OBSTETRICS Flashcards

1
Q

Multifetal pregnancy

A
  • 1% live births
  • TYPES
    • Dizygotic (fraternal) 70%
      • independant fertilization of 2 ova
      • always DCDA.
      • Each ovum has its own placenta and amnion
      • 80% of twins are DCDA
      • Risk factors
        • advanced matrenal age
        • family history twins
        • ethnicity (nigerian)
    • Monozygotic (identical) 30%
      • duplication of single fertilized ovum
      • may be monochorionic or dichorionic
      • independant of maternal age, heredity and race.
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2
Q

Placental Unit in Multifetal pregnancy

A
  • amnionicity: number of amniotic sacs
  • Chorionicity: number of placentas
  • Dizygotic twins
    • always diamniotic, dichorionic
    • The two placentas may fuse but do not have vascular connections
  • Monozygotic twins have different amionicty and chorionicity depending on the stage of cleavage of the signle fertilized ovum.
  • The amnionicity/chorionicuty degtermins the risk of complications.
  • Monoamniotic > monochorionic > diamnionic > dichorionic
  • Monoamniotic:
    • cord entanglement
  • Monochorionic
    • twin-twin transfusion syndrome
    • Twin anemia-polycytemia sequence.
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3
Q

Multifetal pregnancy

USS approach

A
  • APPROACH
    • 1 define the presence and number of twins
    • 2 determine amnionicity and chorionicity
    • 3 Growth estimation: determine fetal weight for each twin.
    • 4 are there complications or anomalies.
  • US FEATURES
    • DICHORIONICTY
      • separate placentas
      • Different fetal sex
      • Thick membrane >2mm separating twins in the first trimester
      • Lambda sign
        • chorion extending into intertwin membrane
    • DIAMNIONICITY
      • thin membrane in the first trimester
      • Two yolk sacs
  • in the second trimester, the sensitivity for finding an amnion is only 30%.
  • In 70% of cases the amnion is present by not visitble
  • DA is easiest to establich in the first trimester.
  • Different genders of fetuses always indicates DC
  • Failure to identify a separating amnion is not a reliable sign to diagnose MA.
  • Twin Peak/lambda
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4
Q

MULTIFETAL PREGNANCY COMPLICATIONS

A
  • ALL TWINS
    • increased risk prem labour
    • FETAL Mortality rate x3 higher than singleton
    • NEONATE mortality x 7 than singleton
  • DCDA
    • perinatal mortality 10%
  • MCDA
    • perinatal mortality 20%
    • TTT
    • TAPS
    • Acardia
    • Demise of cotwin
    • Twin embolisation syndrome
    • Structural abnormalities
  • MCMA twins
    • perinatal mortality 50%
    • Entangled cords
    • Conjoined twins
    • All the MCDA complications above.
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5
Q

Twin twin transfusion

A
  • Only occurs in MC twins.
  • Results from artriovenous communications in the placenta. Very poor prognosis

US Features

  • RECIPIANT TWIN
    • Large twin (increased EFW)
    • Polyhydramnious
    • polycythemia
    • Fetal hydrops
  • DONOR/PUMP TWIN
    • Small twin pinned to side of the gestational sac
    • Decreased EFW
    • oligohydramnious
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6
Q

CONDITIONS ASSOCIATED WITH DEMISE OF A TWIN

A
  • Vanishing twin (blighted twin)
    • the demise of a twin in the early first trimester (15weeks) and subsequent resorption of the dead fetus.
    • The risk to the surviving twin is minimal, especially if dichorionic.
  • Fetus Papyraceous
    • demise of. twin in the 2nd or 3rd trimester and persistence of the dead fetus as an amorphous mass of flattened structure along the uterine margin.
    • Complications
      • prem labor, obstruction in labor, embolization
  • Twin-Twin Transfusion
    • occurs only in MC twins because that share a common placenta. Demis of one twin lease to the passage of thermoplastic material into the Circulation of the live twin.
    • Results in thrombosis and multiorgan failure in the live twin and maternal DIC
  • Acardiac Parabiotic Twin
    • Twin reversal arterial perfusion sequence TRAPS
    • the most extreme manifestation of twin transfusion syndrome
    • occurs in a monochorionic pregnancy
    • reversal of flow in the umbilical artery of the acardiac twin with blood entering via the vein and leaving via the artery.
    • Poor development of acardia twin above thorax.
  • FETAL STRUCTURAL ABNORMALITIES
    • occur with higher frequency in twins (Monozygotic > dizygotic). Most defects are not concordant and occur in only one twin. Some abnormalities are secondary to in utero crowding.
  • Conjointed Twins
    • MCMA twins only.
    • 75% are female.
    • Prognosis is related to the degree of jointing and associated anomalies.
      • Thoracopagus (70%) Thorax is fused
      • Omphalogaus, xiphopagus: anterior abdomen are fused.
      • Pygopagus: sacrococcygeal fusion
      • Craniopagus: cranium is fused
  • Ectopic twin pregnancy
    • There may be an increase in this condition because of the more widespread use of ovulation induction and IVF.
    • 1/7000.
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7
Q

Types of Placenta Formation

A
  • Circumvallate
    • chorionic plate smaller than the basal plate
    • susceptible for abruption
  • membranacea
    • occupies the entire periphery of the chorion. Thin membranous
    • Placenta previa
  • bilobed
  • succenturiate
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8
Q

Placenta accreta spectum

A
  • Accreta - attaches to myometrium. Looss of the normal retroplacental hypoechoic zone (<2mm)
  • Increta - Invasion
  • Percreta - Penetration
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9
Q

Placenta previa

A
  • Within 2cm of os
  • 4 types
    • type 1: within 2cm
    • type 2: doesn’t extend into os
    • type 3: covers part of os
    • Type 4: covers all os
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10
Q

Vasa praevia

A

presence of abnormal fetal vessels in the amniotic membranes that run close to or cross the internal os.

The abnormal fetal vessels connect:

velementous cord insertion within the main body of the placenta

portions of a bilobed placent

placenta with succenturiate lobe.

A/W: low lying placenta, rupture

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11
Q

Two vessel cord

A

1% incidence

1 umbilical artery

50% a/w cardiac and renal anomalies

increased risk of IUGR

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12
Q

nucal cord

A
  • wrapping of the cord around the fetal neck
  • 1-29% of fetuses, increased with advancing maternal age.
  • Most not associated with pernatal morbidity/mortality.
    *
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13
Q

USS features of Absent Corpus Callosum

A
  • Colpocephaly
  • sun-burst sulcal pattern
  • Parallel lateral ventricles
  • High riding 3rd ventricle.
  • Angulated frontal horns
  • The presence of a cavum septum pellucidum excludes complete ACC.

Associations:

  • pericallosal lipoma
  • DW syndrome
  • Holoprosencephaly
  • Heterotopias
  • Chiari malformations
  • T18
    *
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14
Q

What is this and what causes it.

Which structures are absent and which are present?

A

Hydraencephaly

near total abscence of the cerebrum with intract cranial vault, thalamus and brain stem.

Secondary to occlusion of the ICAs.

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15
Q

V - View

A
  • Transverse aorta and transverse ductus arteriosus
  • look for
    • Co-arctation
    • interupted aortic arch
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16
Q
A
  • Twin-to-twin transfusion syndrome

Dr Mostafa El-Feky◉ and Dr Mohamed Refaey et al.

Twin to twin transfusion syndrome (TTTS) is a potential complication that can occur in a monochorionic (either MCDA or MCMA) twin pregnancy.

Epidemiology

This complication can occur in ~10% (range 15-25%) of monochorionic pregnancies giving an estimated prevalence of ~1:2000 of all pregnancies.

Clinical presentation

Marked abdominal distension has been described as a clinical feature.

Pathology

TTTS results from unbalanced vascular (arteriovenous and arterioarterial) anastomoses in the placenta - that is, placental circulation is directed predominantly towards one twin and away from the other.

The resultant hypovolaemia and hypoperfusion in one twin and hypervolaemia and hypertension in the other create a cascade of hormonal changes including the renin-angiotensin system. This in turn leads to chronic tubulopathy and oliguria in the hypovolaemic (donor) twin with consequent oligohydramnios, and polyuria and consequent polyhydramnios in the hypervolaemic (recipient) twin.

Staging

The extent of the syndrome can be staged according to severity. One method proposed by Quintero et al. is as 3:

stage I: oligohydramnios/polyhydramnios

stage II: bladder not visible in donor twin

stage III: abnormal Dopplers in either twin

stage IV: hydrops fetalis in either twin*

stage V: in-utero demise of either twin

*almost always in the recipient; rarely in the donor if there is coexistent TAPS - see below.

Variants

Twin anaemia-polycythaemia sequence (TAPS) is a relatively recently described subset of TTTS, which is discussed separately.

Radiographic features

Antenatal ultrasound

Monochorionicity is a prerequisite at any stage of gestation.

Growth discordance is often but not invariably present, and does not contribute to diagnostic criteria.

First trimester

The following findings on a first-trimester ultrasound of a monochorionic pregnancy have been associated with increased risk of developing TTTS, although predictive value remains poor 8:

NT discordance: 20% or more

CRL discordance: 10% or more

ductus venosus reversed a-wave

folding of the inter-twin membrane as an early sign due to a disparity in amniotic fluid volumes (amniotic fluid discordance)

Second and third trimesters

Features that may be noted individually in each twin include:

recipient twin

polyhydramnios (deepest vertical pocket (DVP) >8 cm)

large or constantly cycling urinary bladder

features of cardiac overload

fetal hydrops

fetal cardiomegaly

in certain cases, fetal echocardiography may also show AV valve incompetence

Doppler abnormalities - predominantly venous

donor twin

oligohydramnios (DVP <2 cm), which may result in the twin appearing pinned to the side of the gestational sac: “stuck twin”

small or non-visualised urinary bladder

Doppler abnormalities - predominantly umbilical artery +/- venous

evidence of fetal anaemia

Doppler

absent or reversed diastolic flow in the umbilical artery is an indication of worsening twin-to-twin transfusion syndrome

abnormal ductus venosus waveform pattern suggests the possibility of cardiac diastolic dysfunction

Treatment and prognosis

Serial sonographic monitoring is common practice. In an uncomplicated monochorionic twin pregnancy, TTTS screening should start from 16 weeks gestation with assessment fetal growth, DVPs and umbilical arterial pulsatility index (UA-PI) performed every two weeks. Detailed morphology ultrasound is routine at 20 weeks. Additional fetal middle cerebral arterial-peak systolic velocity (MCA-PSV) is recommended from 22 weeks.

Untreated, TTTS generally carries a poor prognosis, with up to 90% perinatal mortality 8. Laser coagulation of the chorionic plate is the treatment of choice and significantly improves the prognosis for both twins - although both morbidity and mortality remain considerably higher than in non-TTTS monochorionic pregnancies.

Other management options include:

conservative management with surveillance for Quintero stage 1 TTT

serial amnioreduction, where laser treatment is not available 8

Differential diagnosis

General imaging differential considerations include:

other causes of oligohydramnios and/or polyhydramnios, for example related to fetal structural anomalies

isolated placental insufficiency in one of the twins

will not produce polyhydramnios in opposite twin

17
Q
A