7. Twin Pregnancy.
|a.||has increased in incidence in recent decades.||True|
|b.||has a perinatal
mortality rate >5 times that of singleton
|c.||is most common as a
natural event in
|d.||is associated with hyperemesis.||True|
|e.||is suitable for biochemical screening for Down’s syndrome.||False|
|f.||is usually dizygous.||True|
|g.||is more common with increasing maternal age.||True|
|h.||is associated with an increased risk of congenital malformation.||True|
|i.||should be managed in hospital from 28 weeks||False|
|j.||prophylactic tocolytic drugs are of proven value.||False|
|k.||steroids are of proven value.||False|
|l.||Llamas are important in evaluation of risk in twin pregnancy.||False|
|m.||fetal abnormality rates are increased in multiple pregnancy.||True|
|n||monozygous twins only occur after assisted reproduction.||False|
|o||monochorionic, monoamniotic twins carry the highest risk of fetal loss and damage.||True|
|p||monochorionic twins are at risk of twin-twin transfusion.||True|
|q.||the “stuck-up” twin is a feature of in-breeding in the upper echelons of society and particularly common with monochorionic twins.||False|
|r.||monoamniotic twins are at risk of lethal cord entanglement.||True|
|s.||when fetal death occurs, the survivor of monochorionic twins is at more risk than the dichorionic equivalent.||True|
|t.||twins should be scanned in the 3rd. trimester to look for growth retardation.||True|
Key facts for the DRCOG.
Expanded explanation for the MRCOG and to help facts stick.
Twin pregnancy has increased in incidence, mainly due to the increasing use of fertility drugs.
The natural incidence in the Caucasian population is ~ 1%.
For some reason the natural incidence of twins is highest in West Africa ~ 5%.
And lowest in Japan ~ 0.4 %.
The incidence rises with maternal age.
This has been attributed to the higher FSH levels of older women.
Clomiphene is associated with an incidence of twins of more than 5%.
IVF & GIFT have rates of multiple pregnancy of 20-30%.
Their increasing use is having a significant impact.
NICE has recommended that IVF should be available on the NHS to all who need it, so we can expect to see even more twins.
Twins usually arise from completely independent fertilisation and development of two eggs - hence most (2/3) are dizygous.
The additional pregnancies from clomiphene and assisted reproduction are almost all dizygous.
You would expect these to form separate pregnancies and be inevitably di-amniotic and di-chorionic.
This would put them in the lowest risk group with regard to perinatal mortality and morbidity, so long as it is no more than twins.
However, assisted reproduction pregnancies are at more risk of splitting and producing monozygous twins than natural conceptions.
Monozygous twins result from the splitting of a fertilised egg that should have resulted in a single pregnancy.
The genetic material is shared, so the twins are identical.
Depending on the time of the splitting of the egg, you can get anything from:
conjoined twins through
monochorionic / monoamniotic twins,
monochorionic / diamniotic twins
to dichorionic / diamniotic.
The highest risk falls to the twins sharing an amnion and a placenta.
The lowest to those with separate sacs and placentas.
If twins share a single sac, cords may entangle and cut off the blood supply.
And a shared placenta can lead to one baby shunting blood to its twin, with dire consequences.
A view was expressed a few years ago recommending delivery of monoamniotic twins at 28 weeks to get round the cord-entanglement problem.
The counter argument is that most of the lethal entanglements take place before 28 weeks.
So you would not gain a lot from such early delivery and would put babies at risk from prematurity.
About 1/3 of twins are monozygous, Luesley & Baker, with an incidence of about 4 per 1,000 births.
Abnormality rates as high as 10% have been quoted, mainly heart and intestinal defects and anencephaly.
Screening for T21 has to rely on nuchal translucency, NT.
Interestingly, there is evidence that if there is significant differences in NT, not due to T21, there is an increased risk of TTTS.
Early pregnancy sees an increased risk of miscarriage and hyperemesis.
If second trimester miscarriages are included with perinatal mortality figures, overall losses of around 10% occur, which is pretty horrifying.
The 1989 Scottish report into perinatal mortality gave figures for singletons and twins of 7.6 and 53.6 per 1000 births respectively.
The figures for triplets are substantially worse.
Kumar in Luesley and Baker’s textbook quotes perinatal mortality rates of:
37 per 1000 for twins,
52 per 1000 for triplets,
231 per 1000 births for higher order births,
260 per 1000 for monozygotic twins.
Cerebral palsy rates go up frighteningly: they are 8 times higher in twins and 47 times higher for triplets.
Prematurity and IUGR rates are also much increased.
Twins and triplets have relative risks of IUGR or 10 and 19 respectively compared with single babies.
This raises major ethical issues about the number of embryos to be replaced in IVF treatment.
There is a view that the more that are replaced the better the "success" rates in terms of the number of ongoing pregnancies.
Although this is disputed.
But a sure outcome is higher multiple pregnancy rates, with potentially disastrous outcomes.
There is evidence that replacing three embryos rather than two increases the risk of triplets by a factor of 15; from 0.4% to 6%.
Like all other statistics, those of success rates from IVF clinics have to be interpreted carefully.
As an obstetrician, I feel distinctly jaundiced about the IVF practitioners who install tribes of embryos to optimise their “success” rates.
But never have to pick up the consequent horrors with decisions about:
“multifetal pregnancy reduction” (killing off the excess number of fetuses)
and caring for women who deliver disastrously early and have dead or seriously damaged babies.
When money is changing hands, one is particularly cynical!
In recent years the transfer of not more than 2 embryos has become the norm.
National guidelines now recommend the use of a single embryo. http://www.fertility.org.uk/news/pressrelease/08_09-SingleEmbyoGuidelines.html.
Patients with twins used to be kept in hospital and on bed rest in the hope that this would reduce the incidence of premature labour.
About 10% deliver before 32 weeks and this is the major cause of perinatal risk.
It did not work.
Such regimes may well put the patient at hazard from DVT and I suspect that they increase cigarette consumption.
Tocolytics have been tried but have not been proven to help.
Prophylactic steroids are discouraged in the College guideline, though used by some obstetricians.
They are again of unproven value - given the low incidence of twins, it would need a multi-centre trial to validate their use and one is planned.
Monochorionic twins are at risk because of shared vascular channels deep in the placenta.
This allows one baby to pump blood into the other.
The recipient tends to go into heart failure, pee a lot and produce excess fluid in its sac.
The donor is left in a reduced volume sac.
This is gradually squeezed up against the wall of the uterus by the other twin’s sac, which now displays polyhydramnios.
This is the “stuck” twin.
Twin-twin transfusion carries a horrible perinatal mortality rate – 80% or more.
The main approaches to trying to deal with it involve:
attempted ablation of the communicating vessels,
and knocking holes in the membrane between the sacs so that the pressures and volumes can equilibrate.
Because monochorionicity is such bad news, it is important to try to determine chorionicity accurately.
This is best done by seeking the “Lambda” sign in early pregnancy.
If it is present, the pregnancy is dichorionic.
The test is very accurate in the first trimester.
There is also the “T” sign, which fits with monochorionicity.
You will be shown pictures of it on the course, which is the best way of getting it to stick in your head.
Later in pregnancy diagnosis of chorionicity is not so good.
If the babies are of different sex, the pregnancy is dichorionic.
If there are two separate placentas, the same applies.
If there is evidence of arterial communication between the placentas, “arterio-arterial anastamoses”, the pregnancy is monochorionic.
These communications can be seen in two thirds of such pregnancies.
If the babies share the same sac, that carries its own risks, particularly of cord entanglement, which can prove lethal.
Twins can also “lock” during delivery.
The commonest scenario (still very rare) is for the first baby to be breech.
As it delivers, the second baby’s head gets below the first baby’s head.
So the first baby cannot deliver until the second baby has been moved.
Small print stuff.
Nearly a third of twin pregnancies will show evidence of intrauterine growth restriction.
You would no doubt guess by now, if asked, that monochorionic twins are worse performers than non-identical ones and you would be right.
Biochemical screening for Down’s syndrome cannot be used.
Presumably the results from the abnormal pregnancy are swamped by those from the other fetus.
Nuchal fold assessment is the main risk assessment tool.
If one twin dies, it carries enormous risk to the surviving twin if it is a monochorionic pregnancy.
It may die or have catastrophic neurological or renal damage.
It is thought that the surviving twin pumps blood into the dead one and so becomes anaemic and even shocked.
Doppler studies of middle cerebral artery blood flow may confirm the anaemia.
The risks with non-identical twins are much less and these pregnancies are usually allowed to continue.
Ong et al published a literature review in the BJOG in 2006. Vol 113, no9, pp. 992-998.
The risks to the survivor after death of the other twin were:
Risk of death
Risk of neurological damage
Risk of premature delivery
I give these figures to show the high risk to the monochorionic twin, but no one is going to expect you to remember them.
If the death is discovered in the first day or so, intrauterine transfusion to save the survivor may be feasible.
This is usually coupled with attempts to cut off the circulation to the other twin.
However, I think you would be very lucky to make an early diagnosis.
In cases where the diagnosis has been made later, all you can do is assess the survivor for brain damage, e.g. by ultrasound or MR scanning.
If the test is normal, this will be some reassurance for the parents.
If it is not, terminating the pregnancy may be an option.
TRAP sequence (Twin Reversed Arterial Perfusion Sequence) is a rare complication of monochorionic twins, affecting about 1% of them.
One twin is grossly abnormal, usually with no head and no functioning heart.
It gets its blood supply from the healthy twin, the “pump” twin, which runs the risk of consequent heart failure.
The huge cardiac output from the “pump” twin can also lead to increased renal blood flow.
This leads to more urine output and polyhydramnios with the risk of premature labour.
The “pump” twin has a risk of chromosomal abnormality of ~ 10%, so the chromosomes need to be checked.
A key factor in the outcome is one you probably would not guess, but might conclude if you had a few hours to deliberate.
Cardiac failure is the main determinant of outcome.
The size of the acardiac twin is going to decide how much cardiac work the “pump” twin has to do.
So the bigger it is, the worse the outcome.
Management is by obstructing the blood flow through the cord of the acardiac twin.
This is usually done via the hysteroscope.
Another risk to keep in mind is that retained products of conception, at any gestation, may trigger disseminated intravascular coagulation.
A dead pregnancy falls into this category.
DIC takes some weeks.
In essence, placental tissue and amniotic fluid are rich in thromboplastin.
Thromboplastin is absorbed as the material degenerates, triggering a consumption coagulopathy.
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