisol.
Glucose crosses the placenta easily, and leads to hyperglycaemia and hyperinsulinaemia (from foetal pancreas). The hyperglycaemia is teratogenic, promoting congenital abnormality, and may result in macrosomia and dystocia.
Foetal demise may occur from acidosis or hypoxia from increased metabolism.
Gestational Diabetes - Complications (6 and 6)
MATERNAL > Infections > Polyhydramnios > Preeclampsia > Caesarian > Post-pregnancy Type II Diabetes > Diabetic emergency/other complications (e.g. neuropathy)
FOETAL
> Macrosomia
> Delayed lung, liver and brain development
> Congenital abnormality - heart, brain, neural tube, and other
> Neonatal hypoglycaemia and hypocalcaemia
> IUGR
> Foetal death
Gestational Diabetes - High Risk Pregnancies (5)
> Obesity > Hx of GDM/Macrosomia > Family history of Type II DM > PCOS > Glycosuria
Gestational Diabetes - Screening and Diagnosis (3)
Three (“two”) step method:
1) HIGH RISK PREGNANCIES - require screening in the first antenatal visit with a blood glucose test
2) OGTT IN WEEK 24-28 - aims to catch most women when they are most influenced by hormonal changes, however allowing time for therapeutic intervention. Can be non-fasting, with 50g of glucose
3) IF STEP 2 POSITIVE, DO FASTING OGTT - 8-12 hours of fasting, then drink 100g of glucose, measure glucose levels hourly for 3 hours afterwards - diagnosis of GDM = 2/3 elevated measurements.
Gestational Diabetes - Management (8)
> GOALS - Fasting glucose of 5.3 mmol/L, 1h PP of 7.8 mmol/L, 2h PP of 6.7mmol/L
MONITORING - Trimesterly HbA1C, daily glucose levels
DIET
EXERCISE
PHARMACOTHERAPY - If euglycaemia is not reached, patient may need either Glibenclamide (OHA, works on K channels on β-cells, risk of hypoglycaemia), or Insulin.
OBSTETRIC MONITORING - keep an eye on the baboy with Foetal US, Foetal echo, and serum AFP.
DELIVERY - Try to keep to term, however can be delivered earlier by caesarian if macrosomia. Ensure euglycaemia during labour. Watch for neonatal hypoglycaemia and reduced insulin requirements for mother.
POST-PARTUM - Re-do 75g OGTT 6-12 weeks post-partum.
Hyperthryoidism in Pregnancy
Clinically presents with tachycardia, weight loss, exophthalmos, and tremor, with low TSH and high free T4. Can lead to prematurity, IUGR, and foetal death.
Managed with pharmacotherapy:
> Atenolol
> PTU in first trimester, Methiazole in second and third - block synthesis of thyroid hormone.
Hypothyroidism in Pregnancy
Managed with levothyroxine.
Immune Thrombocytopenia in Pregnancy
NOT TO BE CONFUSED WITH GESTATIONAL THROMBOCYTOPENIA, which never dips below 70,000/uL.
Therapy started if bleeding or if platelets under 50,000/uL, involves prednisone. Closely monitor baby for antibody haemolysis.
SLE in Pregnancy
Diagnosis with 4/11 criteria - MD SOAP BRAIN
Less likely to flare up in pregnancy, may have rebound flare afterwards. Manage with steroids and hydroxychloroquine.
Nausea and Vomiting in Pregnancy
Usually mild, seen in 50-80%, resolves by the second trimester.
Managed by avoiding triggers, eating small meals frequently, avoiding lying down after meals, and ginger and accupuncture, with antiemetic (doxylamine) therapy if these dont work.
Hyperemesis Gravidarum
Defined as persistent nausea and vomiting in a ketotic pregnancy. Clinically presents with intractable nausea and vomiting, as well as weight loss and dehydration.
Treatment is symptomatic, with first line treatment being Vitamin B6 and doxylamine.
Mendelson Syndrome
Aspiration of gastric contents during labour, due to reduced gastric emptying and increased pressure.
Risk factors include sedatives, narcotics, and anaesthesia, as well as eating before labour. Can lead to ARDS, needs urgent airway support.
Thromboembolic diseases in pregnancy
Greatest risk being a few weeks postpartum, due to changes in clotting cascade and mechanical factors.
DVT and PE managed with either unfractionated heparin or LMWH (enoxaparin)
Amniocentesis - Procedure and Risks (3)
Involves removing a sample of amniotic fluid (usually about 20mL) using a 22G needle under US guidance, done transabdominally.
Risks include
> 0.3% chance of pregnancy loss
> 1% of amniotic fluid leakage
> Risk of Rh alloimmunization in Rh- women (ensure prophylaxis)
Amniocentesis - Diagnostic (4) and Therapeutic (2) Indications
DIAGNOSTIC INDICATIONS
> GENETIC TESTING - testing in week 16-20 for identification of chromosomal and single gene abnormalities -> PCR and karyotyping
> BIOCHEMICAL TESTING - α-fetoprotein (AFP) used to detect open walls (e.g. neural tube defects)
> INFECTION - Testing for TORCH infections via culture, PCR, gram staining, glucose and leukocytes.
> LUNG MATURITY TESTING - Testing levels of lamellar bodies (Ratio of lecithin:sphyngomyelin) and pulmonary phospholipids (PG and PI)
THERAPEUTIC INDICATIONS
> POLYHYDRAMNIOS - used to drain excess fluid
> TWIN-TWIN TRANSFUSION SYNDROME - also used to drain excess fluid away from the receiving twin, laser ablation.
Chorionic Villus Sampling
Involves taking a small sample of the chorionic villi, either transcervically or transabdominally, under US guidance.
The sample is then tested for chromosomal abnormality (division can be directly observed)
Can be done earlier than amniocentesis at week 10-12, however is a sterile procedure, AFP cannot be measured, and there is a small chance of false negative (in mosaicism)
Risk of foetal loss is less than 1%.
Cordocentesis
A procedure in which foetal blood is obtained directly from the umbilical vein under US guidance. Used for rapid karyotyping using leukocytes, 1% risk of pregnancy loss.
Cervical Cerclage
Circular stitch placed around the cervix to help cervical incompetence - usually placed at around 13-16.
Indications for Operative Vaginal Delivery (4), and what to avoid (Pearl)
> PROLONGUED SECOND STAGE - lack of progress for 2 hours (3 hours if anaesthesia)
SUSPICION OF IMMINENT FOETAL COMPROMISE - class III FHR patterns
STABILISING THE HEAD DURING BREECH
SHORTEN THE SECOND STAGE FOR MATERNAL BENEFIT - especially in HTN, diabetes, cardiac disease, or epidural
NEVER use one form after another (e.g. vacuum after forceps), due to much higher risk of morbidity
Forceps Delivery - Risks (2)
> Failed delivery (7%)
> Maternal Injury - soft tissue, bladder, perineum
Vacuum Extraction - Risks (2) and when to discontinue
> Failed delivery (12%)
Foetal morbidity - cephalohaematoma, retinal haemorrhage, subgaleal haematoma (under periosteum)
DISCONTINUE if no progress, or if 2 “pop-off’s” occur.
Caesarian Delivery - Indications (6)
ABSOLUTE
> Previous non-transverse uterine incision - e.g. classical caesarian, or myomectomy
> Placenta Previa
RELATIVE > Dystocia > Previous Caesarian > Breech Presentation > Foetal Distress
Caesarian Delivery - Types (3) and associated risks
> LOW TRANSVERSE - preferred, transverse incision behind the bladder. Lower rate of rupture (1%), bleeding, paralytic ileus, and adhesions.
CLASSIC CAESARIAN - massive vertical incision made on fundus, may be done lower down (modified low vertical). Indicated if lower uterine segment is underdeveloped, inaccessible, or there is a planned hysterectomy with the delivery. 4-7% rupture risk, always need caesarians afterwards if to deliver.
Prevention of Caesarians (2)
> External Cephalic Version (ECV) - done in week 36-37, 60% success rate
Vaginal Birth after Caesarian Delivery (VBCD) - trial of labour following low transverse caesarian and no hx of rupture. Emergency team on standby, 70% success rate with benefit of lower maternal morbidity.
