My Obstetrics Notes PDF

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Obstetrics1. Antenatal CareGestation Purpose of visit36 weeks Routine care as above Check presentation - offer external cephalic version if indicated Information on breast feeding, vitamin K, 'baby-blues'38 weeks Routine care as above40 weeks (only if primip) Routine care as above Discussion about o...

Description

Shiffa’s P Year Notes

Obstetrics

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Shiffa’s P Year Notes

1. Antenatal Care

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Shiffa’s P Year Notes

1.1 Antenatal Care  main purpose is to identify women who are likely to need medical input, and to prevent foetal and maternal mortality  ideally, antenatal care begins before conception  may involve a general health check to find previously unidentified disease, optimisation of chronic conditions, switching to non-teratogenic medications, checking vaccination status, and advising on lifestyle factors to promote good health, folate (400mcg) may be given  10 antenatal visits in the first pregnancy if uncomplicated  7 antenatal visits in subsequent pregnancies if uncomplicated  women do not need to be seen by a consultant if the pregnancy is uncomplicated  routine screening tests: Gestation

Purpose of visit

8 - 12 weeks (ideally < 10 weeks)

Booking visit  general information e.g. diet, alcohol, smoking, folic acid, vitamin D, antenatal classes  BP, urine dipstick, check BMI Booking bloods/urine  FBC, blood group, rhesus status, red cell alloantibodies, haemoglobinopathies  hepatitis B, syphilis, rubella  HIV test is offered to all women  urine culture to detect asymptomatic bacteriuria

10 - 13+6 weeks

Early scan to confirm dates, exclude multiple pregnancy

11 - 13+6 weeks

Down's syndrome screening including nuchal scan

16 weeks

Information on the anomaly and the blood results. If Hb 1 in 150) of a disorder so it is important to screen for conditions affecting the mother  haematological disease = anaemia, sickle cell disease, rhesus status  clinical conditions = pre-eclampsia, gestational diabetes, asymptomatic infections (especially UTIs)  tests can broadly be divided into: 1. nuchal translucency → modified by other risk factors, e.g. combined test 2. two stage assessment → combined 1st and 2nd trimester results, e.g. NT + blood tests. 3. second trimester blood tests only → e.g. triple test Test

Components

Dates

Triple test

uE3, hCG, AFP

Nuchal translucenc y Quadruple test

US

14-20 week s 10-13 week s 14-20 week s 10 week s 10 + 20 week s

AFP, uE3, hCG, inhibin A

Combined test

US, hCG PAPP-A

Integrated test

[US, PAPP-A] + AFP, uE3, hCG, inhibin A

Sensitivit y

80% (Downs)

Amniocentesis = removal of amniotic fluid using a fine gauge needle under ultrasound guidance, transabdominally, performed from 15 weeks onwards.  karyotyping if screening tests suggest aneuploidy  DNA analysis if parents are carriers of an identifiable gene mutation e.g. CF, thalassaemia  enzyme assays looking for inborn errors of metabolism  diagnosis of foetal infections e.g. CMV, toxoplasmosis  lower procedure-attributed miscarriage rate than CVS ≈1%  less risk of maternal contamination or placental mosaicism x miscarriage x failure to culture cells x full karyotyping may take 3weeks

85%/5%

90%/5%

90%/2%

 AFP → screens for NTDs  US at 11-13 weeks assesses nuchal translucency  raised in trisomy conditions and structural defects including congenital cardiac deformities 6

 neural tube defects can be picked up on USS or by measuring AFP in the second trimester Higher risk diagnostic tests can then be arranged

Chorionic villous sampling = aspiration of trophoblastic cells under ultrasound guidance, usually transabdominally, between 10-13weeks  karyotype if 1st trimester screening tests suggest high risk fo aneuploidy  DNA analysis if parents are carriers of an identifiable gene mutation e.g. CF, thalassaemia  allows 1st trimester TOP if abnormality detected  can be performed surgically,

Shiffa’s P Year Notes before pregnancy becomes physically apparent x 1% risk of miscarriage, higher than amniocentesis x increases risk of vertical transmission of blood-borne viruses e.g. HIV, hepatitis B

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x false negative results (rare) from contamination with maternal cells, especially in DNA analysis requiring PCR x placental mosaicism gives misleading results

Conditions which all pregnant women should be offered screening

Conditions for which screening should not be offered

Anaemia Bacteriuria Blood group, Rhesus status and anti-red cell antibodies Down's syndrome Fetal anomalies Hepatitis B HIV Neural tube defects Risk factors for pre-eclampsia Rubella immunity Syphilis The following should be offered depending on the history: Placenta praevia Psychiatric illness Sickle cell disease Tay-Sachs disease Thalassaemia

Bacterial vaginosis Chlamydia Cytomegalovirus Fragile X Hepatitis C Group B Streptococcus Toxoplasmosis

Shiffa’s P Year Notes

1.3 Down’s Syndrome  most common genetic cause of mental retardation  trisomy 21 Presentation Appearance  dysmorphic facial features + hypotonia  flat nasal bridge  epicanthic folds  single palmar crease Intellectual impairment  80% profound or severe  developmental delay  mean mental age at 21yrs is 5yrs  increased risk of early-onset dementia Congenital malformations  cardiac abnormalities  46% (VSD, ASD, ToF)  GI atresia Increased risk of other medical conditions  leukaemia  thyroid disorders  heating loss

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 epilepsy Diagnosis  combined test  11–13+6weeks = nuchal translucency + blood test (low PAPP-A and high hCG)  serum integrated test  dating scan (not nuchal), PAPP-A blood test at 10weeks, quadruple test at 15weeks (oestradiol, high hCG, low AFP, inhibin A)  integrated test  nuchal scan and blood tests at 10–13+6weeks (PAPP-A at 10weeks, quadruple test at 15weeks)  triple test  blood test at 15-20weeks (oestriol, hCG, AFP), dating scan (not nuchal)  quadruple test  blood test at 15-20weeks (oestriol, hCG, AFP, inhibin A), dating scan (not nuchal)

Shiffa’s P Year Notes

1.4 Teratogens Definition: any environmental factor that can cause teratogenesis in the foetus = dysgenesis of fetal organs in terms of either structure or function, can also manifest as IUGR and fetal death

Teratogens  drugs: o recreational → alcohol, tobacco, LSD, sedatives, cocaine o medications → ACE inhibitors (2nd/3rd trimester), antiepileptics (e.g. valproate), trimethoprim (alters folate metabolism), lithium, warfarin, aspirin, anti-cancer drugs, sex steroids  chemicals → PCB, toluene  toxic metals → mercury, lead  maternal disease → infection (VZV), diabetes, obesity, thyroid or parathyroid disease, phenylketonuria  physical factors → radiation, hyperthermia, hypothermia 9

Shiffa’s P Year Notes Timing Pre-embryonic = conception to 17days after (implantation and blastocyst formation)  adverse effects result in miscarriage Embryonic = day 17 to 55 after conception (organogenesis)  congenital malformations likely due to rapidly dividing tissues, earlier timings leads to greater damage Fetal phase = 8weeks after conception to term  any effects impact fetal growth + organ function Prescribing principles  benefits of medication in pregnancy/breast-feeding should outweigh risks  prepregnancy assessment should be offered to all women of childbearing age on regular medication with alternative medication options where possible  try to avoid 1st trimester use  use drugs already used in pregnancy  give as few drugs as possible to avoid interactions  ensure patient is informed of risks and offered counselling if required  use minimum dose to achieve desired effect  seek latest information on specific medication  OTIS (organisation of teratology information)  24hr service on aspects of drug/chemical toxicity in pregnancy throughout the UK

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Drug/condition

Effect

ACE inhibitors

Renal dysgenesis Craniofacial abnormalities

Alcohol

Craniofacial abnormalities

Aminoglycosides

Ototoxicity

Carbamazepine

Neural tube defects Craniofacial abnormalities

Chloramphenicol

'Grey baby' syndrome

Cocaine

Intrauterine growth retardation Preterm labour

Diethylstilbesterol

Vaginal clear cell adenocarcinoma

Lithium

Ebstein's anomaly (atrialized right ventricle)

Maternal diabetes mellitus

Macrosomia Neural tube defects Polyhydramnios Preterm labour Caudal regression syndrome

Smoking

Preterm labour Intrauterine growth retardation

Shiffa’s P Year Notes Drug/condition

Effect

Tetracyclines

Discoloured teeth

Thalidomide

Limb reduction defects

Valproate

Neural tube defects Craniofacial abnormalities

Warfarin

Craniofacial abnormalities

1.5 Rhesus Iso-Immunisation Definition  maternal antibody response against foetal red cell antigen entering her circulation  rhesus -ve mothers exposed to the rhesus D antigen recognise it as foreign Pathophysiology  fetal cells enter maternal circulation normally  increased amounts cross in sensitisation events  TOP, ERPC, ectopic pregnancy, vaginal bleeding >12weeks (early if heavy), ECV (external cephalic version), blunt abdominal trauma, invasive uterine procedure (amniocentesis or CVS), IU death, or delivery  RhD/d fetus carries antigens which Rhdd mother does not have  mother mounts an immune response  sensitisation (IgM produced, cannot cross into fetal circulation)  re-exposure in next pregnancy  primed memory B cells produce IgG  IgG actively crosses into fetal circulation  IgG binds to foetal red cells which are then destroyed in reticulo-endothelial system  leads to haemolytic anaemia Clinical sequelae

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 mild → neonatal anaemia (haemolytic disease of the new-born)  moderate → neonatal jaundice,  severe = if erythropoiesis is unable to compensate → in utero anaemia, cardiac failure, ascites, hepatosplenomegaly, kernicterus, death, hydrops = fluid accumulated in ≥2 foetal compartments Prevention  give anti-D immunoglobulin to mother  binds to fetal red cells carrying D antigen so sensitisation prevented = mops up  1500IU anti-D  given to all rhesus -ve women at 28 and 34weeks, within 72hours of any sensitising event or rhesus +ve delivery  large feto-maternal haemorrhage during sensitising event in 2nd/3rd trimester  Kleihauer test to measure amount of fetal blood in maternal blood to determine dose of anti-D, also do this test if neonate RhD +ve  Management Detection  booking, 28 and 34weeks  all women checked for rhesus and atypical antibodies  if antibodies detected, determine fetal blood group  identify partner’s status and PCR of

Shiffa’s P Year Notes fetal cells in maternal blood (if father heterozygous or uncertain paternity)  positive but low levels of antibodies 10IU/mL  assessment of fetal anaemia  measure peak systolic volume (PSV) of fetal middle cerebral artery (MCA) once a week, hydropic foetus = becomes abnormal  increase >1.5MoM = fetal blood sample and blood available for transfusion Treatment  18 weeks onwards, if fetal haematocrit is ≤30  irradiated, Rh –ve, CMV –ve red cells transfused into umbilical vein at cord insertion, or into hepatic vein, haemolysis will continue and transfusion repeated every 2weeks or when MCA becomes abnormal again  35weeks onwards  delivery preferable Postnatal management  all babies born to Rh -ve mother should have cord blood taken at delivery for FBC, blood group & direct Coombs test o Coombs test: direct antiglobulin, will demonstrate antibodies on RBCs of baby

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o Kleihauer test: add acid to maternal blood, fetal cells are resistant  correct anaemia  blood transfusion  coagulopathy may occur  low platelets and clotting factors  hyperbilirubinemia and jaundice  in utero, mother clears but immature neonatal liver cannot cope so phototherapy or exchange transfusion if severe  antibodies can persist for weeks  continued haemolysis so monitor haematocrit carefully Anti-D immunoglobulin also given within 72hours of:  delivery of a Rh +ve infant  live or stillborn  any termination of pregnancy  miscarriage if gestation is > 12weeks  ectopic pregnancy  only if managed surgically; if managed medically with methotrexate then anti-D is not required  external cephalic version  antepartum haemorrhage  amniocentesis, chorionic villus sampling, fetal blood sampling

Shiffa’s P Year Notes

1.6 Hypertensive Disorders in Pregnancy Blood pressure in pregnancy  decreases in early pregnancy until 20-24weeks  decreased vascular resistance  increases after 20-24weeks to pre-pregnancy levels until delivery  increased stroke volume  decreases after delivery but may peak again 34days post-partum Disorders  pregnancy-induced hypertension (PIH) → HTN (≥140/90mmHg) in the second half of pregnancy, in the absence of proteinuria or other pre-eclampsia markers, increased risk of pre-eclampsia, BP returns to normal within 6weeks after delivery OR an increase >30mmHg systolic or 15mmHg diastolic  chronic/pre-existing hypertension  women with a high booking BP >130-140/80-90, more common in older women, increased risk of preeclampsia

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Pre-existing hypertension A history of hypertension before pregnancy or an elevated blood pressure > 140/90 mmHg before 20weeks gestation No proteinuria, no oedema Occurs in 3-5% of pregnancies and is more common in older women

Pregnancyinduced hypertension (PIH, also known as gestational hypertension) Hypertension (as defined above) occurring in the second half of pregnancy (i.e. after 20weeks) No proteinuria, no oedema Occurs in around 5-7% of pregnancies Resolves following birth (typically after one month). Women with PIH are at increased risk of future pre-eclampsia or hypertension

Pre-eclampsia Pregnancyinduced hypertension in association with proteinuria (> 0.3g / 24hours) Oedema may occur but is now less commonly used as a criteria Occurs in around 5% of pregnancies

Shiffa’s P Year Notes

Pre-existing hypertension

Pregnancyinduced hypertension (PIH, also known as gestational hypertension)

Pre-eclampsia

later in life

Management  in pregnancy  treatment reduces hypertensive complications but not course of pre-eclampsia, don’t aim for 140/90 and ≥300mg proteinuria in a 24hour collection  if already hypertensive  rise in SBP ≥30 or DBP ≥15  presents in many ways from mild to severe Pathophysiology  placentas disorder, 2 stages: 1. placental disease → occurs before 20 weeks, asymptomatic, failure of trophoblastic invasion of spiral arterioles leading to maladaptation of these vessels so placental blood flow is reduced 2. maternal response → symptoms of PET, maternal inflammatory response to the ischaemic placenta induces endothelial damage, causing vasoconstriction, increased permeability, and clotting dysfunction.

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Risk factors:  previous severe/early-onset pre-eclampsia  give low dose aspirin 73mg PO od before 16weeks  age  >40, teenager  family history  mother, sister  obesity  BMI>30  primiparity  multiple pregnancy  long birth interval  >10years  fetal hydrops  hydatidiform mole  pre-existing medical conditions  hypertension, renal disease, diabetes, antiphospholipid antibodies, thrombophilias, connective tissue disease High risk factors

Moderate risk factors

hypertensive disease in a previous pregnancy  chronic kidney disease  autoimmune disease, such as systemic lupus erythematosus or antiphospholipid syndrome

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first pregnancy age 40 years or

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older pregnancy interval of more than 10 years  body mass index (BMI) of 35 kg/m² or more at first visit  family history

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Shiffa’s P Year Notes High risk factors type 1 or type 2 diabetes  chronic hypertension

Moderate risk factors

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

of pre-eclampsia multiple pregnancy

Presentation: (pink = severe)  usually asymptomatic and picked up in routine screening  headache  frontal  visual disturbance  flashing lights  epigastric or RUQ pain  liver involvement and capsule distension  N&V  rapid oedema  especially face  papilloedema  hypertension >140/90  ≥170/110 is severe  proteinuria  >300mg/24h (dipstick ++/+++)  confusion  HELLP syndrome  platelet count 42weeks)  premature rupture of membranes (>24hours)  induction of labour  diabetes  antepartum haemorrhage  other significant maternal medical conditions Foetus  IUGR  prematurity  oligohydramnios  abnormal Doppler velocimetry  multiple pregnancy  meconium-stained liquor  breech presentation Intrapartum  oxytocin augmentation  epidural  intrapartum vaginal bleeding  pyrexia >37.5oC  fresh meconium staining of liquor  abnormal FHR on intermittent auscultation  prolonged labour Cardiotocography Definitions  CTG  measures the foetal heart rate and uterine contractions via probes placed on the abdomen  baseline rate  mean level of foetal heart rate when this is stable, after exclusion of accelerations and decelerations  baseline variability  degree to which the baseline varies i.e. bandwidth of baseline after exclusion of accelerations and decelerations, variation of foetal heart rate from one beat to the next, occurs because of interaction between nervous system, chemoreceptors, baroreceptors and cardiac responsiveness so good indicator of how healthy foetus is at that moment as healthy will be constantly adapting heart rate in response to environmental

Shiffa’s P Year Notes changes, variability 5-25bpm = normal, 0-5bpm = reduced, >25bpm = saltatory  acceleration  a transient rise in foetal heart rate by ≥15beats over the baseline, lasting for ≥15seconds  deceleration  a reduction in the baseline of ≥15beats for >15seconds Interpreting a CTG DR C BRaVADO, 1 large square = 1 minute Define risk → is this a high-risk pregnancy? Contractions → x in 10 minutes, >5 is worrying, assess power by placing hand on abdomen Baseline rate → 110-160, measure over 10minutes, ignoring accelerations/decelerations  foetal tachycardia = baseline rate >160bpm  foetal hypoxia  chorioamnionitis – if maternal fever also present  hyperthyroidism  foetal or maternal anaemia  foetal tachyarrhythmia  foetal bradycardia = baseline rate 25bpm for >25minutes or sinusoidal reduced variability:  foetal sleeping = shouldn’t last >40minutes  foetal acidosis (hypoxia) = more likely if decelerations present  foetal tachycardia  drugs = opiates, benzodiazepines, methyldopa, magnesium sulphate  prematurity = variability reduced at earlier gestation 2minutes, 2-3minutes = non-reassuring, >3minutes = abnormal, act quickly (foetal blood sampling, emergency CS) Sinusoidal pattern  rare, very concerning, foetal mortality and morbidity, immediate CS, usually poor outcome  regular smooth wave-like pattern

Shiffa’s P Year Notes  frequency of 2-5cycles a minute  stable baseline rate 120-1260bpm  no beat to beat variability  severe foetal hypoxia

 severe foetal anaemia  foetal/maternal haemorrhage Overall impression → based on the above, grade as reassuring, suspicious, or abnormal:

The normal fetal heart rate varies between 100-160bpm Feature

Description

Causes

Baseline bradycardia

Heart rate < 100 /min

Increased fetal vagal tone, maternal betablocker use

Baseline tachycardia

Heart rate > 160 /min

Maternal pyrexia, chorioamnionitis, hypoxia, prematurity

Loss of baseline variability

< 5 bea...