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Chapter 4: Obstetrics 77
https://t.me/med1917
Other maternal disease in pregnancy
Thromboembolic disease

EPIDEMIOLOGY
Risk of VTE is increased ×6
Greatest risk is postpartum
PE = important cause of maternal
death
SIGNS/SYMPTOMS
Calf tenderness
Cough
Chest/abdo/groin pain
Anaemia
Hb drops to 11g/dl (symptoms if <9g/dl)
PROPHYLAXIS:
Dietary advice
Folic acid 5mg OD
Iron supplements
PROPHYLAXIS: with LMWH*
Antenatally: only if high risk Postnatally: if >1 moderate risk factor
INVESTIGATIONS
PE: CXR, ABG, CT DVT: Doppler USS
d-dimer not useful in pregnancy
*warfarin contraindicated in pregnancy
Risk factors for thromboembolic disease:
assess at booking & postpartum
High risk:
previous VTE
prolonged immobility/hospitalisation
Moderate risk:
BMI >30
age >35
IVDU/smoker
immobility
thrombophilia
varicose veins
C-section
pre-eclampsia
DIETARY ADVICE:
Iron-rich: kidney, liver, eggs, green vegetables Folate-rich: fish, raw green vegetables
Thrombophilias
antiphospholipid syndrome, protein S/C deficiency, factor V Leiden
COMPLICATIONS
VTE IUGR
Miscarriage Pre-eclampsia
Placental abruption Fetal death
MANAGEMENT: as high-risk pregnancy
Aspirin & LMWH
LMWH continued postnatally
Cardiac disease
PATHOPHYSIOLOGY: During pregnancy HR & SV to CO by 40%
IMPACT
Major cause of maternal mortality: pre-existing cardiac condition may mean
heart cannot cope with increased demand during pregnancy
Problems usually occur >28w or during labour
Fetal cardiac abnormalities occur in 3%

blood flow causes in 90%

MANAGEMENT
1. Treat conditions before pregnancy if possible e.g. valve disease
2. Stop contraindicated drugs: warfarin, ACEi
3. Regular checks: of BP, anaemia, fetal abnormalities
78 Chapter 4: Obstetrics
https://t.me/med1917
Reassure that 9 out of 10 women with epilepsy have a healthy baby

Epilepsy
IMPACT
Significant cause of maternal mortality:
seizure control reduced: in labour, if sleep-deprived, during
morning sickness
Increased risk of congenital defects (NTDs) – mainly due to drug therapy
3% risk of fetus developing epilepsy
Safest drugs: carbamazepine, lamotrigine Contraindicated drugs: sodium valproate
MANAGEMENT4: 
1. Seizure control: with as few drugs as possible at lowest dose
2. Folic acid supplementation 5mg OD pre-conception
3. Vitamin K for baby at birth: 1mg IM
4. Offer high resolution USS abnormality scan at 18–20w + serial growth scans
involve neurology teamDO NOT CHANGE MEDS without their advice
Obesity
20% pregnant women have BMI >30
MATERNAL RISKS
Thromboembolism
Pre-eclampsia
GDM
C-section
Postpartum haemorrhage
Wound infection
ANTENATAL MANAGEMENT
1. Preconceptual advice: weight, diet, exercise
2. Supplementation: 5mg folic acid & vit D
3. Thromboprophylaxis
4. Prophylactic aspirin: 75–150mg OD to prevent HTN
5. Monitor: blood glucose, BP
OGTT at 28w
Serial growth scans from 24w
5
FETAL RISKS
Congenital abnormalities
Mortality ×2.5
Miscarriage/stillbirth
NTDs
Macrosomia (shoulder dystocia)
LABOUR/POSTNATAL MANAGEMENT
1. IOL if large baby (elective C-section may be discussed)
2. Continuous CTG in labour
3. Thromboprophylaxis: clexane, stockings, up & moving
4. risk of haemorrhage: IV syntocin for 4h
5. risk of infection: regular checks, expose to air if possible
4
RCOG (2016) Epilepsy in pregnancy [GTG 68]
5
RCOG (2018) Care of women with obesity in pregnancy [GTG 72]
Early pregnancy problems
https://t.me/med1917
15% pregnancies
Miscarriage
fetus dies or delivers dead before 24 completed weeks of pregnancy

CAUSE: Significant chromosomal abnormality in 60% cases
SYMPTOMS: Lower abdo pain (crampy/ ‘period-like’) & vaginal bleeding
Bleeding before pain
INVESTIGATIONS: in order
1. Speculum – open os is suggestive of miscarriage
2. TV USS – shows if fetus is intra-uterine & viable / any RPOC
3. 48h serum hCG – rise >66% in viable pregnancies, remains low in miscarriage
4. Check FBC, CRP, Rhesus status, G&S
CRP often raised
Interpreting USS results
CRL <7.2mm on 1st scan
= very early pregnancy OR miscarriage
rescan in 7–10d to be sure
CRL >7.2mm + no cardiac activity
= miscarriage diagnosed
at this size heartbeat should be present
Chapter 4: Obstetrics 79
TYPES OF MISCARRIAGE
Type Symptoms On examination Mx
Threatened Pain, bleeding – fetus still alive (only 25% miscarry) Os closed, uterus normal for date Home Inevitable Pain, heavy bleeding – fetus may/may not be alive Os open 1, 2 or 3 Incomplete Pain, bleeding – some fetal parts passed Os open, some RPOC* 1, 2 or 3 Complete Slowed bleeding – all fetal parts passed Os closed, uterus not enlarged, no RPOC* Home Missed May be asymptomatic – fetus dead/not developed Os closed, uterus small for date
Septic Pain, offensive vaginal loss ± fever Uterine tenderness, endometritis ABX & 3
MANAGEMENT
1. Conservative/expectant: wait to see if miscarriage occurs naturally 80%
successful
R/V at 14d
no bleeding/pain = pregnancy test at 3w to confirm miscarriage still bleeding/pain = re-scan & consider medical/surgical management
2. Medical: give medication to cause completion of miscarriage 80% successful
PO/PV misoprostol (prostaglandin) ± mifepristone (anti-progesterone)
+ Analgesia & anti-emetics PRN
Pregnancy test at 3w to confirm miscarriage
Risks: bleeding*, infection, failure
6
*RPOC: retained products of conception
1, 2 or 3
(often picked up on 1st dating scan)
Additional management considerations
1. Give anti-D prophylaxis if Rh –ve & >12w
2. Give PV progesterone BD for pregnant
SEs of misoprostol = diarrhoea & fever
*Risk of excess bleeding
gestation AND are having SURGICAL MANAGEMENT
women with vaginal bleeding & history of miscarriage
3. Surgical: remove tissue surgically under local or general anaesthetic
Vacuum aspiration + histological examination to exclude molar pregnancy
Complications: partial removal of endometrium, perforation/scarring of uterus
Recurrent miscarriage
3 or more miscarriages in succession
CAUSES
Antiphospholipid antibodies – cause thrombosis Tx: aspirin & LMWH
Chromosomal defects – refer to geneticist & consider IVF/PGS (rare)
Uterine abnormalities, e.g. LLETZ, fibroid – USS to identify Tx depends
oncause
Hormonal: thyroid problems
Other: obesity, smoking, higher maternal age, PCOS
6
NICE (2019, updated 2021) Ectopic pregnancy and miscarriage [NG126]

All have approx. 3% risk of infection
1% couples
Emotional support/counselling = very important in these cases
80 Chapter 4: Obstetrics
Tubal
Ovarian
https://t.me/med1917
1% pregnancies
Ectopic pregnancy
In a woman of child-bearing age, abdominal pain + abnormal PV bleed = ectopic until proven otherwise.
Must do a URINE PREGNANCY TEST!
*RED FLAGS
  
embryo implants outside of the uterine cavity
RISK FACTORS: particularly things that scar tubes
Advanced maternal age
Previous ectopic pregnancy
IVF pregnancy
PMHx chlamydia/pelvic infection/PID
Previous abdo/tubal surgery
Use of progesterone-only pill or IUD (the coil)
SIGNS & SYMPTOMS: can be variable & vague!
Lower abdominal pain
initially colicky then constant rebound tenderness uterine & adnexal tenderness
Abnormal vaginal bleeding –
scanty, dark
Signs of intraperitoneal blood loss
▶ dizziness & *shoulder-tip pain
(referred)
*syncope/collapse in extremes
Amenorrhoea 4–10w
may be unaware of pregnancy &
interpret bleed as period
Uterus small for date & closed cervical os
Pain before bleeding
INVESTIGATIONS:
1. Urine hCG pregnancy test: will
show +ve in ectopics
2. TV USS to exclude intrauterine
pregnancy
BUT won’t show very early uterine pregnancies
May show clot / free fluid in tubes
3. Serum βhCG to distinguish early &
ectopic pregnancies
Early pregnancy: by >60% in 48h
Ectopic = slower or decrease
If already >1000IU/ml would
see pregnancy in uterus unless it is ectopic
4. Laparoscopy: most sensitive but
invasive*
Interstitial
Cervical
Fig. 4.1 Locations of
ectopic pregnancy.
Side-effects of methotrexate
Mouth ulcers
Liver dysfunction
MANAGEMENT7:
1. Admit to hospital: ABCDE, IV access, X-match, Anti-D if Rh –ve
2. Medical: If unruptured AND no cardiac activity AND hCG <1500 IU/L
• Single dose IM methotrexate 15% need 2nd dose, 10% need surgical
escalation
Followed by serial hCG level monitoring
3. Surgical:
Laparoscopic salpingectomy (tube removal)
consider salpingostomy (remove ectopic & leave tube) if other tube is
damaged – allows future conception
Risks: bleeding, infection, damage to other structures, hernia from
incisions, DVT/PE, anaesthetic risks
Counselling points
1. If medical management or salpingostomy: explain possibility ectopic remains
need for serial hCG levels know warning signs of rupture: severe abdo pain, pale/clammy, tachycardic, LOC/collapse
2. Information about increased risk of ectopic in future BUT reassure 70% go on to have future successful pregnancy
3. Emotional support/counselling
7
NICE (2019, updated 2021) Ectopic pregnancy and miscarriage [NG126]
Chapter 4: Obstetrics 81
https://t.me/med1917
Hyperemesis gravidarum
1 in 750 women
= Severe N&V in early pregnancy causing dehydration, electrolyte disturbances, 5% weight loss, ketosis
starts at 4–7w, resolves by 16w
Severity Prevalence Symptoms Treatment
Mild NVP* 50% Nausea, occasional vomiting No treatment needed Moderate NVP 5% More persistent vomiting Often need admission Severe NVP (hyperemesis gravidarum) 0.15% Vomiting causing systemic Sx Hospital admission
INVESTIGATIONS: Physical exam for signs of dehydration
BP & pulse – for hypovolaemia
Urine dip/urinalysis – for ketonuria & exclude UTI
FBC – raised haematocrit if dehydrated
U&Es – raised urea & Cr if dehydration causes AKI, hyponatraemia, hypokalaemia
Calcium – exclude hypercalcaemia as cause of vomiting
Pelvic USS – check viability of pregnancy & RFs for hyperemesis gravidarum
COMPLICATIONS
DVT/PE – TED stockings ± LMWH prophylaxis
Wernicke’s encephalopathy – due to thiamine deficiency
Hypokalaemia – IV/PO potassium replacement
Mallory–Weiss tear – due to excessive vomiting
Oesophageal rupture/pneumothorax – very rare!
MANAGEMENT
Dehydration: IV fluids (Hartmann’s/saline) may need added K+ if hypokalaemia N&V: antiemetics (IV/IM/SL if oral intake not tolerated) Close monitoring: BP, pulse, renal function Complications: TED stockings/LMWH, thiamine/Pabrinex, Gaviscon, folic acid
8

Feel dizzy/faint Oliguria
Gestational trophoblastic disease
trophoblastic tissue proliferates more aggressively than normal
TYPES:

1. Hydatidiform mole: localised & non-invasive proliferation
Complete: sperm fertilises empty oocyte = mitosis of 46XX tissue no
fetal tissue
Partial: two sperms fertilise oocyte = forms triploid zygote (69XXX/XXY/
XYY) → variable evidence of fetus
2. Invasive mole: invasion localised to within the uterus
3. Choriocarcinoma: invasion followed by metastases
Malignant: need further Ix/Tx
outside of the uterus
SYMPTOMS
Vaginal bleeding – may be heavy
Severe vomiting
Uterus large for date
Early pre-eclampsia &
hyperthyroidism
INVESTIGATIONS
USS – swollen
villi = ‘snowstorm
appearance’
Serum hCG – very
high
Histology = diagnostic
MANAGEMENT
Suction curettage – removes trophoblastic tissue
Serial hCG levels – persistent/rising suggests malignancy*
excess hCG
Risk factors
Multiparous
Multiple pregnancy
Molar pregnancy
Differential diagnosis
UTI
Gastroenteritis
Trophoblastic disease
Possible antiemetics
Promethazine
Cyclizine
Metoclopramide
Ondansetron
RARE: 1 in 700 pregnancies
Gestational trophoblastic neoplasia:
persistently elevated hCG resulting from persistence of any form of trophoblastic tissue
*Malignancy
Diagnosed if: persistent/rising hCG OR persistent vaginal bleeding OR blood-borne metastases
Mx: chemotherapy
8
RCOG (2016) The management of nausea and vomiting of pregnancy and hyperemesis gravidarum
[GTG 69]
82 Chapter 4: Obstetrics
https://t.me/med1917
Late pregnancy problems
Antepartum haemorrhage (APH)
Give anti-D if Rh –ve
Kleihauer test: estimates fetal Hb & therefore
amount of anti-D to give
Classification of placenta praevia
Minor: placenta not covering os Major: partially/fully covering os
90% low-lying placentas will move upwards after 20w with growth of the uterus in the 3rd trimester
Delivery of placenta praevia
Elective C-section at 36–37w
Earlier if severe bleeding
If placenta accreta/percreta
Rusch balloon compression/total
hysterectomy after C-section to bleeding



*Blood ≠ severity. Pain without bleed = ‘concealed’ abruption
Delivery in placental abruption
No fetal distress >37w: IOL with amniotomy
No fetal distress <37w: monitor on antenatal ward, steroids if <34w
Fetal distress = urgent C-section
Fetus is dead: IOL with amniotomy + blood
& FFP transfusion
 

bleeding from the genital tract after 24 weeks’ gestation
Common causes
Undetermined
Placental abruption
Placenta praevia
Rarer causes
Genital tract pathology
Uterine rupture
Vasa praevia
PLACENTA PRAEVIA – placenta implants in lower section of uterus
Complicates 0.4% pregnancies
Risk factors
Twins
High parity
Increased maternal age (>40)
Scarred uterus, e.g. previous C-section/surgery, previous placenta praevia
Placenta accreta: implantation so deep into scar that placental separation
is prevented
Placenta percreta: implantation so deep into scar that it penetrates
uterine wall into surrounding structures e.g. bladder
Symptoms
Intermittent, painless bleeds increase in frequency & intensity
Breech presentation, transverse lie, fetal head not engaged
Investigations: avoid vaginal examination can provoke massive bleed
Ultrasound scan detects low-lying placenta at 20w safety-net: straight to hospital if
bleed occurs
▶ repeat at 32w to exclude praevia
Management
Presentation without bleeding: delay admission until delivery
Presentation with bleeding: admit & keep until delivery FBC, clotting studies, cross-match monitor fetal and maternal wellbeing: CTG, IV access IV steroids if <34 weeks’ gestation anti-D if woman is Rhesus –ve
9
PLACENTAL ABRUPTION – part or all of placenta separates before delivery of the fetus
Complicates 1% pregnancies
Risk factors
Hx of placental abruption (6%)
Pre-eclampsia / pre-existing HTN
IUGR
Multiple pregnancy
High parity
Autoimmune
Smoking / cocaine use
Investigations USS: exclude placenta praevia
may not show abruption
9
RCOG (2011) Antepartum haemorrhage [GTG 63]
Symptoms
Painful, dark bleeds*
Tender, contracting uterus labour
often ensues
If severe = ‘woody-hard’ uterus,
hypotension, HR
Decreased fetal movements
Management: admit
FBC, clotting studies, cross-match
Monitor fetal and maternal
wellbeing: CTG, CVP, IV access
IV steroids if <34w gestation
Anti-D if woman is Rhesus –ve
VASA PRAEVIA – fetal blood vessels run in the membranes in front of the
https://t.me/med1917
presenting part
when membranes rupture, fetal vessels do too = MASSIVE FETAL BLEED
Chapter 4: Obstetrics 83
Symptoms
Moderate, painless vaginal bleed
when membranes rupture
Severe fetal distress
Management
URGENT C-SECTION
UTERINE RUPTURE
occasionally occurs before labour in women with scarred / congenitally abnormal uterus but very rare
BLEEDING OF GYNAECOLOGICAL ORIGIN
Causes
• Cervical carcinoma suspect if small recurrent or post-coital bleeding
Cervical polyps
Ectropions
Vaginal lacerations


BLEEDING OF UNKNOWN ORIGIN
Small, painless bleeds in absence of placenta praevia likely minor placental abruptions
Prolonged pregnancy
DEFINITION: >42w
RISKS
To fetus/neonate
Meconium aspiration
Macrosomia: prolonged labour,
shoulder dystocia
Neonatal seizures/encephalopathy
IUGR (due to placental insufficiency)
Stillbirth / neonatal death
To mother
Prolonged labour
Instrumental delivery/C-section
Perineal damage
PPH
Infection
usually too slow to save fetus if not in hospital
Risk factors for prolonged pregnancy
Hx post-term pregnancy
Primigravidity
High BMI
Higher maternal age
Genetics
MANAGEMENT
Offer IOL after 41w
If IOL declined, increased monitoring: CTG 2× per week
Chorioamnionitis

DEFINITION: acute inflammation of the amniotic fluid/membranes 2° to
ascending bacterial infection
RISK FACTOR: Prelabour ROM
INVESTIGATIONS
FBC, CRP
High vaginal swab – culture &
sensitivities
CTG
SYMPTOMS
Uterine tenderness
Maternal signs of infection: fever,
tachycardia, leucocytosis
MANAGEMENT: Medical emergency
Prompt delivery under IV ABX
may need C-section
84 Chapter 4: Obstetrics
https://t.me/med1917
Risk factors for preterm delivery
General
Hx of preterm labour
Younger/older mothers
Lower socioeconomic status
Short inter-pregnancy interval
Fetal survival response
Biggest risk factor
Maternal disease, e.g. renal, thyroid, DM
Pregnancy complications – IUGR,
pre-eclampsia
Antepartum haemorrhage
Damage to uterus/cervix
STIs/UTIs/vaginal infections
Hx cervical surgeries
Uterine abnormalities/fibroids
Not enough space
Multiple pregnancy
Polyhydramnios
Infection indicated in 60%
Preterm delivery

DEFINITION: delivery between 24w & 37w (if <24w = miscarriage)
CAUSES
Spontaneous preterm labour (50%)
Iatrogenic IOL by doctor due to fetal/maternal risk or PPROM
COMPLICATIONS
For neonate:
Prematurity = 80% NICU occupancy
Chronic morbidity
Death
Lung disease, blindness/hearing loss, cerebral palsy, neurological impairment
For mother:
Infection (endometritis = common)
Increased need for C-section
SYMPTOMS
Painful contractions 50% resolve & no preterm delivery
Dull suprapubic ache & increased discharge if cervical incompetence
Antepartum haemorrhage
Fluid loss suggests ROM

Predicting preterm labour
1. Hx & VE
2. Transvaginal USS:
Serial cervical length
3. Fetal fibronectin
Levels rise shortly before labour
4. QUiPP app10 to calculate risk

Prevention: only high-risk women, e.g. previous preterm labour
10
Offer cervical cerclage: sutures to strengthen cervix & keep it closed
elective at 12–14w if recurrent early losscervical length scans at 16w, 18w, 20w & offer sutures if <25mm‘rescue suture’ of dilated cervix can be performed if first presentation
Progesterone supplementation: suppositories from early pregnancy
Treatment of maternal medical disease
Avoid unnecessary ABX: treat UTIs, STIs, bacterial vaginosis but caution for
other infections
Multi-fetal reduction: of higher order multiples
Treatment of polyhydramnios: needle aspiration (amnioreduction) or
NSAIDs (reduce fetal urine output)
MANAGEMENT11: <27w transfer to NICU
1. Steroids & tocolysis:

infection present
Steroids if <34w to promote pulmonary maturity
Take 24h to work so delay delivery with tocolysis e.g. nifedipine
2. IV ABX: only given antenatally if PPROM
3. MgSO4 if <32w: reduces risk of intraventricular haemorrhage and cerebral
palsy
4. Delivery: VAGINAL WHERE POSSIBLE – ensure in optimal environment
(neonatal unit)
C-section if breech or other obstetric indications increases risk of fetal
respiratory distress
No artificial rupture of membranes if <34w
Forceps only if necessary
Antibiotics* – given intrapartum as GBS prophylaxis (regardless of mum’s
GBS status)
10
QUiPP version 2.0, released Oct 2017, © King's College London
11
NICE (2015, updated 2019) Preterm labour and birth [NG25]
Preterm pre-labour rupture of membranes (PPROM)
https://t.me/med1917
DEFINITION: membranes rupture before labour at <37w
CAUSES
Often unknown
Any of the causes of preterm labour
COMPLICATIONS
Preterm delivery – occurs within 48h in 50%
Infection of fetus, placenta, or cord (chorioamnionitis/funisitis)
Prolapse of umbilical cord
Pulmonary hypoplasia / postural deformities (due to lack of liquor)
SYMPTOMS
Gush of clear fluid + further leaking
Chorioamnionitis Sx:
contractions abdominal pain / uterine tenderness fever, tachycardia offensive liquor
Chapter 4: Obstetrics 85
INVESTIGATIONS
Speculum: pool of fluid in posterior fornix
USS: may show reduced liquor BUT normal liquor volume doesn’t exclude
PPROM
Point of care tests*: ILGF binding protein / placental alpha microglobulin
Infection screen: high vaginal swab, FBC, CRP ± amniocentesis & culture
Assess fetal wellbeing: CTG
Management12: balance risks of infection vs. risks of preterm delivery
No signs of infection
Admit & monitor for signs of infection
Corticosteroids if <34w (promote lung maturity of fetus)
Prophylactic erythromycin (for maximum of 10d)
IOL if reach 37w
Signs of infection
Immediate IV ABX & delivery
IV ABX & septic screen in baby when born
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remember 
12
RCOG (2019) Care of women presenting with suspected preterm prelabour rupture of membranes
[GTG 73]
86 Chapter 4: Obstetrics
Embryonic Disc
Conjoined Twins
Monochorionic/Monoamniotic
https://t.me/med1917
Multiple pregnancies
Twins: 1/80 pregnancies
Risk factors
Assisted conception
Increasing maternal age
Higher parity
Genetics
Triplets: 1/1000 pregnancies
Definitions
Dizygotic twins (2/3) – fertilisation of 2 different oocytes by 2 different sperm Monozygotic twins (1/3) (identical) – meiotic division of a single oocyte
Division before day 3 = dichorionic
diamniotic (DCDA) 2 placentas, 2 amnions (30%)
Division in days 4–8 = monochorionic
diamniotic (MCDA)
Division in days 9–13 = monochorionic
monoamniotic (MCMA) 1 placenta, 1 amnion (rare)
Incomplete division = conjoined twins
1 placenta, 2 amnions (70%)
Biggest risk MC twins
of complications is in
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*All obstetric risks increased!
Complications*
MATERNAL
Gestational diabetes, pre­eclampsia, anaemia = more common
Spontaneous miscarriage – one
fetus dies in 50% cases
Preterm labour – 40% twins, 80%
triplets
Malpresentation of 1st twins at labour – 20%
Postpartum haemorrhage
atonic uterus is common
FETAL
×6 mortality/stillbirth
prematurity = big cause of mortality
×5 handicap (e.g. cerebral palsy)
Congenital abnormalities more
common in MC twins
IUGR ⁄ cases: especially in MC twins
but can occur in any twin pregnancy due to placental insufficiency
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Morula
Blastocyst
Implanted
Blastocyst
Formed
Cleavage
Days 1–3
Dichorionic/Diamniotic
Cleavage
Days 4–8
Monochorionic/Diamniotic
Cleavage
Days 8–13
Cleavage
Days 13–15
Fig. 4.2
Outcomes of TTTS
Severe preterm delivery
IUFD
Prognosis of TTTS
Both survive: 50%
One survives: 80%
Specific complications of monochorionicity
TWIN–TWIN TRANSFUSION SYNDROME (TTTS) – in MCDA only (15%)
Unequal blood distribution through anastomoses in placenta
Donor twin: volume depletion, anaemia, IUGR, oligohydramnios
Recipient twin: volume overload, polycythaemia, cardiac failure, polyhydramnios
Management
complete laser photocoagulation of placental interface via USS & fetoscopy
(seal blood supply between twins)
USS amnioreduction (draw out some amniotic fluid)