Obstetric Lectures PDF

Oraganization and summarization of obstetric lectures The followings are all obstetric lectures taken in stage 5 1. History & Examination 2. Antenatal Care Medical disease in pregnancy 3. Epidemiology 1. Diabetes Mellitus...

Oraganization and summarization of obstetric lectures The followings are all obstetric lectures taken in stage 5 1. History & Examination 2. Antenatal Care Medical disease in pregnancy 3. Epidemiology 1. Diabetes Mellitus 4. Antepartum Haemorrhage 2. Hypertensive Disorders 5. Normal Labor 3. Epilepsy 6. Abnormal Labor 4. Anemia 7. Induction of Labor 5. Renal Diseases 8. Preterm Labor & PROM 6. Thyroid Disorders 9. Prolonged Pregnancy 7. GIT Disorders 10. Instrumental Delivery 11. Caesarean Section 8. Coagulation Disorders 12. Cord Presentation & Prolapse 9. Cardiac & Pulmonary Diseases 13. Breech & Shoulder Dystocia 14. Intrapartum Fetal Monitoring 15. Intrauterine Fetal Death IUFD 16. Intrauterine growth restriction IUGR 17. Amniotic Fluid Abnormalities 18. Multiple Gestation These topics are explained in details same 19. Rh Incompatibility & Hydrops as lecture 20. Postpartum Haemorrhage 21. Early Pregnancy Vaginal Bleeding It start from Hx, Ex and end with GIT disorder (in order) 22. Physiological Changes 23. Puerperium 24. Imaging 25. Maternal Pelvis & Fetal Skull 26. Labor Analgesia Highlighted topics not explained 27. Prenatal Diagnosis 28. Drugs in Pregnancy in this file 29. Antenatal Fetal Infections 30. Malposition 31. Transverse Lie Prepared by Rayan Anwar Thanks for Halder Jamal  History & examination LMP: first day of last cycle (seeing blood) These are some general notes from this lecture but for more EDD by Naegele‘s rule: information about how to take history, do examination go to LMP + 7 days - 3 months + 1 year. its lecture and clinical files LMP + 7 days + 9 months. GA: calculate from LMP forwards or EDD backwards. EDD is GA of 40 weeks. 1 month = 4 weeks +3 days (4+3 wks) 2 = 8 weeks + 5 days (8+5 wks) 3 = 13 wks 4 = 17+3 wks 5 = 21+5 wks 6 = 26 wks 7 = 30+3 wks 8 = 34+5 wks 9 = 39 wks Remember we added 7 days to LMP? → 40 Weeks. Term 37-42 (range of dates to have a normal delivery) Pre-term: 42 weeks Keep in mind that pregnancy is 9 months + 7 days = 40 weeks = 280 days IF you calculate it from LMP (which isn’t technically correct as there will be an entire follicular phase before ovulation & fertilization, so from the point of conception, pregnancy would be only 38 weeks) Gravidity: number of pregnancies regardless the outcome (twin is regarded as one) Parity: number of deliveries after 24 weeks gestation (alive or dead) (twin is regarded as 2) Abortion: number of pregnancies ended before 24 wk. including ectopic and molar pregnancy. ´ Nulligravida is a woman who has never been pregnant. ´ Primigravida: pregnant for the first time, G1 ´ Multigravida: pregnant more than one time, G2 or more ´ Nullipara: never carried a pregnancy beyond 24 weeks, P0 ´ Primipara: given birth once before, P1 ´ Multiparous: given birth more than one time, P2 or more ´ Grand multipara: given birth 3 or more times (some say 4 times) Fetal quickening: is the first movement of the fetus sensed by the mother. It is useful in dating of the pregnancy. Occurs at 18-20 week in primigravida, and 16-18 week in multipara (2 week earlier in multipara women bcz she is now professional at this) What do we mean by NVD (Normal vaginal delivery)? SSTVV: Single, Spontaneous, Term, Viable, Vertex. Without using any instrument, episiotomy could be regarded as normal vaginal delivery (but perineal tears are not NVD) Indications and contraindications of pelvic examinations? Indications: - Excessive or offensive discharge - Vaginal bleeding (in the known absence of a placenta praevia) - Cervical smear - Rupture of membrane (ROM) Contraindications to digital examination: - Known case of placenta praevia - Vaginal bleeding when the placental site is unknown and the presenting part unengaged (take US to exclude placenta previa) - PROM (increased risk of ascending infection). - Virgin females (in our locality…..) Effect of alcohol & smoking on fetus? Smoking causes a reduction in birthweight in a dose-dependent way. It also increases the risk of miscarriage, stillbirth and neonatal death Alcohol cause fetal alcohol syndrome which lead to causes brain damage and growth problems  Antenatal care What is Antenatal care? How & when it is done? It involves checking maternal health and fetal wellbeing, assessing risk factors, screening for disease and abnormalities and providing education and advice all to optimize outcomes for mother and baby. Aims of antenatal care are: To optimize pregnancy outcomes for women and babies. To prevent, detect and manage those factors that adversely affect the health of mother and baby. To provide advice, reassurance, education and support for the woman and her family. To deal with the ‘minor ailments’ of pregnancy. To provide general health screening Start from decision to become pregnant till end of puerperium by History, Examination, Investigation. Frequency of visits: Traditional model: - Once/month from 4-28 weeks - Twice/month from 28-36 weeks - Weekly from 36-delivery NICE model: 7 visit in multiparous 10 visit in nulliparous in uncomplicated pregnancy WHO model: minimum 4 visits 1st on confirmation of pregnancy 2nd at 20-28weeks 3rd at 34-36weeks 4th just before EDD *In each model, additional visits are individualized in complicated pregnancies Booking visit Done as early as possible, usually ≤ 12 weeks, earlier if she had risk factors. If done after 14 weeks, it will be called late booking visit. Confirmation of pregnancy: Symptoms of pregnancy with either: ⊕ serum β hCG (8-12 days after fertilization) ⊕ urinary β hCG (14-18 days after fertilization) TVUS (from 5 weeks), TVUS (from 6 weeks). Hear the fetal heart with sonicaid (from 12 weeks) Stop ACEi when pregnancy confirmed, warfarin one month before pregnancy, isotretinoin 3 months before. Identify high risk women: PET, risk of PTL, IUGR, Vitamin D deficiency, GDM. Start low dose aspirin if chronic HTN. *Advise on breastfeeding within hour of birth, exclusively for 6 months and then continued breastfeeding with foods at least up to age of 2 years. General pregnancy dietary advice Do not eat for two Avoid snacks Eat fibre-rich foods Base your meals on starchy foods such as potatoes, bread, rice and pasta Restrict intake of food, drinks high in added sugars, and fat. Eat at least five portions of a variety of fruit and vegetables each day. Controlling weight gain in pregnancy General exercise advice Aim of exercise during pregnancy is to stay fit Pelvic floor exercises during pregnancy and immediately after birth may reduce the risk of urinary and faecal incontinence Breastfeeding advice Breastfeeding protects against diarrhoea and common childhood illnesses such as pneumonia, reducing the risk of obesity later in life. it is associated with a higher intelligence quotient (IQ) in children. Start breastfeeding within an hour of birth, exclusive breastfeeding for the first 6 months of life and continued breastfeeding beyond 6 months and at least up to 2 years of age. Antenatal urine test Urine is screened for Protein (to detect renal disease or pre- eclampsia) Persistent glycosuria (to detect pre-existing diabetes or gestational diabetes [GDM]) Nitrites (to detect urinary tract infections) and if nitrites detected sample should be send for culture &sensitivity Blood pressure assessment Allows the detection of previously unrecognized chronic hypertension Low-dose aspirin in women with chronic hypertension (reduce pre-eclampsia and decrease perinatal mortality in fetus) Antenatal anti-D immunoglobulin prophylaxis using either a single large dose at 28 weeks, or two doses, given at 28 and 34 weeks Women who have had previous GDM should be offered a glucose tolerance test or random blood glucose in the first trimester Screening for thalassaemia in the UK is offered to all pregnant women at booking visit using the Family Origin Questionnaire (FOQ) and/or FBC results Benefits of dating US Dating U/S is to define GA & EDD: U/S difference with GA should not be T1 (11+3 - 13+6 weeks) based on crown–rump length (CRL) more than 2 weeks T2 (14 - 20 weeks) based on head circumference (HC) > 20 weeks based on femoral length (FL) - Accuracy of GA determined by US is: ± 1 week in T1, ± 2 week in T2, ± 3 week in T3 so dating becomes progressively less accurate as the pregnancy advances due to impact of genes & environment. Other benefits: ⁃ Accurate dating if irregular cycles or can’t remember LMP. ⁃ Decreased incidence of IOL for prolonged pregnancy. ⁃ Maximizing the potential for serum screening to detect fetal abnormalities. ⁃ Detection of multiple pregnancies, chornionicity. ⁃ Confirm viability & detection of otherwise missed miscarriages Benefits of T2 US The anatomical scan (18-22 weeks): to provide an accurate estimation of GA if an early scan has not been performed; to carry out a detailed fetal anatomical survey to detect any fetal structural abnormalities or markers for chromosome abnormality (You may not detect small anomalies but all major ones are identified). to locate the placenta and identify the 5% of women who have a low lying placenta for a repeat scan at 34 weeks to exclude placenta praevia; Majority of those low lying will have upward migration and no placenta praevia. to estimate the amniotic fluid volume. to perform Doppler US of maternal uterine arteries to screen PET if patient has risk factors. to measure cervical length to assess the risk of PTL. Benefits of T3 US To assess fetal growth; Large HC compared to AC is seen in IUGR and the opposite is seen in diabetic pregnancy. These measurements when used in equation can give more accurate EFW To assess fetal well being (biophysical profile & Doppler of fetal umbilical vessels) Check viability or confirm IUFD Measure cervical length in patient at risk of PTL. Confirmation of fetal presentation in uncertain cases; DX of uterine and pelvic abnormalities e,g fibroid & ovarian cysts Guide invasive procedures such as amniocentesis, CVS, cordocentesis, and therapeutic procedures. HC: Head circumference AC: Abdominal circumference EFW: Estimated fetal weight Summary Early scan (11-14 weeks) Viability, GA, multiple pregnancy and chorionicity, gross structural abnormalities and identify markers (fetal chromosome abnormality such as down syndrome) 20 weeks Scan (18-22 weeks) GA, structural abnormalities, location of placenta, amniotic fluid volume, cervical length (PTL), doppler U/S for maternal uterine arteries (pre-eclampsia) U/S in third trimester Assess fetal growth, assess fetal wellbeing (biophysical profile&doppler of fetal umbilical vessels), IUFD, fetal presentation, cervical length in PTL, guide invasive procedures (amniocentesis, CVS, and cordocentesis) Fetal growth and well being is checked by Kick count: adequate maternal perception of fetal movement (at least 10 in 12 hours). NST (non stress test): CTG without tocography: reactive if 2 movements with accelerations of 15 bpm of ≥ 15 s within 20 min (adequate O2 & intact CNS). non-reactive, may be the baby is sleep → tell the mother to go for a walk, or shake the head of the baby or do vibrio-acoustic stimulation. CST (contraction stress test): CTG with tocography, contractions are by oxytocin or nipple-rolling: ⊕ results (bad): with persistent late decelerations is evidence that the fetus will not be able to withstand the hypoxic stress of the labor (it is a hypoxic fetus) ⊖ results (good): No persistent decelerations noted with at least 3 contractions. BPP score: normal (8-10) suspicious (6) abnormal (0-2-4). Doppler US of fetal umbilical vessels, abnormalities are: Early diastolic notch (PE, IUGR, abruption). Reduced end diastolic flow. Absent end diastolic flow. Reverse end diastolic flow (needs immediate delivery) Increased MCA flow (hypoxic fetus) Not a single method confirms fetal wellbeing and thus we should use a combination of them.  Epidemiology Perinatal mortality definition Live birth: complete expulsion or extraction from its mother of a baby, irrespective of gestational age, which then shows any signs of life such as breathing, beating of heart, pulsation of the umbilical cord, or definite movement of voluntary muscles. Stillbirth: birth of a baby, from 24 completed weeks of gestation, who show no signs of life after birth. Stillbirth rate: number of stillbirth per 1000 total births (stillbirth and livebirths). Early neonatal mortality rate: number of live born dying within first week of life. Late neonatal mortality rate: number of live born dying from the end of first week of life till end of fourth week. Infant mortality rate: number of live born dying within the first year of life. Perinatal mortality rate: the number of stillbirths and first week deaths (stillbirths and early neonatal deaths). Maternal death: death of woman while pregnant or within 42 days of delivery or abortion, irrespective of the duration or site of pregnancy, from any cause related to or aggravated by the pegnancy or its management. Maternal mortality ratio: number of maternal deaths during given time period per 100,000 livebirths during the same time period. Maternal mortality rate: number of maternal deaths during given time period per 100,000 women of reproductive age in same time period. Life-time risk of maternal death: probability of maternal death during a womans reproductive life. Most maternal deaths occur within the first week after delivery and it is 100 times more likely to occur on the first day after birth and in the hospital. death rates rise with parity and maternal age. PPH, eclampsia and sepsis are leading causes for maternal deaths in the developing countries. Major causes of perinatal and neonatal mortality FETAL Placental insufficiency Intrauterine infection Severe congenital malformations (anomalies) Umbilical cord accident Abruptio placentae Hydrops fetalis PRETERM Severe immaturity Respiratory distress syndrome Intraventricular hemorrhage Congenital anomalies Infection Necrotizing enterocolitis Bronchopulmonary dysplasia (BPD) FULL TERM Congenital anomalies Birth asphyxia, trauma Infection Meconium aspiration pneumonia Persistent pulmonary hypertension (PPHN)  Antepartum haemorrhage APH APH: bleeding from genital tract after 24th competed weeks of gestation and before onset of labor, occur in 2-5% of cases. At time of labor there is show which some times misdiagnosed with APH Causes — Placenta praevia: 1/3 — Abruption placenta: 1/3 — Local cause: 1/3 Cervical erosion, polyp, ectropion, cancer Genital tract infection: cervicitis, vaginitis Vaginal varicosities — Blood dyscrasias — Undetermined causes — Fetal (Vasa praevia: 1%) Blood dyscariasis rare as Idiopathic thrombocytopenia, Von willibrands disease, Leukemia, Hodgkin's disease Placenta previa: Placenta implanted wholly or partially on the lower segment of the uterus. The lower segment does not contract in labor but is stretched in response to contractions. Risk factors Multiparty Multiple pregnancy Increasing maternal age C/S or uterine surgery D&C, IVF Smoking Grades: I: reaches the lower segment but not the internal os (almost 2,5 – 3 cm away from it) → low lying placenta. II: reach the internal os but doesn’t cover it → marginal. III: covers the internal os before dilatation but not when dilated (accentric) → partial. IV: completely covers the internal os of the cervix even when dilated (central) → complete. Grade I & II are Minor, Grade III & IV are Major. Associated with: Abnormal lie & Malpresentation PROM IUGR Operative delivery Morbidly adherent placenta (accreta) Migration occur because of development of lower uterine segment, so most of low lying placenta will be corrected by term. All patient with Previa before 24 weeks should have a U/S at 28, 32 & 34 weeks to reassess the position of the placenta. Diagnosis History Asymptomatic diagnosed by routine U/S Painless, causeless, recurrence Bright red vaginal bleeding (1/3 before 30 weeks, 1/3 in 30-36 & 1/3 after 36 ) 10% will reach term without bleeding Examination Abdomen & uterus is soft Fetal parts, heart are easily detected Presenting part is high not engaged Could be abnormal lie & presentation -PV is contraindicated but you can do cusco speculum to exclude local causes Investigation U/S (enough) MRI, X-ray to see the presenting part angiography Placenta accreta spectrum (morbidly adherent placenta) There is risk that the placenta implant and invade into the previous scar. This is called morbid adherent placenta. Three types of morbidly adherent placenta are: Placenta Accreta: placenta is abnormally Adherent to the lower uterin wall, there is no decidua basalis, & the fibrinnoid layer is incompletly developed Placenta Increta: placenta is abnormally Invading into the uterin wall ( myometrium ) Placenta Perecreta: placenta Penetrates myometrium & may invade nearby viscera Treatment of placenta previa Initial management of PP & Abruptio placenta is very similar: Hemodynamic state of the mother should be immediately evaluated & stabilization performed if necessary. Gestational age should be assessed & the fetal heart rate should be monitored continuously. 1) insert a broad – bore I.V cannula and start an infusion with crystalloid solution. 2) cross matching 4 units of blood & heal 3) packed RBC should be given if sever anemia is evident or there is continuous uterine bleeding, the goal hematocrit is at least 30%. 4) UOP should be maintained above 30 ml/h 5) anti D for Rh ⊖ mother. Delivery is always indicated if: ► there is a non reassuring fetal HR despite resuscitation effort ► there is life-threatening maternal hemorrhage ► GA is ≥ 34 weeks & there is known fetal lung maturity In 24-36 weeks, if maternal, fetal stability are assured conservative expectant management will be tried: ►Hospitalization till bleeding is stopped ►hydration & blood transfusion are given if necessary ►Continues fetal heart monitoring required if there is continued bleeding or uterine contraction ►Bed rest, restrict activity, give stool softener, iron supplementation ►Steroid to promote fetal lung maturity if ≤ 34 weeks, then if no uterine activity & no bleeding, home therapy can be considered: Patient should be instructed return to hospital if she experience contractions or bleeding Have 24 H contact via telephone & ability to return to the hospital at any time. Fetal growth, amniotic fluid index & placental localization should be assessed by U/S every 2 weeks. At 36-37 weeks, a final US should be performed and acted upon:- ► Grades III, IV should have a C/S at 37-38 weeks. ► There is a possibility of perform hysterectomy ► If the presenting part is below lower edge of placenta in grade I, II anterior, trial of vaginal delivery could be given. Caesarean hysterectomy is required in 2/3 of patient with P accrete, there are several surgical option if uterine preservation is important 1) The placenta removed & the uterine defect over-sew 2) The area of accrete re-sected & the uterus repaired 3) Leaving the placenta inside, acceptable in patient who are not actively bleeding, the cord ligated & cut close to the base & the patient treated with antibiotics & methotrxate postpartum. Prognosis: Major cause of death in mother is PPH because lower segment does not contract as upper segment, so maternal vessels of placental bed continue to bleed after delivery. This may lead to an emergency hysterectomy if the bleeding can’t be stopped Fetal risk from GA. Complications of placenta previa Maternal C/S Abnormal lie, presentation PPH Puerperal sepsis Fetal IUGR, low birth weight Premature baby Birth injury IUFD Congenital malformation Abruptio placenta Premature separation of placenta before delivery of baby but after 24 weeks, as antepartum or intrapartum event - Concealed vs revealed. - Major: > 1/3 separated, life threatening. - Minor: < 1/3 separated, can result in placental infarct, or multiple minors become major. Risk factors of abruptio placenta Causes of abruption are not known but the following factor are associated: HTN, PET Smoking, cocaine Revealed: following separation of placenta, blood comes out of cervical canal to be visible externally. This is the most common type. Thrombophilia. Concealed: blood collects behind separated placenta or between membranes and Multiparity, ↑ age decidua. collected blood is prevented from coming out by presenting part which presses Previous episode. on the lower segment. this is rare. Trauma as ECV, abdominal trauma ↑ AFP in the absence of fetal malformation , folate deficiency Decompression of overstretched uterus during rupture membrane (polyhydramnios, multiple pregnancy) Presentation of abruptio placenta Triad: bleeding, contractions, distress (↓ placental exchange surface area or from severe maternal hypotension) Major: painful, bleeding less than degree of shock, on examination there will be woody hard uterus, cannot feel fetus, and fetus maybe dead. Minor: not diagnosed often until after delivery. mild pain, tenderness, with threatened PTL, APH. Complications: Maternal: shock, DIC, oliguria and anuria, puerperal sepsis, PPH Fetal; impaired growth, Hypoxic ischemic encephalopathy → cerebral palsy Treatment of abruption Major is a life threatening for both the mother & fetus, if the fetus is still a live: -Insert two large -bore IV cannula of normal saline / Colloid -Cross match of four units, Hb, coagulation profile -Perform an immediate C/S to save the fetus life (high risk of PPH) -Adequate fluid replacement following the C/S -Leave an indwelling urinary catheter -Consider insertion of a central venous line Dead Fetus: Allow deliver vaginally. Usually happens rapidly (with 4-6 hours) as the abruption stimulate labor. if not in labor rupture of membranes usually leads to a rapid delivery. Relevant points: - Epidural analgesia contraindicated bcs of risk of coagulopathy but patient controlled of opiate infusion can be used - If coagulopathy has developed ( prolonged APTT, PTT, increased fibrin degradation product, low platelets): Give four unit of fresh frozen plasma Ask the blood bank to get 6 units of platelets ready Consumptive coagulopathy began to improve immediately after uterus has been evacuated of its content. Marked abnormalities of coagulation test usually resolve within 4-6 hours of delivery of the placenta Prevention: No intervention has been shown to prevent abruptio, Stop smoking, cocaine & treat HTN maybe benificial. Fetal cause (Vasa previa) Occur from rupture of vasa praevia when there is velamentous insertion of cord vessels and these cross the cervical os. Risk factors Velamentous insertion Bilobed or succenturiate placenta (by US) Diagnosis Scant APH with rupture membrane and sinusoidal fetal HR Check bleeding by kliehauer test (resistant to alkalanization). Treatment Delivery as soon as possible and prepare transfusion of neonate.  Normal labour Labor: regular uterine contractions combined with cervical changes that bring about the delivery of fetus & placenta through the birth canal. Diagnosis: all by history except cervical changes: - Regular contractions that increase in frequency, duration and intensity. - Cervical changes: effacement and dilation (bishops score) - Show of small amount of blood mixed in cervical mucus plug. - Water break: gush of amniotic fluid due to rupture of membranes. Stages: First: contractions every 3-5 min (length of 8-16 or 5-8 h, 1.2 or 1.5 cm/h in primi or multi respectively) Latent phase: onset - 4 cm, up to 7 h in nullipara. Active phase: 4-10 cm, 1-2cm/h Second: 10 cm to the delivery of baby. Contractions every 2-3 min (3-5/10 min). (Length of 5-30 min in multi but up to 2 hour with analgesia, 1-2 hour in primi but up to 4 hour with analgesia) Engagement Descent Flexion Internal rotation (shoulder through TD inlet) Extension Restitution and external rotation (shoulder through APD outlet) Delivery of shoulders and fetal body Third: Delivery of placenta (20-30 min), better to do active management. Fourth: Involution of uterus, watch for PPH (each 15 min for 2 h then each 30 min for 1h → 10 times) Theories of labor onset Progesterone withdrawal theory “hormone of pregnancy”: progesterone relax uterus, maintain uterine lining, and pregnancy. if withdrawn, uterus will begin to contract. Oxytocin theory: oxytocin leads the uterus to contract Prostaglandin theory: prostaglandins in cervix and stimulating the uterus to contract. Management of labour Five essential components of labor: 5P First stage: Passage (pelvis) - Emotional support to the mother Passenger (fetus) - Observation of the progress of labor - Monitoring of the fetal wellbeing Power (uterine contractions) - Analgesia, and hydration Psychology (phycological condition) Position of mother (e.g lithotomy, in water) Active management of third stage of labor: PPH incidence reduce from 15 to 5% 1- IM injection of 10 IU oxytocin (1 ampoule) with delivery of the anterior shoulder or immediately after delivery of the baby. 2- Early clamping and cutting of umbilical cord 3- Controlled cord traction (CCT): done when the signs of placental separation are seen. Methods (Schultz method when separate from centre, Matthew Duncan method when separate from peripherally) If CCT failed (in 2% of cases): CCT: when contraction is felt, left hand should be moved supra- Repeat CCT after 10 minutes pubic and fundus elevated with palm facing towards the mother. At Or manual evacuation under anaesthesia the same time right hand should grasp the cord and exerts steady traction so that the placenta is separated and delivered gently. Or injection of oxytocin into umbilical vein Signs of placental separation Apparent lengthening of the cord Small gush of blood from the placental bed Rising of uterine fundus to above the umbilicus Uterine contraction resulting in firm globular feel on palpation Definition Presenting part: is the lower part of the fetus palpable on vaginal examination. In cephalic presentation the normal presentation is vertex , which indicate that the head is flexed. Vertex: is the area of fetal skull bounded by 2 parietal eminences & anterior & posterior fontanelles. Any other presentation is called mal-presentation like breech, cord, brow, face or compound presentation. Lie: relationship between longitudinal axis of fetus to that of mother to uterus as: longtudinal, oblique, transverse lie Station: level of decent of presenting part as assesed on vaginal examination, when lowest part of presenting part reached the ischial spine the presenting part at level of 0 station. prescribed by centimeters above or below ischial spine. Engagment: when the widest diameter BPD passed pelvic brim, assessed on abdominal examination by 5 fifth. Amniotomy: artificial rupture of membrane , may be after spontaneous labor, or part of augmentation of labor. Attitude: relation of different part of fetus to each other, usually the attitude is flexion. Caput succedneum: edema over the presenting part of the head, common in prolonged labor. Moulding: change in fetal skull to adapt maternal pelvis during its passage. sutures allow some movement between bones (parietal slide over frontal & occipital bones), severe moulding is sign of cephalo-pelvic disproportion. Position: for each presenting part there is a dominators, for cephalic is occiput, for face is mentum , for breech is sacrum, refers to the position of fetal occiput in relation to the maternal pelvis. OA–occipito- anterior“normal”  Abnormal labour Abnormal, Prolonged, Obstructed, Difficult, Dysfunctional labour, Dystocia means: Poor progress of first or second stage. Fetal compromise Malpresentation, Malposition Uterine scar Poor progression of labour indicate Induced & Precipitate labour problem in one of Ps Progress of labour is depend on 3 P: Power i.e. the efficiency of uterine contractions. Passage i.e. uterus, cervix, and bony pelvis. Passenger i.e. fetus (with particular respect to the size, presentation, and position). Power Inefficient uterine action: most common cause of poor progress of labour, more common in primi and older women characterized by weak and infrequent contractions. — Subjective assessment by history — Objective assessment by Examination (Palpation) External uterine tocography (Tocodynamometer): gely frequency and duration of contractions. Intrauterine pressure catheters (IUPC): measure strength or pressure but rarely used. - Normally 4-5 contractions: Weak < 20 s, Moderate 20-40, Strong > 40 - Montevideo unit (MVU): collective peak strength of contractions (mmHg) in 10 minutes, >200 is adequate. For cervical dilation to occur each contraction must generate 25 mmHg with 50-60 mmHg being considered optimal. Treatment Rehydration, ARM, IV oxytocin (also treats irregular contractions in multiple pregnancies) Passage Abnormal pelvis (only gynecoid is normal) 4 types of pelvis gynecoid, android, anthropoid, platypelloid, (gynecoid is normal, others cause obstructed labour) Abnormal shape of pelvis due to: rickets, osteomalacia, tuberculosis, tumors of bones, childhood poliomyelitis, previous accidents, DDH, congenital deformity of sacrum or coccyx, kyphosis and scoliosis Contracted inlet (AP 41, or twin ≥ 38 weeks) - PROM at term, or at 34-37 if has additional factor (suspected maternal infection, fetal compromise, IUGR). PPROM < 34 weeks is not clear indication. - HTN disorder (esp PET), IUGR, IUFD (or Hx of it) - DM & macrosomia - Deteriorating maternal illness - Unexplained APH - Cholestasis - Maternal isoimmunization - Social reasons (she has exams later-on and want to deliver now) Contraindications - Placenta previa - Severe fetal compromise - Deteriorating maternal condition with major APH - PET or cardiac disease may favor C/S - Breech (relative) - Previous C/S (inform about risk of uterine rupture) * Preterm is not an absolute contraindication Methods Membrane sweep (weekly from 40 weeks with exclusion of PP, is adjunct to other methods). insertion of finger through the cervix and its rotation around the inner rim of the cervix. This safe technique strips off the chorionic membrane from the underlying decidua and releases natural prostagl andins. PGE2 (dinoprostone) gel, tablet, pessary to ripen cervix and initiate contractions, two doses required, given at least 6 hours apart. controlled-release pessary is left in place for up to 24 h ARM artificial rupture of membrane (cervix must be favourable Bishop score) Oxytocin infusion (should have ruptured membrane, increase dose every 30 min till 3-5 contractions/10 min). Extra-amniotic saline infusion (EASI) by foleys catheter Mifepristone and misoprostol: high complications rate so only used for IUFD When induction fails, the options include Rest period followed by induction again in future Caesarean section Delaying delivery further is acceptable if there is no threat to fetal or maternal condition e.g social induction. Failed induction in setting of pre-eclampsia or IUGR will necessitate caesarean delivery. Complications Pain Epidural analgesic (high rate of instrumental delivery) Long labor ➝ PPH due to Uterine atony Uterine hyperstimulation as a side effect of prostaglandin and oxytocin causing fetal bradycardia and may require emergent C/S if FHR fail to resolve promptly  Preterm Labor & PROM Preterm labour (PTL): onset of labour before 37 weeks gestation and after 24 weeks of pregnancy Causes Cervical weakness: painless premature cervical dilatation and is suggested by a history of painless second trimester pregnancy loss. weakness is either congenital or acquired by D&C, instrumental delivery or delivery of large baby. Infection: chorioamnionitis (major cause of PTL particularly before 32 weeks with intact membrane), infection ascends from the vagina, may be transplacental or introduced during invasive procedures. delivered baby may be associated with fetal brain damage (fetal inflammatory response), release of cytokines during maternal infection is harmful to brain of the unborn infant, causing periventricular white matter damage also known as periventricular leukomalacia PVL. increased AF IL-6 associated with intraventricular haemorrhage (IVH), PVL. high levels of cytokines found in brains of infants who die with evidence of PVL. Multiple pregnancy: risk of PTD rises with fetal number, with triplets delivering on average at 32 weeks and quadruplets delivering at 28 weeks. Twins have a six to seven fold increased risk of cerebral palsy Polyhydramnios: can be managed with amnio-drainage, but this by itself precipitate PTL and PPROM, alternatively indomethacin (reduces fetal urine production) may be used, but flow through the ductus arteriosus should be monitored as inhibition of PGE production by indomethacin may result in premature closure thus should not be given after 32 weeks Mullerian anomalies: occur as a consequence of abnormal embryologic fusion and canalization of müllerian ducts and result in abnormally formed uterine cavity (range from arcuate uterus to complete failure of fusion). Other outcomes include first and second trimester miscarriage, PPROM, PTL, IUGR, breech presentation and C/S APH (placenta abruption): bleeding lead to release thrombin (stimulates myometrial contractions) Stress: premature increase in circulating corticotrophin releasing hormone (CRH). Management Threatened PTL → test for cervicovaginal fetal fibronectin fFN: If ⊖ → Discharge home If ⊕ → Admission, start following treatments: -Progesterone (this with cerclage are also used for prevention) -Corticosteroids “ improves neonatal outcomes” (betamethasone, dexamethasone) -Tocolytics (to give steriods time to work, contraindicated if PPROM): OTR-A (Atosiban), MgSO4, CCB (nifedipine), NSAID (indomethacin), β2⊕ (ritodrine, salbutamol, terbutaline) -Antibiotics (erythromycin only if PPROM) They are similar in delaying delivery (efficacy) but the side effects and neonatal outcomes (NRDS, NEC, IVH, jaundice) are best with atosiban, and worst with β2⊕ and intermediate with CCB. β2⊕ can lead to maternal pulmonary edema (especially if large fluids given, multiple pregnancies and known cardiac disease) MgSO4 decrease risk of Cerebral palsy (neuroprotective) NSAID (indomethacin) has risk of PDA closure (after 32 weeks), NEC, renal dysfunction (oligohydramnios bcs of PG inhibition it cause ↓ renal perfusion). delay delivery for 48 hours, 7–10 days and beyond 37 weeks. Ritodrine, salbutamol, terbutaline are predominantly β2 agonists, mediate myometrial relaxation by stimulating cyclic AMP production. effective in delaying delivery, but do not improve neonatal outcome. Atosiban is competitive antagonist of oxytocin and vasopressin, binding to OTRs and vasopressin V1a receptors within the myometrium. PPROM Prelabor or premature rupture of the membranes (PROM): Rupture of the membranes before onset of labor. If PROM is ≥ 37 week → term PROM, if PROM is < 37 weeks → preterm PROM (PPROM). Rupture of membranes for > 18-24 hours before delivery is called prolonged rupture of membranes Differential diagnosis: leukorrhea, infection, incontinence. Diagnosis History: pain is first sign, leaking (complete or partial) indicates PPROM, bleeding (Gush till the ground) Examination: (Polling of fluid into posterior fornix), sterile specular examination should be used bcs of risk of chorioamnionitis, take swab from the fluid Investigation Nitrazine test (paper turns blue) Fern test US (oligohydramnios) Amniocentesis (for lung maturity and infection) CBC, swabs from genital tract Complication of PPROM Maternal: Infection: endometritis, sepsis Placental abruption PTL Operative delivery Fetal: Preterm baby with their complications : (RDS / Fetal and Neurologic dysfunction, Intracranial hemorrhage) Pulmonary hypoplasia and fetal compression syndrome (Potter Sequence) Prolapse or compression of umbilical cord Placental abruption Treatment: balance of risk of prematurity (if IOL) and infection (if delivery delayed). -IOL if >37 weeks or evidence of chorioamnionitis -Conservative if 42 weeks) Prolonged rupture of membranes (>24 h) Hypertension Diabetes Antepartum hemorrhage (placental abruption) Medical disorders such as systemic lupus erythematosus Fetal problems Fetal growth restriction Prematurity Oligohydramnios Abnormal Doppler artery velocimetry Multiple pregnancy Meconium stained liquor Intrauterine infection Intrapartum risk factors Oxytocin augmentation Epidural analgesia Vaginal bleeding in labour Maternal pyrexia Fresh meconium stained liquor Interpretation of CTG: DR C BRaVADO: DR: Define risk (indication) C: Contractions BRa: Baseline rate 110-160 V: Variability 5-25 A: Accelerations (reassuring): abrupt ↑ FHR > 15 bpm for > 15 s. D: Decelerations: early (normal), late (abnormal, left lateral position, O2, fluids, stop oxytocin), prolonged (worst, immediate delivery), variable (inconclusive) O: Overall impression: reassuring, suspicious or abnormal.  CTG Contractions: record the number of contractions present in a 10 minute period. Each big square is equal to one minute, so look at how many contractions occurred within 10 big squares. Individual contractions are seen as peaks on the part of the CTG monitoring uterine activity. Assess contractions for the Duration (How long last), Intensity (How strong are the contractions assessed by palpation) Baseline rate of the fetal heart: normal fetal heart rate is between 110-160 bpm , but now they consider 120- 160 Variability: baseline variability refers to the variation of fetal heart rate from one beat to the next. Normal variability indicates an intact neurological system in the fetus. Normal between 5-25 bpm. Variability can be categorised as either reassuring, non-reassuring or abnormal. Reassuring: 5 – 25 bpm Non-reassuring: less than 5 bpm for >30 minutes more than 25 bpm for 15-25 minutes Abnormal: less than 5 bpm for > 50 minutes more than 25 bpm for more than 25 minutes sinusoidal Accelerations: abrupt increase in baseline fetal heart rate > 15 bpm for > 15 S The presence of accelerations is reassuring. Accelerations occurring alongside uterine contractions is a sign of a healthy fetus. Absence of accelerations with an otherwise normal CTG is of uncertain significance. Decelerations: abrupt decrease in the baseline fetal heart rate of > 15 bpm for > 15 seconds. Types of decelerations Early deceleration (physiological): start when the uterine contraction begins and recover when uterine contraction stops, due to increased fetal intracranial pressure causing increased vagal tone. Late decelerations (abnormal): begin at the peak of the uterine contraction and recover after the contraction ends. it indicates there is insufficient blood flow to the uterus and placenta. As a result, blood flow to the fetus is significantly reduced causing fetal hypoxia and acidosis. Causes of reduced uteroplacental blood flow include: Treatment of late deceleration Maternal hypotension Left lateral position Pre-eclampsia IV fluid Uterine hyperstimulation Stop oxytocin Give O2 Variable decelerations: are observed as a rapid fall in baseline fetal heart rate with a variable recovery phase. they are variable in their duration and may not have any relationship to uterine contractions. They are most often seen (during labour, oligohydramnios) and usually caused by umbilical cord compression. All fetuses experience stress during the labour process, as a result of uterine contractions reducing fetal perfusion. Whilst fetal stress is to be expected during labour, the challenge is to pick up pathological fetal distress. prolonged deceleration: is defined as a deceleration that lasts more than 2 minutes: If it lasts between 2-3 minutes it is classed as non-reassuring. If it lasts longer than 3 minutes it is immediately classed as abnormal. Overall impression: once you have assessed all aspects of the CTG you need to determine your overall impression. Can be described as either reassuring, suspicious or abnormal Reassuring Baseline heart rate (110 to 160 bpm) Baseline variability (5 to 25 bpm) Decelerations (None or early) Non reassuring Baseline heart rate ( 160) Baseline variability (Less than 5 for 30 to 50 minutes, More than 25 for 15 to 25 minutes) Decelerations Abnormal Baseline heart rate ( 180) Baseline variability (Less than 5 for > 50 minutes, More than 25 for > 25 minutes, Sinusoidal) Decelerations Causes of the following Fetal compromise Placental insufficiency Placental abruption Uterine hyper stimulation Maternal hypotension Cord compression Tachycardia (>160 bpm) Maternal fever Fetal hypoxia Fetal anemia Ammonites Fetal tachyarrhythmia (SVT 200-240 bpm) Fetal heart failure Drugs (Beta sympathomimetic) Bradycardia (< 110 bpm) Heart block (little or no variability) Occiput posterior or transverse position Serious fetal compromise Hypoxia Decreased baseline variability Fetal metabolic acidosis Pre existing neurologic abnormality CNS depressants Fetal sleep cycles ( 40) 6. Thrombophilia 7. Maternal BMI > 30 8. Placental complications (If the umbilical cord inserts into the placenta abnormally) 9. Obstetric cholestasis (pruritis with no rash after 24 weeks + abnormal liver function tests which improve after delivery suggests obstetric cholestasis Causes - Chromosomal (trisomies), congenital anomalies. - Infections (non recurring, E-coli, GBS, both induce preterm. B19, toxo, malaria) - DM, Extreme ages (40), Obesity, obstetric cholestasis. - Nuchal cord, abnormal insertion of cord to placenta - Thrombophilias (C,S, ATIII ↓, APCR, FVL, PTGM, APAS, hyoerhomocysteinemia → PET, IUGR). Diagnosis ↓ fetal movement, ↓ progression of pregnancy, no FHR should confirm by US. Color flow map if obese. Determine timing of death by checking: Skin edema, hydrops, spalding sign (overlapping of skull bones), liqour amount (would decrease). Investigation to be done (for the causes): - Exclude PE, abruption, DIC (fibrinogen) - CBC, BG/Rh, kleihauer & coombs test - ANA, APA screen. - ToRCH screen. - RBS, A1C, Bile salt. - Baby examination, postmortem exam (if refused, you can try fetal MRI, skeletal x-ray, histopathology, karyotype & cytogenic test of placenta) Treatment Up to 90% deliver spontaneously with 2 weeks (if delayed → risk of DIC) Aim for vaginal delivery with adequate analgesia. C/S is appropriate if High risk of uterine rupture Suspected scar dehiscence Failed induction Major placenta previa. C/S carries 50% risk of endomyometritis. After delivery: Psychological support, suppress lactation by (Cabergoline), contraception.  IUGR Types Neonatal Complications Meconium aspiration Asphyxia Polycythemia Hypoglycemia Mental retardation Greater risk of perinatal morbidity and mortality Diagnosis of IUGR Determine GA early SFH at each visit, if high risk or SFH lags by 2 cm → more thorough assessment by: - US (BPD, head and abdomen circumference, femoral length, fetal weight, liquor, anomalies) - serial biometry & liquor each 2-4 weeks - BPP (biophysical profile) Perinatal complication of IUGR include fetal and neonatal deaths, - doppler umbilical blood flow prematurity, fetal compromise in labor, neonatal morbidity, IOL, and C/S. - venous doppler Neonates with IUGR are at increased risk for impaired neurodevelopment, type 2 DM and hypertension in adult life. Treatment & effects of IUGR It is a balance of: If kept undelivered → stillbirth. If IOL or C/S → prematurity → neonatal morbidity & mortality (meconium aspiration, asphyxia, polycythemia, hypoglycemia, mental retardation) DM & HTN later in life. So there is wide variation at timing of delivery but should have optimal expertise and skilled resuscitator and a low threshold for C/S. The goal is to deliver the most mature fetus in the best condition with minimal risk to the mother... General measures - Stop smoking, alcohol, drug abuse, optimise mother health. - Low dose asprin has a role in prevention. - If severe → bed rest to maximize placental blood flow - Intensive fetal surveillance - Steroids if need delivery before 36 weeks.  Amniotic fluid abnormalities Polyhydramnios: >2 L, AFI >25 cm or Single Pocket >8cm (Severity: 8-11, 12-15, >16) in 1-2% of cases. Causes Pathogenesis Idiopathic (65%) Increase in daily fetal urine production Placental Chorioangeoma (1%) Decrease in fetal swallowing Maternal (15%): DM, RH Incompatibility, TORCH Fetal (19%): NTD, Anencephaly, GIT Obstruction, Cardiac, Anemia, TTTs. Clinical presentation Acute: Onset occurs before 20 weeks and present with symptoms, and labour start before 28 weeks of pregnancy. Symptoms: acute abdominal pain and distension, nausea, vomiting, breathlessness which increase on lying down, palpitation, leg swelling, varicosities in legs and vulva, hemorrhoids. Signs: patient looks ill, abdomen enlarged with shiny skin, fluid thrill may be present, SFH is larger than date, difficulty in feeling fetal part. PV shows taking up of cervix or even dilatation with bulging membrane. Chronic: More common and may be asymptomatic. Symptoms are mainly due to mechanical results: dyspnoea is more in supine position, palpitation, edema of legs and vulva. Similar signs, external ballotment is more easily elicited, high presenting part. Diagnosis US: Confirms it and to look for twins, anomalies, macrosomia. AFP (NTD) Fetus is surrounded by AF everywhere except at its attachment with the umbilical cord. AF is derived from fetal urine & fetal lung secretion although additional contribution comes from Coombs amniotic membrane secretions. Torch Screen 8wks: 15ml, volume increases 10ml/wk 17wks: 250ml, increases at 50ml/wk DM Screen 28-35wks: ~750-1000ml 42wks: < 500ml Function of amniotic fluid Treatment Shock absorber – protects from external trauma Protects cord from compression Acute Cases → Terminate Pregnancy Permits fetal movements – development of musculoskeletal system, prevents adhesions. Swallowing of AF enhances growth & development of GIT Chronic: AF volume maintains AF pressure – reduces loss of lung liquid – pulmonary development Hospitalization, bed rest permits lung growth Maintenance of fetal body temperature Treat The Cause Bacteriostatic properties – It protect the fetus and provides barrier against infection. Indomethacin (1.5-3 mg/kg/day ↓ lung liquid, urine production & increase absorption through fetal membrane), can close PDA. Severe Cases → Repeated Amniocentesis (Can Cause Prom, PTL) Mild to Moderate Hydramnios: Rarely Requires Treatment. No Diuretics, Water and Salt Restriction Complication Malpresntation, PROM, PTL, Abruption, Cord Prolapse, Cord Knot → IUFD. Oligohydramnios: AFV 35 Multiparity Family history Classification based on: - No of fetus: twins; triplet, quadruplets… - No of fertilized eggs: Zygosity - No of placenta: Chorionicity - No of amniotic cavities: amnionicity Post conception days: - 0-3 days(morula)……Dichorionic -diamnionic - 4-8 days(blastocyst) …. Monochorionic-diamnionic - 9-12 days(embryonic disk) ….Monochorionic-monoamnionic - > 12 days (embryo)…. Conjoind Determination of zygosity by DNA fingerprinting, amniotic fluid (amniocentesis), placental tissue (chorion villus sampling), or fetal blood (cordocentesis). chorionicity is determined by an ultrasound in the first trimester. Complication of twin pregnancy Antepartum (Anemia, Preeclampsia, Gestational diabetes, and Thromboembolism) Intrapartum (preterm, malpresentation, and C/S) Postpartum (PPH) Pregnancy complications according to chorionicity: Miscarriage and severe preterm delivery (if before 24 weeks die, after 32 weeks survive, between 24-32 high chance of neontal death) Perinatal mortality in twins (perinatal mortality rate in twins is six times higher than in singleton, due to prematurity- related complications, and its twice as high in monochorionic than dichorionic twin due to TTTS) IUGR (delivery should be avoided before 32 weeks even if there is evidence of imminent intrauterine death of the smaller twin) Fetal abnormalities e.g NTD Chromosomal defects and twining e.g Down syndrome ( screening by measurement of fetal nuchal translucency thickness in each fetus by ultrasound at 10-14 weeks, invasive procedures like amniocentesis or chorion villus sampling). Death of one fetus in a twin pregnancy Malpresentation & C/S Complications unique to monochorionic twinning (TTTS) Others (Hyperemesis gravidarum, hypertension, gestational DM, anemia, hemorrhage, pre eclampsia) TTTS Donor become hypovolemia, hypotension while recipient become hypervolemia, polyhydramnios, high output heart failure. Severe disease becomes apparent at 18-24 weeks. Treatment Amniocentesis every 1-2 weeks and drainage of large volumes of amniotic fluid; this treatment improves survival by prolonging the pregnancy. More recent method involves the introduction of a thin endoscope into the uterus and the use of laser to coagulate the placental blood vessels that connect the circulations of the two fetuses; in about 70 per cent of pregnancies one or both babies survive. Mode of delivery in multiple pregnancy If no other obstetrical indications of C/S and leading fetus is cephalic → vaginal delivery at 38 (but usually labor will start by 37), Otherwise if other indications (e,g DM, HTN, PE, previous CS, or leading fetus is not cephalic → C/S How do you delivery first baby if cephalic presentation? Vaginally How do you delivery second baby? (If cephalic → vaginally, if breech & intact membrane → ECV, if membranes ruptured → IPV) What are indications of C/S to deliver second baby? Fetal distress, shoulder presentation. Time of delivery Uncomplicated monochorionic twin pregnancies should be offered elective delivery from 36 weeks gestation and this should be performed after course of antenatal corticosteroids has been given Dichorionic twin pregnancies delivery from 37 weeks Continuing uncomplicated twin pregnancies beyond 38 weeks gestation increases the risk of intrauterine fetal death monochorionic → 36 Dichorionic → 37  Rh Incompatibility & Hydrops Pathophysiology When a Rh-negative mother is exposed to Rh + fetus blood (D antigen), the D antigen is perceived as a foreign threat similar to how bacteria and viruses are perceived. This leads to a series of activation of immunogenic pathways that culminates in the production of anti-D antibodies. These antibodies can freely cross the placenta to the fetus, bind to the D antigen present on the erythrocytes of Rh- positive fetuses to further activate immunologic pathways that lead to the hemolysis of the fetal erythrocytes. This condition is called Rhesus (Rh) incompatibility. Clinical presentation of Rh isoimmunization Varies from mild to severe to fatal hemolysis: - In utero, bilirubin is removed by the placenta to maternal circulation and part of it go to the liquor. Fetus will be anemic with risk of HF (hydrops fetalis). - After delivery: varying degree of anemia & hyperbilirubinemia with risk of kernicterus Prevention of Rh incompatibility Identify blood group & Rh of all pregnant women in first visit: - If Rh⊕ → don’t worry, If Rh⊖ → check the partner - If he is also Rh⊖ → don’t worry, while If he is Rh⊕ (or if we don’t know his blood group) → there is chance of getting Rh ⊕ fetus (100% if he is homozygous & 50% if heterozyhous) If woman is unsensitized (⊖ indirect coombs test): Anti-D (Rh immunoglobulin) covers at 28-32 weeks (or 2 low doses at 28 & 34 weeks) If the neonate Rh ⊕ → another anti-D to mother within 72 hours of delivery. (Up to 9 days) Rh Ig immunoprophylaxis: Any time risk of feto-maternal hemorrhage like: Early pregnancy bleeding (miscarriage, ectopic, GTD), APH, ECV, Invasive procedure as CVS, abdominal trauma. *for miscarriages: give if GA is > 9-12 weeks. But if severe or recurrent bleeding can give even at 8 weeks. Failure of prophylaxis is either due to: Dose too small or Dose too late >72 hours Each prophylactic dose is 300 μg, covers 15 ml fetal cells and works for 10 weeks Factors affecting sensitization (immunization) & severity: - Amount of Antigen (fetal RBCs) - Strength of antigen (antigenicity) - Host factors (Integrity of maternal immune system) Investigations 1. Indirect Coombs test: test of sensitization. 2. Kleihauer-Betke test or flow cytometry: for fetomaternal hemorrhage (know how many doses to be given) 3. Amniocentesis: Indirect method to measure degree of haemolysis of fetal RBC by measuring concentration of bilirubin in amniotic fluid. Zone I: mild. Zone Il intermediate, follow by amniocentesis every 1-2 weeks. Zone III may require transfusion or delivery (risk of hydrops) Indirect Coombs test: it use blood sample of mother to look for the presence of cell destroying antibodies within the plasma. positive test is a sign of Rh incompatibility (sensitization) Management of sensitised patient (need family planning): Maternal antibody titers (serial indirect coombs test). repeated every month until 24 weeks of gestation and more frequently in T3. if it is < 4 = HDFN unlikely, 4-15 moderate risk, >15 high risk of hydrops. Fetal DNA testing (If Rh — , don't worry more). US: polyhydramnios & hydrops Doppler US: ductus venous blood flow and peak systolic velocity of fetal MCA for severity of anemia. Amniocentesis in case of fetal anemia to measures bilirubin. Treatment Term: deliver then: Phototherapy if mild jaundice, Exchange transfusion if moderate to severe jaundice Preterm fetus: - If Hb >10g/dL & no hydrops → conservative with regular follow up till lung maturity is assured then deliver. - Zone Il or III: depending on GA, clinical assessments, CTG, U/S, BPP: Transfer to suitable place for Intra-uterine blood transfusion Steroids, repeat intrauterine therapy, if lung matures → deliver OR Steroids + delivery + extrauterine therapy. * Blood for Intrauterine therapy should be Fresh blood, compatible with mother & feuts, CMV, HBV, HCV ⊖. * These women need prenatal counselling & family planning esp if father is homozygous. Hydrops fetalis is prenatal form of heart failure with subsequent accumulation of fluid in ≥2 compartments. or life threatening hemolytic anemia which defined as abnormal accumulation of fluid in fetal soft tissues and body. Appearance or After birth symptoms - Enlarged organs, effusions, ascites - Pale coloring - Respiratory distress associated with polyhydramnious, placental edema, mortality rate > 50%, Bad prognosis Types, causes & pathophysiology of hydrops: Immune hydrops fetalis (IHF) caused by Rh incompatibility Non-immune hydrops fetalis (NIHF) commonest type, occur when another disease interferes with regulation of fluid: - Cardiac or lung defects. - Fetal anemia: e.g alpha thalasaemia, TTTS, feto-maternal hemorrhage - Genetic: Turner, down or patau syndrome. - infection like congenital parvovirus B19 Diagnosis US: polyhydraminous, Thickened placenta, enlarged liver, spleen, or heart, fluid buildup around the abdominal organs, heart, or lungs and ascites. Fetal blood sampling for karyotyping, virology, full blood count enzymatic studies and liver function test Doppler ultrasound for MCA Amniocentesis Fetal Echo Maternal risk: Rapid onset Pre- eclampsia due to placental edema PPH due to polyhydramnios Amniotic fluid embolism Treatment based on baby's overall health, GA, Severity, Cause: Supportive measures required including: - management of respiratory status - management of fluid and electrolyte status. - pleural drainage, Chest tubes may need - Arrhythmia of fetal heart can be treated by drugs to the mother or fetus nutrition management - intravascular volume replacement, blood pressure support immune support - correction of anemia by intrauterine transfusion ABO incompatibility Is haemolytic disease when mother blood group is O and baby is A or B (baby cannot be AB) - 20% chance of ABO incompatibility if feto maternal hemorrhage occur (risk of stillbirth is not increased) - < 5% chance of developing noticeable hemolytic disease (mild) - Is less severe but more common than Rh incompatibility - does not cause stillbirth but frequently affects primigravida (unlike Rh Incompatibility) - chance of recurence is 87%. - Diagnosis: Direct Coomb’s antiglobulin test may be ⊖ or weakly ⊕ - Anti-A & B produced in the mother being natural are IgM molecules & so do not cross placenta. - No antenatal treatment is necessary & 67% of affected infants will not need any treatment.  Postpartum hemorrhage PPH Primary with 24 h. 0.5L/VD, 1L/CS, ↓Hct by 10%. Secondary 1 day - 6 weeks (usually due to tissue or infection) Causes: 4 T Tone, Atony, inertia: Retained product Prolonged or obstructed labour Operative delivery spatially if GA is used (may cause relaxation of myometrium as halothane & cyclopropane) Over distention of uterus as in polyhydraminus & multiple pregnancy Large placental site as in multiple pregnancy. Placenta previa because of inability of the lower segment to contract. Abruptio placenta due to interstitial uterine hemorrhage & later due to hypofibrinogenemia. Multiparty due to increase in fibrous tissue & decrease in muscular tissue. Multiple uterine fibroids spatially the intramural type. Full bladder. Couvelaire uterus: abruption → retroplacental blood → penetrates myometrium Thrombin (clotting disorders): hereditary or DIC due to: abruption, amniotic embolism, IUFD Tissue (Retained tissue--placenta accreta spectrum) Trauma: Complete or incomplete uterine rupture during pregnancy (is rare, weak scar like classical C/S, myomectomy, metroplasty) during labor (Obstructed labour, internal pudalic version, Forceps may lead to extended cervical tear, The improper use of oxytocic drugs, Scar in the uterus, Multi-parity) Lacerations of cervix: Precipitated rapid labor, Forceps on un-fully dilated cervix, Rapid delivery of the after coming head in breech presentation, Scar in the cervix from previous injury. Perineal tear: 4 degrees (vaginal mucosa, perineal muscle, anal sphincter, rectal mucosa) Treatment Call for help, ABC 1. Ensure that at least 2 peripheral infusion lines are established using a wide bore cannula (gauge 14). 2. Blood group & cross matching. 6 units of blood (preferably fresh whole blood). 3. Vital sign 4. CVP 5. Restoration of blood loss by IV fluids (Hartman’s or hemacel) till cross matched blood is available & if group Oˉ blood is given till preparation of the appropriate blood group. 6. Insert a urinary catheter. 7. Start replacement and identify the cause Tone: Atony; Lax uterus: Utero-tonic drugs are effective (see below). Uterine massage, Bimanual compression Intrauterine balloon, Uterine packing Uterine artery embolisation B lynch suture, uterine artery ligation, Internal iliac artery ligation, hysterectomy. Trauma: If placenta is delivered & the uterus is well contracted → Transfer the patient to the operation theater for examination under anesthesia. Tissue: If the placenta is not delivered but separated →”CCT” If the placenta is not separated → should be removed manually under GA after stabilization of the patient & correction of shock & we should avoid giving oxytocic drugs till after removal of the placenta. Oxytocin: ampoule is 1 mL = 10 units. – Augmentation of labor: dilution & slowly IV – Vaginal delivery:10 unit IM with delivery of anterior shoulder or of baby. – C-section: 5 units IV slowly. – PPH: infusion of 40 unit (4 ampules) in 500 mL of normal saline over 2-3 h. Side effects: Nausea, vomiting, abnormal taste, abdominal crumps, persistent contraction if the baby is inside, hyponatremia/cerebral edema if high dose for long period (oxytocin works on ADH receptors as both come from posterior pituitary) Does not have absolute contraindications but should be cautious in case of heart or pulmonary disease. Ergometrine: ampoule is 0.2 mg. Give 1-2 ampoule IM. Side effects & contraindications: – Nausea & vomiting – HTN (contraindicated if patient already had HTN, heart or pulmonary disease) – Bronchospasm (contraindicated in asthma) – Contraindicated if baby is inside the uterus (risk of uterine rupture bcz it contracts the uterus and closes the cervix) Misoprostol (PG E1): tab is 200 mg. (give 3-4 tabs rectally) Side effects: nausea, vomiting, shivering, diarrhea. Prevention of PPH + Correction of anemia (heart, dehydration, PE). + Be aware if Hx of PPH + Active management of 3rd stage of labor: 1. Early cord clamping and cutting. 2. Brandt-Andrews maneuver: Gentle CCT with uterine counter-traction when the uterus is well contracted. 3. Utero-tonic (Oxytocic) drug administration (preferably oxytocin): IV Ergometrin 0.5 mg (1-2 ampoule of 0.2 mg) or IM Oxytocin (pitocin or syntocinon), (1 ampoule: 10 units) (with delivery anterior shoulder or fetus). These drugs when given IV will act during 30-45 seconds. IM Syntometrin (1 ml contain 5 units oxytocin & 0.5 mg ergometrin) with the crowning of fetal head (except multiple pregnancy that it is given after the delivery of the last baby PG IM, IV or rectaly PPH hematoma Infralevator: Perineal, vulvar, paravaginal, ischiorectal. leads to Severe pain & very tender purple vulval swelling. Causes Rupture of paravaginal plexus of veins fom distention of lower genital tract even though vaginal epithelium may remain intact Imperfect repair of an episiotomy Supralevator: Above pelvic diaphragm spreads into the base of the broad ligament & a soft mass appear in one of the iliac fossa. Causes: - Cervical laceration extending into the vaginal vault. - Extra peritoneal rupture of uterus - CS Treatment: conservative & transfusion. if severe and shock →operation  Early pregnancy vaginal bleeding Early Pregnancy Vaginal Bleeding: Age of viability: gestational age at which we can save the life of a baby outside the uterus. It is variable according to each country & mainly depends on the quality of the healthcare system (especially NICU).: USA: around 22 weeks or 500 grams. UK: 24 weeks. Iraq: it is technically 28 weeks but we count it as 24 because our system is based on that of UK. This age is a cutoff for categorisations of pregnancy conditions: ○ Bleeding: either early pregnancy vaginal bleeding (if before) or antepartum hemorrhage (if after). ○ Pregnancy loss: either abortion (if before) or IUFD (if after). ◆ A baby that was alive in utero just before delivery and was born with no signs of life is stillbirth. Serum β hCG titer → must write titers not just pregnancy test. serum β hCG become positive 8-12 days after ovulation urinary β hCG become positive 14-18 days after ovulation Causes of abnormal β hCG titers: High: Multiple pregnancy, GTD and Down syndrome. Low: ectopic/failing pregnancy, Edwards syndrome and Patau syndrome. Causes of early pregnancy vaginal bleeding: 1. Abortion 2. Ectopic pregnancy 3. Gestational trophoblastic disease (GTD) 4. Low lying placenta (not placenta praevia) 5. Non obstetrical causes: cervical polyp, cervicitis, bleeding disorders…. Order a β hCG titer: If very high → GTD Duplication of β hCG after 48 hours → normal pregnancy If the titer rises but is not duplicating → ectopic pregnancy If the titer is going down → miscarriage. A positive result virtually excludes PID as a differential diagnosis of pain/bleeding. Abortion: Pregnancy loss before the age of viability. Types: Threatened: It is a clinical entity where the process of miscarriage has started but Spontaneous abortion (miscarriage) has not progressed to a state from which recovery is impossible ○ Threatened (only bleeding ± pain, normal SFH, only type with survivable fetus) ○ Inevitable (dilated cervix → nothing can keep it alive) ○ Missed (patient unaware and diagnosed accidentally by US or at follow up of threatened one) ○ Incomplete (some pieces expelled) ○ Complete (empty uterus) ○ Septic (retained pieces get infected because blood is a good media for bacterial growth): patient is toxic with abdominal pain, no bleeding, fever, tachycardia, tired and deteriorating condition. Induced ○ Illegal ○ Legal = Therapeutic abolition: need a committee to sign for it either for maternal or fetal purposes: ◆ Valvular heart disease in mother → patient cannot survive. ◆ Oncology of the mother → chemotherapy (teratogenic) ◆ Fetus incompatible with life (anencephaly, multiple anomalies…) ◆ Abroad, mother can CHOOSE not to precede a pregnancy and this is her right that is not applied here….  The following indicates unfavorable outcome: falling serum β-hCG, decreasing size of the fetus, irregular shape of the Rx: gestational sac or presence of fetal bradycardia Threatened: Analgesia (paracetamol), Tonics (iron & folic acid), Rest, Progesterone. ○ Routine pregnancy tests needed to be done just as any antenatal care: CBC, blood group & Rh, Virology, GUE, TFT, RBS, U/S. ○ We need to follow up after 2 weeks by US to know will she continue or lose pregnancy, but if developed any attacks of bleeding she should consult. ◆ Absence of fetal heart sound on US → Missed miscarriage. – Watchful waiting twice per week for 2-3 weeks, progesterone will be Antibiotic prophylaxis stopped, but iron & folate can be continued. (Penicillin, Cephalosporin) – If not delivered in 2-3 weeks (risk of infection) or if she had continued Bcs blood is good media for bacteria bleeding (risk of shock), we will not wait more: either do medical termination by misoprostol (oral, rectal, vaginal, sublingual “fastest”) or surgical termination by D&E or suction evacuation. Inevitable: Resuscitation (methargine to stop bleeding + IV fluid or blood transfusion), then: ○ Before 12 weeks: D&E or suction evacuation followed by curettage. ○ After 12 weeks: oxytocin to accelerate the abortion if patient accepts. Incomplete: tonics, broad spectrum antibiotics, completing the abortion (if patient clinically stable by misoprostol, if clinical unstable by admission, IV fluid, D&E). Complete: tonics, antibiotics to prevent endometritis (would lead to Asherman) D&E curretage Septic abortion: rescucitation then send for U/S ○ Admission ○ Two wide bore cannula, take a blood sample, start fluids & parenteral antibiotic bollus dose) ○ Send blood for CBC, cross matching, CRP, RFT, LFT & prepare blood and blood product ○ Take high vaginal or cervical swab for culture and sensitivity ○ Prepare the patient for surgery ○ At least 7 days on parenteral antibiotic: 3rd gen cephalosporin, penicillin, metronidazole, aminoglycoside. ○ If she developed DIC (digital infarction, petechiae, ecchymosis) ◆ CBC twice weekly: WBC (septic abortion), Hb, PCV, retics count (anemia), platelet (DIC) ◆ Coagulation screen (everything will be abnormal): Fibrinogen (normal > 200), PT, PTT, BT. ◆ Treat it as any case of DIC Risk factors: Multiple Pregnancy, DM, PCOS, Hypothyroidism, Autoimmue disease, TORCH, smoking, Exercise, Caffeine, Cocaine, Trauma, Age > 35, Antidepressant especially paroxetine and venlafaxine, IUD during conception time Recurrent abortion: ≥ 3 consecutive abortions. Investigate for the causes: Anatomical: Septate uterus, fibroids, adhesions, cervical incompetence Systemic: DM, thyroid disease, progesterone deficiency, PCOS, genetic disorders, infections, thrombophilia (e.g., antiphospholipid) Fetoplacental: Chromosomal, Anomalies, Anembryonic pregnancy, Cord or placental problems. Miscellaneous: Trauma (exercise), latrogenic (e.g CVS, LEEP), Environmental (smoking, cocaine, caffeine, antidepressants). Cervical incompetence (insufficiency): presents with recurrent mid-trimester (T2) abortion (usually inevitable type) or preterm labor because the weak cervix cannot hold the growing size of pregnancy products. Each pregnancy is held for shorter than before. Diagnosis as following: ○ If Pregnant “more accurate” → TVUS: dilation & shortening cervix (< 25 mm) ○ Not pregnant: do HSG at day 21 of cycle (peak progesterone, you will see funnel shape cervix), or do Heger test (size 8 of hegar dilator passes easily into the cervix). ○ Treatment is by McDonald cervical cerclage to close the cervical os, done at the end of T1 or begging of T2 (13-14 weeks) because T1 miscarriages are related to chromosomal causes. It is removed when: Chromosomal anomalies is the most common cause of ◆ Patient reached term (37 weeks) abortion in first trimester ◆ Signs of labor (preterm labor) Cervical incompetence is the most common cause of abortion in second trimester ◆ IUFD ◆ PROM, PPROM ○ Shirodkar cerclage is a permanent suture that needs C/S for delivery. Abortion occurs more in multiple pregnancies & older age. Chromosomal abnormalities & progesterone deficiency more likely causes T1 miscarriages. Blighted ovum (anembryonic pregnancy) is a sonographic diagnosis with gestational sac but absence of fetal pole (no embryo is seen). missed miscarriage Dx by history -fetal movement suddenly stop -other signs of Pregnancy like nausea, vomiting, micturition.... (suddenly stop) -No features of Pregnancy Progression like Abdominal enlargement Ultrasonography (TVS) findings in: Threatened well-formed gestation sac, indicating healthy fetus. Observation of fetal cardiac motion. Anembryonic sac is diagnosed when the mean gestational sac diameter (MSD) is >= 25 mm and no embryo is seen on TVS. It suggests early pregnancy failure. Inevitable examination reveals dilated internal os through which the products of conception are felt Complete empty uterine cavity Incomplete echogenic material (products of conception) within the cavity Missed abortion an empty sac early in the pregnancy or absence of fetal cardiac motion and fetal movements Treatment of missed abortion Expectant (spontaneous) if less than 12 weeks Medical (misoprostol) Surgical (D&E) When you do D&C, These are the indications for stopping the procedure: 1. When you hear crackle sound 2. When you see air bubbles  Abd pain is commonest presentation, others as missed period and Ectopic Pregnancy: vaginal bleeding also may present Tubal 98%: Fimbrial, Ampulla (most common), isthmus (diagnosed earlier), cornual. Non tubal: Ovaries, Cervix, Abdominal, Scar of previous C/S (especially repeated CS), Heterotopic (a normal and an ectopic together often from IVF). RFx: PID (damages tube or asherman), Surgery (abdomen, pelvic, CS), previous ectopic pregnancy, IUD, IVF, smoking, DES syndrome. infertility, tubal surgery and ligation Diethylstilbestrol syndrome intrauterine surgery (e.g. D&C) Ix: Serial β HCG TITTER (will not double after 48 hours). Also measured weekly after treatment until becomes undetectable. TVUS (gold standard): Empty uterus, Thickening of endometrium, adnexal cyst/mass This doesn’t probe ectopic so we need to follow up with β hCG & TRUS, probably that cyst would be corpus luteum of normal pregnancy and later on we will see intrauterine gestational sac Rx: Medical: Methotrexate 1 mg/kg. if β hCG does not fall by 15% from day 4 to day 7 then repeat MTX. Indication of medical treatment ○ Hemodynamically stable Expectant: follow up by β-hCG titer every 3-7 days if: ○ Gestational sac < 3.5 cm β-hCG < 3000 Hemodynamically Stable ○ Absence of fetal heart rate No pain (just US diagnosis) ○ β HCG < 3000. ○ Patient accepts the side effects of MTX (it is a chemotherapy) ○ No contraindications to MTX (as liver/kidney disease) Surgical: indications are opposite to those of medical treatment or failure of 2nd dose of MTX. ○ Laparotomy If unstable patient: Salpingectomy or Salpingostomy → further ↑ risk for next ectopic pregnancy. ○ Laparoscopy If patient is clinically stable. Differential diagnosis: Appendicitis PID Abortion Ureteral calculi Tubo ovarian abscess Ovarian cyst rupture  Arise from trophoblast (future placenta) Presentation (bleeding, large for date uterus, exacerbation of Gestational Trophoblastic Diseases: physiological change of pregnancy, early signs of pre eclampsia) Benign (pre-malignant): Hydatidiform mole (molar pregnancy) complete vs partial (see image). Malignant: Invasive mole, Choriocarcinoma, Placental site trophoblastic tumor, Epithelioid trophoblastic tumor. Rx: D&E (avoid curettage because risk of bleeding, perforation& seeding) Send the sample for histopathology to confirm diagnosis & exclude malignancy If confirmed H Mole → follow up by β HCG weekly until 3 results are negative then monthly for 6 months (here also do US, CXR, MRI to check for metastases) Should be on contraception (bcz pregnancy would make hCG unreliable) Hysterectomy is an option if patient has finished family but even then you need to follow up as above. Indication of chemotherapy: If histopathology confirms malignancy If β hCG level after D&E is continuously rising, decreased but remain plateau for 3 successive results or decreased but raised again. (the level 24 h after D&E is taken as a reference point) If there is metastasis to distant organ (lung, brain, liver, others…) Later develop a mass in the uterus with positive β hCG. Decision of which type of chemotherapy depends on WHO Scoring system: Single drug regime: MTX or actinomysin D. ○ Score ≤ 6 ○ May need 6 cycles, each cycle is repeated every 2 weeks alternative with fulminic acid and 3 doses can be given in 1 cycle. Combined EMACO regime: Etoposide, MTX, Actinomycin D, Cyclophosphamide, Oncovin (vincristine). ○ Score ≥ 7 or failure of single drug regime. ○ Each cycle is repeated every 3 weeks, No need for folinic acid. Risk factors: < 20 years or > 35 years, and previous GTD ABO blood groups of the parents appear to be a factor in choriocarcinoma development, i.e. women with group A has greater risk than group O. Dx: HCG , and confirmed by US show mass Rx: Termination, evacuate and suction Follow up by BHCG Complications: Malignancy, Metastasis Vaginal bleeding, enlarged uterus, pelvic pain or discomfort, and hyperemesis are the most common symptoms of GTD. The initial clinical diagnosis of GTD should be confirmed histologically, which can be done after the evacuation of pregnancy However, malignant GTD is highly vascular. If malignant GTD is suspected clinically, biopsy is contraindicated, because biopsy may cause life threatening haemorrhage. Medical disease in pregnancy  Diabetes in pregnancy Pre pregnancy counselling (part of antenatal care) Optimization of glycaemic control to achieve an HbA1c of < 6% (FBS 4 kg) Diabetes with complications or difficult to control Fetal compromise as observed in antepartum fetal monitoring Elderly primigravidae Multigravidae with a bad obstetric history Obstetric complications like pre-eclampsia, polyhydramnios, malpresentation  Summarized all together Effect of DM on pregnancy: Achieve A1C 160/100 mmHg in early pregnancy - Aim to deliver at 39-40 weeks. Pre-pregnancy BMI > 35 Drugs only prevent stroke, not PET & abruption!! Previous pre-eclampsia Antiphospholipid syndrome PET or Pre-eclampsia “Toxaemia” De novo (new-pnset) HTN + proteinuria or end-organ dysfunction starting after second half of pregnancy (>20 weeks) and disappear by the end of puerperium → multi-system disorder. H mole can induce PET in first half of pregnancy. - HTN means BP >140/90 mmHg 2 occasions 4 hours apart. - Proteinuria means ≥300 mg/24h urine collection - End-organ dysfunction means ↓ platelet, DIC, ↑ LFT, ↑ RFT, Cerebral edema & hemorrhages, pulmonary edema, eclampsia (seizure), HELLP. Risk factors of PET First pregnancy Previous history of PET Pathophysiology of pre-eclampsia 10 years or more since last baby First stage, trophoblast invasion and spiral arteries retain their muscular walls. Age 40 years or more This prevent development of high-flow, low-impedance uteroplacental circulation BMI ≥ 35 and leads to uteroplacental ischaemia FHx of PE Second stage, uteroplacental ischaemia results in oxidative and inflammatory Multiple pregnancy stress, with involvement of secondary mediators leading to endothelial dysfunction, vasospasm and activation of coagulation system. Booking DBP ≥ 80 mmHg Booking proteinuria (≥1+ on more than one occasion or quantified at ≥300 mg/24 h) PMHx: HTN, DM, CKD, Coarctation of aorta, APAS Risk factors of imminent eclampsia: uncontrolled HTN, poor ANC, primi, obesity, black, DM Clinical features of PET Symptoms: Classically frontal headache, visual disturbance and epigastric pain. However, the majority are asymptomatic or merely complain of general, vague flu-like symptoms. Imminent eclampsia: severe frontal headache, visual disturbance and epigastric pain, irritability, restlessness, agitation, twitching, drowsiness, oliguria, tachycardia, RUQ tenderness, uncontrolled HTN, hyperreflexia, clonus. Prone to DVT & DIC thus need hematologist help for treatment. Signs: Degrees of hypertension HTN, maybe absent until late stages. Mild: 140–149 / 90–99 mmHg Rapidly progressive edema of the face and hands Moderate: 150–159 / 100–109 mmHg Epigastric tenderness Severe: ≥160 / ≥110 mmHg Hyperreflexia and clonus SFH & fetus maybe small for date (oligohydramnios & IUGR) +1, +2 protein on dipstick or ≥ 30 mg protein:creatinine ratio warrants quantifying 24h protein. Investigation for pre-eclampsia To monitor maternal complications: CBC ((↓ platelet and ↑ haematocrit), If platelet values are normal, additional clotting studies are not indicated RFT (serum uric acid level to assess the severity of disease ) LFT To monitor fetal complications: U/S assessment of fetal size, amniotic fluid volume, maternal and fetal Dopplers Antenatal CTG (loss of baseline variability or decelerations may indicate fetal hypoxia) Treatment of PET Dx requires admission but mild cases can be managed as outpatient while moderate to severe cases require inpatient treatment (as shown in table below) No cure for pre-eclampsia other than to end the pregnancy by delivering the baby and placenta. Antihypertensives: - Methyldopa: slow onset, take 24 hrs to work, can cause sedation & depression (thus avoid in postpartum period). - Labetalol: first line. - Nifedipine: rapid onset, can cause severe headache. - IV hydralazine, labetalol, nitroglycerin or sodium nitroprusside: for fulminating disease. Low threshold for MgSO4 in severe PE or imminent eclampsia. Cerebral hemorrhage is commonest cause of death in pre-eclampsia, stroke is #1 in HELLP. Prevention: screening of only high risk women by doppler US of uterine artery waveform and prevention by low dose aspirin (75mg daily) and calcium supplementation if low dietary intake. Aim for vaginal delivery at 34 weeks if her condition allows Give steroids if delivered before that time and usually by C/S with high risk of VTE (need heparin). If clotting studies are normal, epidural analgesia would help to decrease blood pressure in labor. Avoid ergometrine in 3rd stage. Postpartum care: Why in pre eclampsia we want to reach 34 weeks and not more ?? Bcs lungs mature in 34 weeks (enough to deliver), we will not wait ⁃ Third of eclamptic fit occur postpartum more bcs process of pre eclampsia is continous and mother condition ⁃ BP at its height 3-4 days postpartum may deteriorate and lead to complications ⁃ Intensive monitoring 48 hr postpartum necessary ⁃ Antihypertensive therapy need to be continued after discharge home ⁃ Postnatal clinic fellow up 6-12 weeks: If HTN not resolved then it is chronic, if proteinuria not resolved then it is CKD. If there was severe PET before 34 weeks, we need to search for underlying cause e.g renal disease.  Epilepsy Good control of epilepsy means last seizure was ≥ 1 year ago while on monotherapy Causes of seizures in pregnancy Epilepsy Eclampsia Encephalitis or meningitis Space-occupying lesions (e.g. tumour, tuberculoma) Cerebral vascular accident, Cerebral malaria or toxoplasmosis Thrombotic thrombocytopaenic purpura Drug and alcohol withdrawal, Toxic overdose Metabolic abnormalities (e.g. hypoglycaemia) Effect of pregnancy on epilepsy: Seizure free: 64%, Increased seizure frequency: 17%, Decreased seizure frequency: 16%, Intrapartum seizures: 3.5%, Status epilepticus: 1 per month Multiple seizure types Drug-resistant epilepsy High-dose polytherapy Poor compliance with AEDs Reduced drug concentration in pregnancy due to increased renal clearance and metabolism, alteration in protein binding ,expansion of intravascular volume Pregnancy specific triggers: nausea and vomiting (reduced AED concentration), sleep deprivation Labour (pain and hyperventilation) Pre-pregnancy counselling in epilepsy Alter medication according to seizure frequency, reduce to monotherapy where possible. Stress importance of compliance with medication. Folic acid 5 mg should be started at least 3 months prior to conception Explain risk of congenital malformation. Explain risk from recurrent seizures. Seizures represent a direct threat to maternal health (e.g. drowning, physical injury), and recurrent seizures put the fetus at risk from hypoxia. Complications or risk to developing fetus: Risk is generally low. It depends on frequency of attacks, number & dose of drugs. Lamotrigine, Levetiracetam and carbamazepine are commonly used and safest agents Sodium valproate can cause neural tube defects, increase risk of cognitive difficulties/learning disability. Fetal hypoxia, sudden unexpected death in epilepsy. LBW/IUGR, falling and injuries during attack if has multiple attacks. Major fetal abnormalities associated with anti epileptic drugs are: NTD, facial clefts and cardiac defects Anomalies: - valproate, highest risk (NTD, low IQ) - benzodiazepine (cleft lip, CHD) - phenytoin (vitamin K and D deficiency, fetal hydantoin syndrome) - phenobarbital (low birth weight) anomalies scan should be done at 20-22 weeks in epileptic Patients Antepartum management: Women of childbearing age who has epilepsy should be managed by neurologist and obstetrician Intrapartum management: Adequate analgesia (transcutaneous electrical nerve stimulation (TENS), nitrous oxide and oxygen, regional analgesia, Pethidine used with caution, diamorphine used in preference to pethidine. Minimise risk factors for seizures such as insomnia, stress and dehydration. Long-acting benzodiazepines such as clobazam can be considered if there is very high risk of seizures in the peripartum period. AED intake should be continued during labour either orally or parenteral. Postpartum management Continue AED postnatally, and those who are taking AEDs in pregnancy should be encouraged to breastfeed Support to ensure that triggers of seizure deterioration such as sleep deprivation, stress and pain are minimised. All babies born to women with epilepsy taking enzyme-inducing AEDs should be offered 1 mg of intramuscular vitamin K to prevent haemorrhagic disease of the newborn. Contraception Copper IUD, levonorgestrel releasing intrauterine system (LNG-IUS) and medroxyprogesterone acetate injections are reliable methods of contraception that are not affected by enzyme-inducing AEDs. All methods of contraception may be offered to women taking non-enzyme-inducing AEDs (e.g. sodium valproate, levetiracetam, gabapentin). Women who take enzyme-inducing AEDs should be informed that a copper IUD is the preferred choice for emergency contraception emergency contraception pills with levonorgestrel and ulipristal acetate are affected by enzyme-inducing AEDs. Women taking lamotrigine monotherapy and oestrogen-containing contraceptives should be informed of the potential increase in seizures due to a fall in the levels of lamotrigine. Treatment of epilepsy in pregnancy summarized Mother should be on lowest dose and least number of safest drugs, may even stop drugs if very mild epilepsy. High dose folic acid (5-6 mg) at least 3 months prior to concepon Avoid risk factors in pregnancy, labor and postpartum like stress, pain, insomnia, social deprivation, dehydration, non-compliance. Labor analgesia is very important. If on enzyme inducing drugs: give vitamin K to neonate to prevent hemorrhagic disease of newborn (risk of cerebral haemorrhage and coagulopathy), copper IUD is best contraception but you can use progesterone based contraceptives, avoid estrogen containing contraceptives. (estrogen also ↓ effect of lamotrigine)  Anemia Normal HB level in T1, T2,T3, Post Partum and after puerperium Hb level should be: > 11 in T1 Two most common causes of anemia during pregnancy and the > 10.5 in T2,T3 puerperium are iron deficiency and acute blood loss > 10 Post Partum > 11 after puerperium Causes of anemia according to MCV level Microcytic 100 Megaloblastic anemias, Liver disease/alcohol, Hemoglobinopathies, Metabolic disorders, Marrow disorders , Increased destruction Effect of anemia on pregnancy (from reference) During pregnancy Pre eclampsia Pre term labor Heart failure During labor PPH Shock Cardiac arrest Puerperium Puerperal sepsis Poor lactation Thromboembolism Poor wound healing Effect on baby Low birth weight IUD Anemia in infancy due to reduced iron store Symptoms of IDA Difficulty concentrating, Pica, Glossitis, Cheilosis, Koilonychia, Dysphagia (bcz iron is needed for smooth muscle contraction) When to send patient for CBC Booking visit (9-12 weeks (if Patient is anemic, it mean that patient was anaemic before pregnancy)) 28 weeks (if patient is anaemic, it is good time to replace iron and prevent PPH) 32 weeks (if Patient was anemic at 28 weeks to know whether there is response to treatment or not) Multiple pregnancy bcs they are more prone to IDA and pre term Regarding the management of IDA, ways to correct anemia are: 1- iron supplements (oral and parenteral) 2- blood transfusion Choice of method depend on three main factors: Severity of the anaemia Gestational Age. Presence of additional risk factor like HF and hypertension Indication for blood transfusion 1- Hb 2.5 (>70% preterm labour and >40% experience preeclampsia) Diabetic nephropathy may develop worsening proteinuria and hypertension. Complications- preeclampsia still birth Good control of blood glucose, BP before and during pregnancy improves perinatal, maternal out come. Lupus nephritis —women with SLE are at high risk especially: Women with SLE and antiphospholipid antibody Proliferative lupus nehritis — Immunosuppressive (e.g steroid, azathioprine) used to manage lupus flares during pregnancy. — It can present same as pre eclampsia, so you can distinguish by: RBC cast, low C3 and C4, low leukocyte (in SLE present but not in PE) Abnormal liver function test results (in PE but not present in SLE) Renal transplant and pregnancy Risk of low birth weight, pre term delivery and ectopic pregnancy Women on stable, low doses of immunosuppressive agents, with normal renal function, and with no prior rejection episodes, conception could be safely considered as early as 1 year post transplant. Antihypertensive agents of choice include methyldopa, nonselective β-adrenergic antagonists (i.e., labetalol), and calcium channelblockers. Cyclosporine (or tacrolimus) and steroids, with or without azathioprine, form the basis of immunosuppression during pregnancy  Thyroid in pregnancy Physiological changes: ↑ hCG → ↑ fT4 → ↓ TSH. ↑ E2 → ↑ TBG, ↑ tT3, tT4. T4 is transferred to fetus (for brain development especially in T1), accounts for >30% of T4 in fetal serum at term. Fetal thyroid begins concentrating iodine and synthezising thyroxin from 12 weeks thereafter. Hypothyroidism: Most common cause of hypothyroidism during pregnancy is Hashimoto’s thyroiditis caused by glandular destruction by autoantibodies (antithyroid peroxidase antibodies), iodine deficiency is #1 world wide. Associated with pregnancy loss (miscarriage, IUFD, stillbirth), abruption, GHTN/PE, PTL, developmental delay. TFT should be performed at each trimester and 4-6 weekly if need dose adjustments. Levothyroxine dose 100-125, increased dose in pregnancy, TSH goal 90% chance of becoming chronic carriers of hepatitis B virus, with associated risk of subsequent cirrhosis and hepatocellular carcinoma Management plan should thus include administration of passive immunoglobulin in the 1st 24hr after birth to the newborns of mother with high infectivity. Administration of active hepatitis B vaccine to neonates whos mothers have low infectivity. Liver disease of pregnancy Obstetric cholestasis: liver disease specific to pregnancy due to genetic predisposition to cholestatic effect of estrogen more common in african, indian & finland. So recurrence in subsequent pregnancy is very high, can even occur with OCP bcs of estrogen. Present in T3 (30-32 weeks) with pruritis mainly palms & soles, mild ↑ ALT, AST, bile acids, should take US, serology for viral hepatitis, CMV, EBV & autoantibodies. Complications: fat malabsorption →↓ vit k → PPH, fetal distress, meconium stained liquor, IUFD, PTL. Treatment: discuss the risk, monitor LFT, clotting studies, CTG & US Daily 10 mg vit K, antihistamines & emollients for pruritis, ursodeoxycolic acid (↓ pruritis & LFT but not the fetal risk), delivery at 37-38 weeks. AFLP (acute fatty liver of pregnancy): a pregnancy-specific liver disease, usually presents in T3 with abdominal pain, nausea, vomiting, anorexia and sometimes jaundice. ↑ ↑ ↑ LFT, RFT, uric acid, ↑ WBCs, hypoglycemia, and sudden coagulopathy → perinatal and maternal mortality and morbidity. Treatment: ICU and multidisciplinary team, immediate delivery after correction of hypoglycemia and coagulopathy with 50%dextrose, FFP, and IM vit K), management after delivery is conservative.