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Obstetrics Flashcards

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1
Q

Risk factors for recurrent APH

A 
HTN/PET
Substances
Antiphospholipid
IUGR
Short inter pregnancy interval
Abdominal trauma
Polyhydramnios
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2
Q

Risk factors placenta praevia

A

Maternal
- AMA
Ethnicity - Asian
Smoking

Obstetric
IVF
Previous praevia
Previous cs
Multiple
Short inter pregnancy interval
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3
Q

Fetal fibronectin

A

Glycoprotein in amniotic fluid, placental tissue, and extracellular substance of decidua basalis.
Release through mechanical or inflammatory mediated damage to membranes or placenta before birth

PPV for birth <34 weeks approx 20%, quantitative may have mor value.

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4
Q

Cases preterm birth

A

IATROGENIC (40%)

PPROM (60%)
Cervix - (ERPOC, multiple LLETZ, fully cs)
Infection - MSU, chlamydia, BV
SES - smoking
Multiple
Endocrine
Haemorrhage
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5
Q

Consequence PTB

A
  • Visual problems related to retinopathy of prematurity
  • Sensorineural hearing loss
  • Impaired gross and fine motor skills due to cerebral palsy
  • Delayed speech and language acquisition
  • Impaired concentration, increased rates of attention deficit disorder
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6
Q

Components safer baby bundle

A 
Smoking cessation
Side sleeping
Fetal growth restriction
Decreases fetal movements
Timing of birth
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7
Q

Mirror syndrome and differences from PET

A

Generalised maternal oedema, often with pulmonary involvement, hydroponic placenta producing sFLT1

Anytime during antenatal or postpartum, rapid weight gain, increasing peripheral oedema, progressive SOB,

Contrast;
HCT usually LOW (haemodilut)
Amniotic fluid HIGH (rather than low)
Fetus always shows signs of hydrops

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8
Q

Brest milk production.

A

Alveoli - lacterious ducts, lacteriferous sinus, milk duct, ejection via nipple

AN: prolactin and placental lactogen producing milk, suppressed by estrogen and progesterone, once placenta delivered, sudden drop E+P allowing prolactin to stimulate milk production, oxytocin via nipple stimulation causes contraction of myoepithelial cells, milk expelled via lactiferous ducts—->sinus—> milk duct, nipple

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9
Q

Subgaleal haemorrhage

A

Subaponeurotic. Bleeding into space between epidural aponeurosis and periosteum, caused by rupture emissary veins (btwn dural sinuses and scalp veins).
LARGE space, tehrefore high mord and mort.

Can contain 250mL of blood with only 1cm increase scalp thickness. Mort 12-25%.

Apgar <7 without sign asphyxia, particularly if prolongd vacuum.
Later-haemodynamic instability, tachycardia/tachypnoea, poor activiy, pallor, anaemia, coagulopathy, hypotension, acidosis, death.

Localised - scalp swelling + laxity “older leather pouch” filled w fluid, pitting oedema over had/in front of ears, gravity dependent, displacement ear lobes, perieauricular oedema.

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10
Q

Caput succedaneum

A

Serosanguinous, extra-aponeurotic collection may extended over midline and suture lines.
Vacuum = prominnent articial caput at site of chignon, but chignon reduces within AN HOUR of birth, not assoc w NN haem.

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11
Q

Cephalohaematoma

A

Friction during birth gives bleeding between periosteum and underlying SKULL, can happy any time, more likely w instrumental. Soft, fluctuant, swelling, well defined. May increase over 12-24 hours, may take WEEKS to resolve.

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12
Q

Pathophys AFE

A

Fetal debris + amniotic fluid breaches maternal circulation, causes anaphylactoid reaction and peripheral vasodilation and reduced venous return/hypotension, triggers extrinsic coagulation cascade and get consumptive coagulopathy

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13
Q

Tocolytic agents

A

Terbutaline 250mcg sc or IV
Salbutamol 100mcg IV
GTN 400mcg sublingual

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14
Q

Factors that control FHR variability on CTG

A

Blood pressure/volume - baroreceptors
Oxygenation - chemoreceptors
Parasympathetic nervous - ACh from vagal nerve on SA node
SNS - adr/norad on myocardium

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15
Q

FIGO criteria for HIE/CP in term infants

A

Metabolic acidosis (pH <7.0, Base deficit >12, lactate >10)

Low apgars at 1 and 5 minutes

Early onset HIE

Early imaging studies showing acute and non-focal cerebral anomaly

Spastic quadriplegic or dyskinetic cerebral palsy

Exclusion of other etiologies such as birth trauma, COAg, infection, generic

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16
Q

Pathophysiology of RDS

A

Surfactant deficiency associated with prematurity

Surfactant reduces surface tension and allows aeration at end expiration. Without surfactant reduced aeration of lungs at end expiration, collapsed alveoli, reduced compliance, and mismatched ventilation and perfusion. Reduced surfactant also can cause irritation and inflammation, epithelial injury thus exacerbating the mismatch. This can result in hypoxia which manifests as tachypnoea, nasal flaring, indrawing, grunting, hypoxia

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17
Q

Strategies to prevent post CS endometritis

A

Pre-op antibiotic prophylaxis: 1st Gen cephalosporin within 30-60 mins knife to skin, RR0.5, CSOAP trial showed reduction with additional antibiotic of azithromycin

Appropriate skin prep - alcohol based

Pre op vagina cleansing: 30s with iodine containing solution RR 0.5 for endometritis, fever, wound infection

avoidance MROP

Closure of sc fat if >2cm

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18
Q

How to reduce cs rate (NIcE guideline)

A 
Avoidance undiagnosed breech
IOL from 41/40 for low risk women
Use of partogram with 4 hour action line
FBS for suspected fetal distress
1:1 support in labour
Involve a consultant obstetrician in decision making for cs
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19
Q

Pregnancy risks and percentages bmi >40

A

HTN in preg 10%
GDM 7%
T1 or T2 4%
CS 52%

Perinatal death 2%
Mechanical ventilation 10%
Macrosomia 20% 
SGA 19%
LGA 16%
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20
Q

Evidence for risking risk PET

A

LDA 100mg from 12/40, inhibits COX and TXA2 synthesis resulting in reduced platelet aggregation/vasodilation/reduced inflam response.
Reduced risk of PET 18%, stillbirth 14%, SGA16%. NNT 61 Cochrane 2019.
If at high risk, <20 weeks, NNT 19, somanz

Calcium 1g daily, reduced PTH and renin release, reduces intracellular calcium which leads to reduction in vasoconstriction. Reduces PET by 50% in high risk women and even greater if low dietary intake

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21
Q

Benefits of breastfeeding

A

Maternal: weight loss, strengthens bonding, helps uterus contract post delivery and reduce PPh risk, reduces risk breast, ovarian, endometrial cancer

Neonatal: decreases sudden infant death syndrome, protects against diabetes, reduces risk obesity, reduces atopy, reduces NEC, passive immunity, lower risk of infections (otitis media, upper respiratory tract infection, UTI) acts as a mild laxative

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22
Q

Priorities in PPH

A

Mechanical
Pharmacological
Surgical

Recognise
Communicate
Resuscitate
Manage
Monitoring
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23
Q

ANtiphospholipid criteria

A

Anticardiolopin IgG or IgM at high levels (IgG >40 or IgM >99th centile)

Lupus anticoagulant - positive
AntiB2glycoprotein IgM or IgG >99th

Two or more occasions, 12 weeks apart, only one positive test

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24
Q

Leading causes DIRECT maternal death (austrlia 2009 -2018)

Study These Flashcards
A 
VTE
Obstetric haemorrhage
AFE
Sepsis
Hypertensive
Suicide
25
Leading causes indirect maternal death australia 2009-2018
``` CVD Non obstetric haem Suicide Sepsis Substance use ```
26
Timing of maternal deaths
1/3 died while pregnant, 43% in first trimester 1/5 (22%) during labour or first 24 hours 43% postnatally
27
Maternal mortality ratio
(direct + indirect) / number of women who gave birth, per 100 000
28
WHO Sustainable developmental targets
By 2030 Reduce global mortality ratio to <70 per 100 000 live births Neonatal mortality as low as 12 per 1000 live births Universal access to sexual and reproductive health-care services including family planning, information, education
29
Evidence based ways to avoid OASIS
- Perineal massage in the second stage. Level 1 evidence from CSR. - Avoidance of instrumental delivery. Level 1 evidence from CSR. - Restrictive use of episiotomy. Level 1 evidence from CSR.
30
Risk factors for OASIS
Do not allow total prediction ``` Asian OR 2.27 Nullip RR 6.97 >4kg OR 2.27 Shoulder dystocia 1.9 OP position 2.44 Prolonged 2nd stage (2-3 RR 1.47, 3-4 1.79, >4 2/02) Instrumental Ventouse no epis 1.89 Ventouse epi 0.57 Forceps no epis OR 6.53 Forceps epis 1.34 ```
31
RCOG bundle for avoiding OASI
AN education to women Hands on birth Episiotomy if needed Thorough PR exam
32
Obstetric risks regional anaesthesia | Cochrane 2018
Instrumental delivery (not in new data since 2005) Longer first and second stage, more likely to need synt Maternal hypotension, fever, urinary retention Increased CS for distress but not overall
33
Vitamin D
Not consistently shown to improve maternal or neonatal outcomes Universal prescribibng, 400IU, present hypocalcaemic seizures and rickets BF infants 400IU for 1st 6/12, formaula not needed Increases maternal and cord blood levels vit D Does not improve maternal obstet outcomes Does not improve infant levels at 3,6,12 months Does not improve NNatal bone density @ 2/52 Assoc w 20% reduction childhood wheezing @ 3 years, regardless of maternal Vit D level
34
2 postulates theories of hyperemesis
Sensitivity to HCG - more hcg associated with more vomiting, such as in multiple pregnancy or GTD, acts as thyroid stimulator and correlated with degree of biochemical thyrotoxicosis Elevated estrogen- reduced gastric motility and emptying
35
When is inpatient monitoring recommended for hyperemesis ?
Severe electrolyte disturbance <3.0 Significant renal creat >90 Concurrent comorbidity: T1DM, short bowel, critical meds-epilepsy/transplant patients Malnutrition/continuing significant weight loss despite therapy Associated conditions Eg infection, haematemesis
36
Pemphigoid gestationis
1 in 10 000 - 60 000 Autoimmune, IgA attacking basement membrane Seen w bullous pemphigoid, T1DM, graves, pernicious, vitiligo, RA, HLA DR3, HLA DR4 Abrupt onset, 2nd trimester, earlier each time. May recur w menstruation, COCP, preg. Intensely pruritis Papules, plaques, target annular lesions then get vesicles, bullae, become tense, can get secondary bacterial infection. TESTS Biopsy - subepidermal vesicles, oedema, basal layer, , necrosis basal cells IMMUNOFLUORESENCE - c3 complement deposition at basement membrane, IgG antibodies ``` Rx MDT Cool baths, emollients, Steroids, topical and systemic Immune suppression ```
37
PEP/PUPP
1 in 200 No hormonal abnormality, related to stretching skin, damage to connective tissue Assoc with: increased wt gain, inc birth weight, primips, multiples THIRD trimester, self limited, resolves rapidly, does not recurr. Abdominal and proximal limbs Along striae, umbilical sparing. NEGATIVE immunofluroesnce
38
How common is perinatal anxiety and depression ?
``` Baby blues 80%, 3-5 days of birth, lasting for 10 AN anxiety/depression 10% PN anx/dep 16% anxiety alone 20% Puerperal psychosis 1 in 1000 PTSD 2-3% ```
39
Causes of nonimmune hydrops
``` Chromosomal - T13/18 Anaemia - fetomaternal haemorrhage Structural - CPAM, thoaracic abN Twin to twin, tumours Infective - toxo, syphilis, cmv Cardiac arrythmia ```
40
What shows evidence of haemolysis ?
Schistocytes LDH >600 Bilirubin >20 REduced haptoglobin
41
Differentials for thrombocytopenia
Pregnancy: PET, HELLP, AFLP, DIC Immune ITP, HUS, antiphospholioid, TTP, aHUS, HUS Non immune b12 deficiency, aplastic anaemia, toxins, congenital, infection - HIV, hepatitis, H pylori
42
Initial investigations for thrombocytopenia
``` FBC + reticulocyte count Peripheral blood film Optical platelet count Coagulation screen Renal and liver function tests TFTs Direct coombs Antiphospholipid: Lupus, anticardiolipin, b2glycoprotein 1 antibodies ANA Hep B/c/HIV H pylori Vit 12/folate Immunoglobulins ```
43
Thresholds for treating thrombocytpoemia
Symptomatic with active bleeding - any threshold <20 Delivery required and <50 x10^9
44
Findings + pathophy AFE
1. Cardiopulmonary arrest or acute hypotension 2. Acute Hypoxia 3. DIC or severe haemorrhage in absence of other explain 4. No other cause and within 30-60minutes of labour/delivery Amniotic fluid or fetal debris breaching maternal circulation, anaphylactoid type reaction Hypotension - peripheral vasodilatation, loss of venous return Thrombocytopenia - debris triggering extrinsic coag pathway, consumptive coagulopathy Bleeding - development DIC, vaginal bleeding, bleeding other sites
45
Causes of decreased variability on CTG
``` Sleep trace (up to 40mins) Early gestation age, <32 weeks Medications: opioids, b blockers, mag, steroids Incorrect recording speed Chronic hypoxia ```
46
Intraoperative placenta praevia risks:
``` Massive haemorrhage 21% Hysterectomy 11% ICU admission 10% Further laparotomy 7-8% Bladder or ureteric injury 6% VTE 3% Death 1 in 12 000 ```
47
USS findings spina bifida 2nd trimester
Anencephaly, hydrocephaly, ventriculomegaly Abnormally shaped + open vertebrae Dorsal ossification centres/lateral pedicles splayed apart Lemon sign - abN size and shape fetal head, narrowing bones at frontal portion Banana sign: cerebellum wrapped around medulla as part of Chiari malformation
48
3 tests @ preconceptual counselling for lupus nephritis
anti Ro/La antibodies --> congenital heart block dsDNA (ANA, complement C3/4) risk of flare APL status - anti cardiolipin, beta 2 glycoprotein Risk of flare approx 15-20%
49
Anatomy of pudendal nerve
Arises from S2,3,4 Leaves pelvis via greater sciatic foramen Re-enters and hooks around ischial spine, within lesser sciatic foramen Passes beneath sacrospinous ligament Branches out to form dorsal nerve of clitoris, perineal nerve, inferior rectal branches --> supplying perineum CLOSE to ischial spine means idenitifiable and LA can be infiltrated to produce anaesthesia for perineum
50
Risks of cs @ Fully compared to instrumental: | maternal AND fetal
``` Tears in incision Haemorrhage Blood transfusion Bladder trauma ICU Future risks: scar rupture, abnormal placentation, adhesions ``` Fetal: neonatal acidosis, ICH, need for resus
51
Factors associated with higher rates of instrumental failure:
BMI >30 EFW >4 OP Mid cavity or >1/5 head palpable abdominally Should have CS available within 30 mins if attempting instrumental
52
Episiotomy with instrumental?
Womens Healthcare initiative australia says all women having first vaginal birth thats assisted. 24% oasis if forceps 16% if ventouse NNT 19 episiotimes in primips
53
Forceps vs vacuum rates of complication
``` Fail RR 0.65 Cephalohaematoma RR 0.64 Retinal haemorrhage RR 0.6 Neonatal jaundice 0.79 Fewer shoulder dystocia RR 0.4 ``` higher OASIS 1.89 Any vag trauma 2.48 Incontinence RR 1.77 NO change in nn injury, low apgars at 5 mins, acidaemia
54
USS features of CMV
Microcephaly CNS Calcification intracranial/abdominal Hydrops, ascites, oligo/poly, hepatomegaly, pleural effusions HyperEchogenic bowel, psuedomeconium ileus IUGR
55
Diagnosing CMV
1 in 300 women get infected approx 30% transmit to babies 10% get congenital issues may be incidental finding elevated LFTs in Mum IgM and IgG If IgM positive, then look at IgG, if LOW avidity then recent infection
56
Main neonatal concerns CMV
Early mortality 5-10% Neurological sequalae microceph, seizures (10%), chorioretinitis (10-20%0, developmental delay SNHL (25-50%, progression expected in about half) ASYMPTOMATIC SNHL 5% (only 1/2 will be detected in newborn period) Chorioretinitis 2%
57
Age related probability of T21
Baseline population 1 in 400 Age 35 - 1 in 300 Age 40 - 1 in 100
58
Other than nuchal, what other factors can improve sensitivitity of CFTS?
Presence of nasal bone Tricuspid valve Ductus venosus waveform

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