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0+G REVISION

TOPICS
OBSTETRICS Hypertension in Pregnancy Diabetes in Pregnancy Bleeding in Pregnancy Obstetric Emergencies Focusing on PPH GYNAE PMB Pelvic Pain

SCENARIO 1
ANC: 33 year old primigravida of 37 weeks gestation. Patient presented with oedema, headache and PV bleeding. BP was 187/116.

Differential Diagnosis
PET

investigations should look for signs of HELLP syndrome checking LFTs and platelet count as well as US scan to look for placental site (as cause for the PV bleeding) and assess fetal growth (as IUGR is a complication of PET & LIQUOR VOLUME).

complications of PET - eclampsia and fetal death. Trainee knew that the patient would need Labetalol and to continue being followed up with antenatal clinic with bi-weekly BP measurement.

After discussion, trainee learnt about further specific management such as induction at term and prescribing Aspirin in the next pregnancy for the patient to take until 37 weeks. Trainee also learnt about important features to recognise on Cardiotocography.

Read further about Magnesium treatment toxicity hyporeflexia as a sign Study more CTGs - recognise that pre-eclampsia can cause reduced utero-placental blood flow which appear as decelerations on CTG. Read further on doppler ultrasound in detecting end diastolic flow in IUGR.

Preeclampsia
Classification of hypertension in pregnancy; hypertension and the placenta; clinical presentation and diagnosis. Management assessment of severity, both fetal and maternal, over time; antihypertensives; magnesium; timing of delivery; intrapartum and post natal management. Gestational Hypertension Chronic Hypertension Pre-eclampsia Eclampsia HELLP syndrome

Maternal and Fetal complications

SCENARIO 2

Tracy, an 18 year old single woman presents to the delivery suite with a two hour history of intermittent abdominal pains and vaginal bleeding. The pains have been getting stronger and more frequent. She is 29 weeks into her pregnancy and had one previous admission at 15 weeks with vaginal bleeding. She lives with her mother and 3 younger brothers. She smokes 15 cigarettes per day but stopped drinking when she became pregnant. Vaginal examination revealed the cervix to be 2cm dilated and fully effaced.

APH
Obs - History from an "pregnant" actress presenting with PV bleeding. It was meant to be an Obs palpation but the patient left halfway through the day so they went to plan B. Was asked about booking visits, routine investigations, and about the 3 stages of labour. History Examination Differential Diagnosis: Management Aim?

Bleeding in Pregnancy BEFORE 24 WEEKS:


Pain then PV Bleeding ECTOPIC PREGNANCY Rupture (Pregnancy outside of uterus. Most wont past 24 /40) Bleeding +/- pAIN = SPONTANEOUS ABORTION (See elsewhere) PV Bleeding (may have uterine contractions) = HYDATIDIFORM MOLE (Random type of placental tissue growth mimicking pregnancy) AFTER 24 WEEKS: No Pain + PV bleeding + Uterus: Soft & Non Tender = APH: PLACENTA PRAEVIA (Placenta is at cervical os stopping fetus from passing) Pain + PV bleeding + Uterus: Contracted = APH: PLACENTAL ABRUPTION (Placenta detached from uterus) IN SUMMARY!! Pain Only (Bleeding Later) ? Ectopic Bleeding +/- Pain(<24/40) ? Spontaneous Abortion / H Mole (though rare!)

Recurrent miscarriage: incidence; causes anti phospholipid antibody syndrome, parental chromosome abnormalities, cervical incompetence; investigations, including examination of the products of conception. List 4 reasons for a positive pregnancy test with an empty uterus on ultrasound scan (pregnancy of unknown location).

Bleeding in Pregnancy AFTER 24 WEEKS:


Bleeding Only (> 24/40): ? Placenta Praevia Pain + Bleeding ? Placental Abruption?

ANTEPARTUM HAEMORRHAGE (APH) Def Bleeding > 24/40 but < Delivery (< 24/40: Bleeding PV) PP Incidence: 4.7% (6% For twins) 20% due to Placenta Praevia, 30% Abruption, 50% uncertain. Cause Abruption, Placenta Praevia, Vasa Praevia (baby may bleed to death) Local Vaginal Bleeding: Polyp, CIN, Vaginal infection. Predis Post coital, Trauma, SROM Inv / Dx PV: Placenta Praevia may bleed if finger introduced. Also: PV with PRM (Risk of introducing infection)] Mx ASSESS Degree of bleeding Maternal Observations (HR, BP) Fetal HR (CTG) SEVERE: () IVI, Blood tests, raise legs. Left lateral position (minimises effects of aortocaval comp) O2, Blood (eg 6U), Send blood for clotting screen IVI replacement & Central line. Catheterise (keep >30mL/h). Summon help. Delivery Baby by C Sect (Especially if PP) MILDER: IVI, Hb, Xmatch, Coagulation studies, U&Es. Check Regularly: Pulse, BP, Blood loss. Est Dx with US / Spec. Prophylactic steroids (fetus lungs), Avoid intercourse, Bed rest. If PP Monitor in H after 34/40 until delivery (C section). Advisable to still give Anti D as not able to 100% distinguish from PA. If PA + pain & bleeding settled + no compromise to fetus may go home after Anti D (Tx as risk pregnancy thereafter)

Diabetes

PLACENTAL ABRUPTION VS PLACENTA PRAEVIA Shock out of keeping w visible loss Pain constant Tender, tense uterus Normal lie, presentation Fetal heart: absent, distress Coagulation problems Beware preeclamsia, DIC, anuria

PP
Shock in proportion to visible loss No Pain Uterus not tender Both may be abnormal Fetal heart usually normal Coagulation problems rare Small bleeds before large

CTG

ABNORMAL LABOUR: Labour becomes abnormal when there is: Poor progress Fetus shows signs of compromise Malpresentation Uterine scar Labour has been induced

Poor progress in labour:


Poor progress in the first stage of labour: Progress in labour is dependent on 3 variables: 1.The powers 2.The passenger 3.The passages Abnormalities in one or more of these factors can slow the normal progress of labour.

Inefficient uterine action:


This is the most common cause of poor progress in labour It is more common in primigravidae Characterized by weak & infrequent contractions A frequency of 4-5 contractions per 10 minutes is considered ideal Treatment is by maternal rehydration, ARM & IV oxytocin

Cephalo-pelvic disproportion (CPD):


o This implies anatomical disproportion between the fetal head & maternal pelvis o It can be due to a large head o It can be due to small pelvis o Combination of the two o It can occur in women of small stature (<1.6m) o Previous fracture of the pelvis o Metabolic bone disease o Relative CPD can occur with malposition of the fetal head (deflection) such as occurs in OP position

CPD is suspected in labour if:


Progress is slow or arrested despite efficient uterine contractions. the fetal head is not engaged V/E showed severe moulding & caput formation The head is poorly applied to the cervix Oxytocin can be given carefully to a primigravida with mild to moderate CPD as long as the CTG is reassuring. Relative CPD may be overcome if the malposition is corrected Oxytocin use in a multiparous woman with slow or obstructed labour carries the risk of causing uterine rupture.

Malpositions: Occipitoposterior position (OP position):


o Occipitofrontal diameter 11cm o The head usually rotates to OP position in normal labour o About 10% rotate to OP position o There are usually longer 1st & 2nd stages of labour o There is increased chance of instrumental delivery & caesarean section.

labour may be poor. Brow presentations are associated with the mento-vertical diameter (13.5cm). This is too large to fit through the bony pelvis. Shoulder presentations cannot deliver vaginally & poor progress will occur. Malpresentations are more common in women of high parity. They carry a risk of uterine rupture

Abnormalities of the passages that cause delay in the progress in labour:


Bony pelvis Uterus (fibroids) Cervix (scarred) leads to cervical dystocia

Poor progress in the 2nd stage of labour:


o Causes of 2nd stage delay can be classified as abnormalities of the powers, the passenger & the passages. o Delay can also occur because of a persistent OP position. o Narrow mid-pelvis (android), prevents internal rotation of the fetal head. o This results in arrest of the fetal head at the level of the ischial spines in the transverse position (deep transverse arrest (DTA) ).

Pattern of abnormal progress in labour:


The use of the partogram to plot the progress of labour improves the detection of poor progress. Indeed, three patterns of abnormal labour are described on the partogram: 1.Prolonged latent phase 2.Primary dysfunctional labour 3.Secondary arrest

Prolonged latent phase (LP):


LP is longer than the arbitrary time limits (3-8 hours). More common in primiparous women. Can be extremely frustrating & tiring for the woman. Intervention in the form of ARM or oxytocin infusion will increase the likelihood of poor progress later in labour & the need for caesarean birth. It is best managed away from the labour suite with simple analgesics, mobilization & reassurance.

Primary dysfunctional labour (PDL):


PDL is a term used to describe poor progress in the active phase of labour (<1cm/h cervical dilatation). More common in primiparous women. It is most commonly caused by inefficient uterine contractions. It can also result from CPD & malposition.

Secondary arrest:
This occurs when progress in the active phase is initially good but then slows or stops altogether Typically after 7cm dilatation Causes are: Fetal malposition Malpresentations CPD Inefficient uterine contractions It is vital to make diagnosis Great care must be exercised in the use of syntocinon if CPD, malposition or malpresentation is suspected is suspected in a multiparous labour. This may cause uterine rupture. Uterine rupture is extremely rare in primipaorus.

Failure to progress & instrumental delivery


Under these circumstances (DTA), delivery may be achieved by: Rotational forceps (kiellands) Ventouse extraction Caesarean section When there is doubt as to whether vaginal delivery is achievable, the obstetrician may decide to perform a trial of forceps in the OT.
Instrumental delivery incidence, preparation, anaesthetic options, modes of delivery,
complications.

Augmentation of contractions with syntocinon should only ever be commenced if the CTG is normal. If progress fail to occur over 4 hours, C/S will be necessary.

Sue, a 28 year old woman in her second pregnancy was seen at the clinic at 41 weeks. She requested induction of labour and was admitted 3 days later. Her pregnancy had been uncomplicated (her previous baby weighed 4.2kg and was delivered normally). The cervix had a modified Bishop score of 4 and PGE2 2mg gel was inserted in the posterior fornix. Four hours later she was contracting every 3 minutes and the cervix was 2cm dilated and effaced. Her contractions eased, and so an amniotomy was performed and an Oxytocin infusion commenced. Six hours later the registrar told Sue that monitoring of her baby's heart was showing fetal distress and that delivery by Caesarean Section should be considered.

Definition of fetal distress; detection of fetal distress; fetal physiology during labour; fetal acid-base balance; association between fetal distress and acute and chronic effects on the baby. Obstetric management timing of delivery, methods of treating fetal distress.

OBSTETRIC EMERGENCIES
Definition of dystocia; primary dystocia; disproportion; malposition; uterine activity; secondary arrest of labour. Management amniotomy; oxytocin; value of operative delivery.

PPH

post partum haemorrhage; management of haemorrhagic shock.

GYNAE

PMB
In a woman over 40 irregular vaginal bleeding may be due to any of the following; cervical ectropion, cervical polyp, cervical cancer, endometrial hyperplasia (cystic or atypical), endometrial polyp, submucosal fibroid and rarely endometrial cancer. It is unlikely that she has pelvic inflammatory disease, and chlamydia rarely causes irregular vaginal bleeding

A speculum examination is an opportunity to detect cervical abnormalities and perform a smear. CERVICAL SMEAR List four factors associated with an increased risk of CIN (Cervical Intra-epithelial neoplasia). COLPOSCOPY Define the terms CIN, dyskaryosis and dysplasia (in less than 30 words).

A digital vaginal examination will detect an enlarged uterus suggestive of fibroids. Endometrial biopsy alone is indicated in women under 40 because the risk of malignancy is greatly reduced. A transvaginal ultrasound scan will detect endometrial polyps/ submucosal fibroids and measure the endometrial thickness. A hysteroscopy and endometrial biopsy is the gold standard for detecting endometrial abnormalities in women over 40.

ist the 4 elements of ovarian RMI (risk of malignancy) score

PCOS
Simon and Susan Knott have been referred to a gynaecologist because of inability to conceive despite regular intercourse, for 4 years. Their GP has already checked Simon's hormone profile and sperm count, and they are quite normal. Susan has very irregular periods, often only having 4 or 5 in a year. She is also overweight and has excess body hair. After blood tests and a pelvic ultrasound scan, the gynaecologist diagnoses polycystic ovary syndrome. He gives some lifestyle advice and puts her on daily metformin tablets. Later, when she reads the drug information leaflet, Susan is surprised to find that the tablet is usually used to treat diabetes.

Subfertility
Jill and Peter Brown have been trying to have a baby for 6 months. Jill is very upset that nothing has happened and is worried about her irregular periods which are very heavy and painful. They go and see Dr Jones, their General Practitioner, who asks Peter to have his hormone levels checked and to have a semen analysis at the local hospital. He also asks Jill to have hormone tests, the first with her next period and another 21 days later. When the couple return to the surgery 10 days later they are told that no sperm were seen in the sample but that Peters hormone levels were normal. Jills menstrual hormone levels were normal but her day 21 progesterone was very low. The doctor decides to refer the couple to a subfertility clinic at their nearest teaching hospital.

Describe the anatomical and endocrine abnormalities in both male and female that may lead to infertility. Discuss the genetic contribution to infertility. Explain abnormal embryogenesis and infertility. Revisit anatomy of the testis, efferent ductules, vas deferens; spermatogenesis, normal and disordered; external influences, anabolic steroids, blockers and alcohol; causes of azoospermia germ cell failure, obstruction; varicocele and hydrocele. Revisit anatomy of the uterus, cervix, fallopian tubes and ovaries; menstrual cycle, hypothalamic-ovarian axis; oogenesis, normal and disordered; causes of disorders of ovulation, including anovulation; endometriosis, tubal disease. Genotypes and karyotypes and their effect on fertility, Downs syndrome, cystic fibrosis; male and female translocation carriers; Turners and Klinefelters syndromes; azoospermia and testosterone deficiency.

ANATOMICAL HORMONAL GENETIC LIFESTYLE (INCLUDING COITUS)

Prolapse
List three conservative treatments for female urinary incontinence and the underlying mechanisms for their actions 3 possible surgical options for the treatment of female urinary incontinence Sketch a series of diagrams to explain the problems / anatomical changes which occur in the four different types of prolapse. (These are the sort of diagrams you would use to explain the differences to a patient)

DYSPAREUNIA

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