Aust N Z J Obstet Gynaecol 1997 p1

download Aust N Z J Obstet Gynaecol 1997 p1

of 5

Transcript of Aust N Z J Obstet Gynaecol 1997 p1

  • 7/27/2019 Aust N Z J Obstet Gynaecol 1997 p1

    1/5

    Aust.

    z

    Obstet Gynaecol

    997;

    37:

    1: 1

    THE AUSTRALIAN

    &

    NEW

    ZEALAND

    JOURNAL

    OF

    OBSTETRICS

    GYNAECOLOGY

    February

    1997

    VOl. 37 No.

    OCCASIONALREVIEW

    From Delivery Suite

    to

    Laboratory:

    Optimizing Returns

    from

    Placental Examinationin

    Medico-legalDefence

    T.Y. Khong

    Department of Pathology Womens

    and

    Childrens Hospital North Adelaide South Australia

    Summary:

    While examinations of the placenta may reveal significant lesions that are

    helpful in a medico-legal context, its value may

    be

    diminished by a lack of attention

    to detail in the period between delivery of the baby and receipt of the placenta in the

    pathology department. These fall generally into

    2

    groups: initial description and

    handling of the placenta and lack of relevant clinical information. This

    communication describes some of these pitfalls. By observing these details, the onus

    then falls on the pathologist to provide a meaningful assessment of the placenta.

    The average Australian obstetrician might be

    expected to be involved in obstetric litigation once in

    10 to

    15

    years. The common reasons for litigation are

    fetal death in utero, fetal distress and alleged cerebral

    hypoxia resulting from obstetric management.

    Placental examination may be important in perhaps

    25

    of obstetric cases that are litigated. Most cases in

    which the placenta has been available conclude in the

    favour of the defending obstetricians and hospitals

    (1).An insurance company review found that verdicts

    were in favour of the defence in all 12 neurologically

    impaired infant claims tried to a conclusion when the

    placenta and/or cord was available for examination

    (2). It is estimated that 15 of all pregnancies have

    abnormalities hat can be explained by an experienced

    pathologist who has examined the placenta (3).

    Nevertheless, failure to pay attention to detail in the

    period

    between delivery of the baby and receipt of the

    Address

    for

    correspondence:

    DrT.Y. Khong,

    Placenta Research Unit

    Department

    of

    Histopathofogy

    Adelaide Womens and Childrens Hospital

    North

    Adelaide

    South

    Australia

    5006,

    Australia.

    placenta by the pathology department can negate the

    value of placental examination and it5 place in

    risk

    management. This aspect appears to be neglected

    or

    overlooked although there have been several recent

    texts and articles detailing the pathology of the

    placenta and of the significance of placental

    examination in the medico-legal context

    4-7).

    The

    purpose of this review is to highlight some of these

    pitfalls and to note practicalaspectsof the initial

    gross

    placental examination and its submission to the

    pathology department that will ensure that the

    placental pathology report will be meaningful.

    Examination

    of

    placentas: triage

    It is a truism that no information can be gleaned if

    the pZacenta is not examined. While some advocate

    examination of all placentas by a pathologist

    (6)

    most

    pathology departments realistically agree that a triage

    of placentas is necessary so as not to overwhelm the

    diagnostic pathology service. Which placentas should

    be sent for pathological examination will depend, to

    an extent, on the interests of the local obstetrics and

    pathology departments but guidelines

    re

    available

    for indications for placental examination 3,8). It is a

  • 7/27/2019 Aust N Z J Obstet Gynaecol 1997 p1

    2/5

    2

    AUST.AND N.2. JOURNAL OF OBSTETF3CS

    AND GYNAE COL oGY

    good idea to incorporate a system where those

    placentas that are not sent for pathological examin-

    ation can

    be

    stored in a refrigerator for about

    I

    week

    so

    that the placenta of the seemingly healthy infant

    who experiences early postnatal problems can be

    retrieved for examination (4,8,9).

    Maternal indications for pathological examination

    include diabetes mellitus, preeclampsia, premature

    rupture of membranes, prolonged rupture of mem-

    branes, preterm delivery,

    placenta praevia, post-

    maturity and poor previous obstetrical history. Fetal

    indications include stillbirth, neonatal death, multiple

    gestation, prematurity, intrauterinegrowth retardation,

    congenital anomalies, hydrops, meconium-stained

    liquor, low Apgar scores, admission to a neonatal

    intensive care unit, abnormal fetal cardiotocography

    and suspected infection.

    Handling of placentas n delivery suit

    Each placenta should be examined promptly after

    delivery in the delivery suite, allowing findings of

    immediate importance to be detected and acted upon

    clinically.

    It also allows placentas that otherwise

    would not have been sent for pathological examin-

    ation for maternal or fetal indications to be identified

    for submission for pathological examination for

    placental reasons. Placental indications are placental

    abruption, infarcts, placenta praevia, abnormal

    calcification and any abnormal appearance of placenta

    and/or cord and/or membranes.

    Missing cotyledons or membranes could highlight

    the possibility of retained placental fragments that

    could give rise to postpartum haemorrhage, failure of

    uterine contraction and involution or endometrial

    infection. Some placentas, however, have a disrupted

    maternal surface rendering accurate assessment of

    completeness impossible. The pathologist should be

    alerted to any tissue taken for research, although such

    tissue usually has a sharp cut edge,

    so

    that an

    erroneous report of incomplete placenta is not

    generated. Ruptured fetal vessels, such as ruptured

    vasa praevia or necrosis

    of

    umbilical arteries, should

    alert the neonatologist to the possibility

    of

    needing

    neonatal transfusion. In the latter case, additional

    neonatal problems, such

    as

    intestinal atresia, may be

    suggested (10.1 1). Opaque membranes or malodorous

    placenta would suggest acute chorioamnionitis and

    neonatal infection.

    Other observations routinely performed include

    weighmg of the placenta and checking for the number

    of umbilical cord vessels. Recording of the placental

    weight fell into disrepute when it was shown that the

    placental weight is subject to great variation and

    inaccuracies (12). There is no standard routine for

    weighing the placenta and the inaccuracies may derive

    from inclusion or exclusion of the membranes,

    umbilical cord n its entirety or in part, maternal

    blood entrapped in the intervillous space, fetal blood

    trapped in the placenta subject to timing or cord

    clamping and the use of oxytocics and, sometimes,

    amniotic liquor. Notwithstanding these criticisms, the

    recent epidemiological findings of Barker and his

    colleagues relating intrauterine events to adult disease

    1

    3) justifies continued weighing of the placenta and

    attempts to standardize the technique. Furthermore,

    placental weights below the 10th percentile or above

    the 90th percentile should alert the examiner to

    pos-

    sible maternal and fetal disorders.

    The dimensions of the placenta are often measured

    in the delivery suite. Apart from the extensive placenta

    membranacea, no relation between placental dimen-

    sions and perinatal outcome has been demonstrated

    and the routine should be desisted. The placenta

    membranacea is defined as an abnormally diffuse

    placenta covering all,

    or

    most, of the membranes and

    is associated with recurrent antepartum bleeding,

    premature onset of labour, postpartum haemorrhage

    and morbid adherence of the placenta (14). The length

    of the umbilical cord is often measured. An unusually

    long cord, defined as greater than 100 cm, leaves it

    susceptible to cord prolapse and venous thrombosis

    while a short cord, defined

    as

    less than 32 cm, may

    restrict fetal descent and result in placental separation,

    fetal distress or cord rupture. It is obvious that these

    measurements are best done in the delivery suite since

    the midwife or accoucheur will know how much of

    the cord is left on the baby or if additional segments

    had been taken for blood gas measurements or for

    research, etc

    (9);

    the pathologist is in no position to

    defend allegations

    of

    fetal distress due to short cords

    if he is unsure

    if

    the cord received in the laboratory

    was the entire length. In this regard, it is also helpful

    for the accoucheur to record the location of the

    placenta in utero since the placental location and

    umbilical cord insertion must be considered when

    studying short cords

    1 5 . A

    note should

    be

    made of

    the site of umbilical cord insertion since velamentous

    cord insertions could

    be

    associated with lacerations,

    compression or thrombosis of vessels

    (

    16).

    Manipulation of the placenta may be detrimental to

    subsequent examination by a pathologist. Thus, in

    trying

    to

    ascertain the lucency

    of

    the membranes,

    wiping the membrane with the hand to promote better

    visualization may inadvertently remove amnion

    nodosum, which are nonadherent,

    in

    contrast to

    amniotic squamous metaplasia which is less easily

    removed. Similarly, loose andor adherent blood clot

    may be removed in handling the maternal surface.

    Unless these findings are recorded and communicated

    to the pathologist, the possibility of a fresh retro-

    placental haematoma or placental abruption may be

    overlooked when the placenta is assessed histo-

    logically since there may be only microscopic

    evidence of acute changes in intervillous blood flow.

  • 7/27/2019 Aust N Z J Obstet Gynaecol 1997 p1

    3/5

    T.Y. h O N G

    3

    With twin placentas, labelling of the umbilical cord

    with 1 clamp for the first twin and 2 clamps for the

    second twin eliminates any confusion that can arise if

    a no clamp/l clamp labelling is used as it may not be

    apparent if the 1 clamp in the no clamp/l clamp

    system is for

    the

    first or the second twin.

    This is

    important because pregnancy and/or delivery compli-

    cations may affect only 1 twin. Thus, for example,

    meconium staining, acute chorioamnionitis or amnion

    nodosum could be present or be more pronounced in

    only 1 gestational sac; while correlation between

    clinical outcome and pathology could be achieved

    later, this is unsatisfactory and may not be possible.As

    part of their clinical practice to attempt to inform

    parents of the zygosity of multiple

    births

    midwives

    often examine the chorionicity of the placenta in

    multiple births by stripping the dividing membranes.

    Unless

    this

    is done correctly and recorded accurately,

    stripping of the dividing membranes may leave the

    pathologist with a dog-ear of dividing membranes to

    reconstitute and may render impossible any comment

    of the chorionicity. This is important since perinatal

    morbidity and mortality are dependent on chorionicity

    and not on zygosity (17). A related issue in litigation

    cases is whether the twins had twin-twin transfusion

    syndrome. Establishing dichorionicity virtually mles

    this out (18). Nevertheless, the preservation of an

    adequate length of umbilical cord and leaving the

    chorionic plate vessels intact allow unhampered

    injection studies to be performed by the pathologist in

    all cases of multiple pregnancies.

    It should also be stated that stripping of the amnion

    from the underlying chorion can make subsequent

    swabbing of the subamniotic chorionic plate for

    bacterial and fungal cultures more difficult. Further-

    more, it may obliterate any evidence of a chordee

    insertion of the umbilical cord wherein a fold of

    amnion extends from the cord insertion site on the

    surface for a distance proximally; this may

    be

    associated with limited cord movement and possible

    circulatory compromise (16). Care should be taken in

    examining the membranes

    so

    that

    the

    site of rupture is

    not artifactually extended as that may obscure

    assessment of its relation to the placental margin in

    cases of placenta praevia.

    The umbilical cord is often clamped with plastic

    clips for stemming blood flow after delivery of the

    baby. Unless umbilical cord haematomas are specifi-

    cally looked for prior to cord clamping, it can be a

    difficult diagnostic problem deciding if such a

    haematoma is artifactual or had occurred spontan-

    eously. Significant spontaneous cord haematomas are

    associated with long cords and with cord prolapse and

    can result in fetal exsanguination and fetal distress

    (19).

    Comments are sometimes made in delivery suite

    notes regarding the finding of infarcts or excessive

    fibrin deposition. These remarks, once annotated,

    almost become anointed. It can be difficult to dis-

    tinguish between massive perivillous fibrin deposition

    and infarct

    or

    even a chorioangioma from an

    examination of the maternal surface alone and the

    credibility of the defence may be called into question

    if the ultimate histological findings are at variance

    with the initial

    gross

    placental examination. If these

    findings need to be documented in the delivery notes,

    it would be preferable to use descriptive t e r n such as

    red, yellow or white plaques and to submit these

    placentas for histological examination. Furthermore,

    the extent of these lesions are important as are the

    locations and these could be determined only after

    examining slices of

    the

    cut placenta. The placenta can

    withstand

    20-30

    villous loss through massive

    perivillous fibrin deposition without any clinical ill-

    effects but may be compromised by 510 villous

    loss through infarction (12).

    Before the placenta is despatched to the pathology

    department, it is essential that it is labelled properly

    and then sent fresh without any rinsing. Clinicians are

    beseeched to send specimens in adequate volumes of

    fixative (20) but the placenta is an example of an

    exception to the rule. Receipt of the placenta

    in

    a

    fresh

    state permits

    the pathologist to swab the

    subamniotic space for evidence

    of

    amniotic fluid

    infection or to take parenchymal samples for

    biochemistry, virology and cytogenetics or to

    perform

    injection

    studies of

    the fetal-placental

    vasculatum

    in

    multiple pregnancies.

    Clinical

    information

    The omission of relevant clinical details in the

    laboratory request form is not a monopoly of obstet-

    ricians: many nurses and doctors commit this

    misdemeanour

    (2

    1). The placenta is a rapidly evolving

    organ in its approximate 40weeks life-span and its

    responses to pathological processes

    are

    limited.

    Unless the pathologist is provided with all relevant

    information, interpretation of microscopic abnorm-

    alities may be meaningless or, more worryingly,

    misleading

    (22).

    The minimum clinical information

    required include

    the

    gestational age, birth-weight and

    the reason the placenta is submitted for examination.

    A

    very frequent omission is the gestational age of

    the pregnancy at the time of delivery. Histological

    comment on appropriateness of placental maturity is

    often made and great reliance is placed on the gest-

    ational age provided in the laboratory request form.

    Villous immaturity may be seen in fetal anaemia due

    to maternal-fetal rhesus isoimmunization or twin-twin

    transfusion, maternal diabetes mellitus, anencephalus

    and syphilis and is significantly infrequent in

    preeclampsia 22).Accelerated villous maturation has

    been described in preeclampsia and has been used as

    a surrogate for uteroplacental vascular insufficiency

  • 7/27/2019 Aust N Z J Obstet Gynaecol 1997 p1

    4/5

    4

    AUST.ANV

    N.Z.

    JOURNALF OBSTETRICS

    ND

    GYNAECOLOGY

    and defective placentation (23-25). Unless the

    estimated date of delivery is provided, histological

    assessment will be limited. The ideal request form

    should provide the estimated dates of delivery from

    both early pregnancy ultrasound and the last men-

    strual period if they are discrepant.

    Two other examples where clinical information

    may be helpful are placenta praevia and morbid

    adherence of the placenta. While placenta accreta

    is

    largely a clinical diagnosis, it would help the path-

    ologist to be aware so that more blocks of the placenta

    could be sampled to attempt to c o n f i i the diagnosis

    on the placental histology when a hysterectomy has

    not been performed (26,27). If the site

    of

    rupture in a

    vaginal delivery is at the placental edge,

    this

    suggests

    that the edge of the placenta may be encroaching on

    the cervical

    0s.

    A site of rupture greater than

    10

    cm

    from the placental edge is likely to follow a fundal

    implantation.

    Antenatal interventional procedures, such as cordo-

    centesis and amniocentesis or intrauterine trans-

    fusions, should be communicated to the pathologist

    so

    that complications such as funisitis can be sought

    vigorously.

    In

    the case

    of

    cordocentesis, gross

    evidence of the funicular puncture site can be readily

    detected during the first month after the procedure but

    may be inconspicuous after a month (28). Umbilical

    cord haematomas may be associated with the

    procedure (28) and need to be distinguished from

    spontaneous or artifactual lesions.

    The pathologist should also

    be

    informed about the

    results of antenatal investigations. There are many

    causes of elevated maternal serum alphafetoprotein

    and placental examination may reveal unusual causes

    unrelated to pregnancy complications (29,30).

    Findings of positive serology for anticardiolipin

    antibody or for lupus anticoagulant should prompt the

    pathologist to sample the placenta extensively

    or

    to

    modify the technique in order to assess the

    uteroplacental vasculature

    (31).

    Obstetricians pathology colleagues

    As stated earlier, it was not the intention of this

    communication to review the various specific aspects

    of placental abnormalities. Many placental abnorm-

    alities are associated with perinatal morbidity and

    mortality and with a poor short-term and long-term

    outcome. However, all these abnormalities may also

    be

    associated with no untoward perinatal or maternal

    sequelae. While it is important that the obstetrician,

    and pathologist, recognize the limitations of placental

    examination its potential utility should not be

    compromised by a lack

    of

    detail

    in

    the interval

    between delivery to receipt by the pathology depart-

    ment. By strict adherence to detail and delivering the

    placenta in an optimal state with all relevant clinical

    information, the obstetricians can, and should,

    demand a quality placental examination expertly

    performed by their pathology colleagues: the onus of

    providing a meaningful assessment

    of

    the placenta

    shifts

    to

    the pathologist. It is then the pathologists

    obligation to educate themselves about the placenta,

    its morphology in health and disease and the relevance

    of its morphological findings (32). Hopefully, the

    numerous recent texts and publications, admittedly

    largely in the domain of pathology (33-46), will have

    raised the consciousness of the pathology community

    to the placenta, hitherto a neglected organ.

    cknowledgements

    frequency

    of

    obstetric litigation.

    I

    thank

    Dr

    Hugh Aders for comments regarding

    References

    1. Lambird PA. Resource allocation and the cost of quality. Arch

    Path01 Lab Med 1990; 1 14 1168.1172.

    2.Schinder NR. mportance of the placenta and cord in the

    defense of neumlogically impaired infant claim. Arch Pathol

    Lab Med 1991; 115: 685-687.

    3. Driscoll SG. Placental examination in a clinical setting. Arch

    Pathol

    Lab

    Med 1991; 115: 668-671.

    4.Benirschke K. The

    placenta in the litigation

    prwess. A m

    J

    Obstet Gynecol 1990; 16 2 1445-1450.

    5. Kaplan CG. Forensic aspects of the placenta. Perspect Pediatr

    Pathol 1995; I 9 2042.

    6.Salafia CM Vintzileos

    AM

    W h y all placentas should be

    examined by a pathologist in 1990. Am J Obstet Gynecol

    1990,

    163: 1282-1293.

    7 Altshuler G. Placenta within the medicolegal imperative. Arch

    Pathol Lab Med 1991; 115: 688-695.

    8.

    Altshuler G Dcppisch LM. College

    of

    American Pathologists

    Conference

    XIX

    on the examination of the placenta: Repon of

    the working group on indications for placental examination.

    Arch Pathol Lab Med 1991: 115: 701-703.

    9. Driscoll SG, Langston C. College of American Pathologists

    Conference

    XIX on

    the examination

    of the

    placenta: Report of

    the working group on methods for placental examination. Arch

    Path01 Lab Med 1991; 115: 704-708.

    10. Bendon RW. ?son RW. Baldwin VJ.Cashner

    KA.

    Mimwni

    F,

    Miodovnik M. Umbilical cord ulceration and intestinal atresia:

    a new association? Am

    J

    Obstet Gynecol 1991: 164: 582-586.

    1

    . Khong

    TY.

    ord

    WDA.

    Haan

    EA. Umbilical cord ulceration in

    association wt intestinal amsia in a child with deletion 3q

    and Hirshsprungs discax.

    Arch

    Dis Child 1994; 71: M12-213.

    12. Fox

    H.

    athology

    of the

    placenta. London. WE Saunden. 1978.

    13.Barkm DJP. The fetal and infant origins of adult disease.

    London BMJ Publishing Group. 1992.

    14. Hurley VA. Beischer NA. Placenta membranacea. Case reports.

    Br J Obstet Gynaecol 1987; 94: 798-802.

    15. Collins J. The

    short

    umbilical cord. Am J

    Obstet

    Gynecol 1992;

    166:

    268-269.

    16.Kaplan C. Lowell DM Salafia C. College of American

    Pathologists Conference XIX on the examination of the

    placenta: Report of the working group on the definition

    of

    structural changes associated with abnormal function in the

    maternal/fetal/placental unit in the second and third trimesters.

    Arch Pathol Lab Med 1991; 115: 709-716.

    17. Fisk NM Bryan E. Routine prenatal determination of

    chorionicity in multiple gestation: a plea t the obstetrician. Br

    J Obstet Gynaecol 1993; 100: 975-977.

    18. Baldwin VJ. Pathology of multiple pregnancy. New York.

    Springer-Verlag 1994; 215-275.

    19. Benirschke K Obstetrically important lesions of the umbilical

    cord. J Reprod Med 1994:

    39:

    262-272.

  • 7/27/2019 Aust N Z J Obstet Gynaecol 1997 p1

    5/5

    T.Y. KHOtiG

    5

    20. Editorial. Fixing specimens properly. Lancet 1991; 338:

    984.

    21. Bull AD, Cross SS, James

    DS

    Silcocks PB.

    Do

    pathologists

    have extrasensory perception?

    BMJ

    1991; 303: 1604-1605.

    22. Khong TY, Staples A, Bendon RW et al. Observer reliabilitv in

    assessing placental maturity by histology. J Clin Path01 1h 5 ;

    48: 420423.

    23. Naeye

    RL.

    Pregnancy hypertension, placental evidences of low

    uteroplacental blood flow, and spontaneous prematwe delivery.

    Hum Path01 1989; 20: 4 4 1 4 .

    24. Raybum W, Sander C, Barr M, Rygiel R. The stil lborn fetus:

    placental histologic examination in determining a cause. Obstet

    Gynecol 1985; 65: 637-641.

    25. rias F, Rodriquez L, Rayne SC,

    Kraus FT.

    Maternal placental

    vasculopathy and infection:

    two

    distinct subgroups among

    patients with preterm labor and preterm ruptured membranes.

    Am

    J Obstet Gynecol 1993; 1 68 585-591.

    26. Khong

    TY,

    Robertson

    WB.

    Placenta creta and placenta

    p v i a

    creta. Placenta 1987; 8: 399-409.

    27. Jacques SM.

    Qureshi F,

    Trent VS. Ramirez NC. Placenta

    accreta: mild cases diagnosed by placental examination. Int J

    Gynecol Path01 19 ; 15: 28-33.

    28. Jauniaux

    E

    Donner C. Simon P, VanesseM u s h J, Rodesch

    F. Pathologic aspects of the umbilical cord after

    percutaneous

    umbilical cord sampling. Obstet Gynecol 1989; 73: 215-218.

    29. Boyd PA. Why might maternal serum AFP be high in

    pregnancies in which the fetus is normally formed? Br J Obstet

    Gynaecol 1992; 99: 93-95.

    30. Khong

    TY,

    George K. Maternal

    serum

    alpha-fetoprotein levels

    in chorioangiomas.A m

    J

    Perinatol 1994; 11: 245-248.

    31. Khong

    TY,

    Chambers

    HM.

    Alternative method for sampliig

    placentas for the assessment of uteroplacental vasculature. J

    Clin Path01 1992; 45: 925-927.

    32. Naeye R, Travers H. College

    of

    American Pathologists

    Conference XD:

    on

    the examination of the placenta: Report of

    the working group on the role

    of

    the pathologist in malpractice

    litigation involving the placenta. Arch Path01 Lab Med 1991;

    115: 717-719.

    33.MacPherson

    T,

    Smlman AE. The placenta and products of

    conception.In:Principles and practice of surgical pathology. ed

    Silverberg SG. New York,

    Churchill

    Livingstone 1990, 1825-

    1856.

    34. Rushton DI. Pathology of

    the

    placenta.

    In:

    Textbook of fetal and

    pennatal pathology. ed Wigglesworth JS, Singer DB. Oxfor&

    Blackwell Scientific 1991; 161-219.

    35.

    Kaplan

    C. Placental pathology for the nineties. path01 Annu

    1992; 2: 15-72.

    36.Naeye

    RL.

    Disorders of

    he

    placenta, fetus, and neonate:

    diagnosis and clinical significance. St Louis, Mosby Year

    Books, 1992.

    37. Khong

    TY.

    Placenta and umbilical cord and

    immunology

    of

    pregnancy. In:Fetal and Neonatal Pathology, 2nd

    ed. Ed.

    Keeling

    JW

    ondon, Springer-Verlag. 1992; 47-85.

    38.

    GerseIl

    DJ, Kraus PT. iseases of the placenta. In: Blausteins

    Pathology

    of

    the female genital

    tract,

    4th

    ed d K m a n UJ.

    New York Springer-Verlag

    1994;

    975-1048.

    39.Lage

    JM.

    The placenta.

    in:

    Pathology

    in

    Gynecology and

    Obstetrics,

    4th

    ed

    Ed.

    Gompel C, Silverberg SG. Philadelphia,

    18

    Lippincou 1994,448-514.

    40.

    Benirschke

    K

    Kaufmam P. Pathology of

    the

    human

    placenta.

    New Yo , Springer-Verlag. 1995.

    41. Fox

    H.

    General pathology of

    the

    placenta.

    In:

    Haines and Taylor

    Obstetrical and Gynaecological Pathology. Ed. Fox H. London.

    ChurchillLivingstone 1995; 1477-1507.

    42. Kohler H, Batcup G. Pathology

    of

    the umbilical cord.In:Haiues

    and Taylor Obstetrical and Gynaecological Pathology.

    Ed.

    Fox

    H. London. Churchill Livingstone 1995; 1559-1580.

    43.Batcup G, Kohler

    H.

    Pathology of the fetal membranes In:

    Haines and Taylor Obstetrical and Gynaecological Pathology.

    Ed. Fox H. London,

    Churchill

    Livingstone 1995; 1581-1595.

    44.

    Redline RW. Placenta and adnexa in late pregnancy.

    In:

    Diseases

    of the fetus and newborn, 2nd

    ed.

    Ed. Reed GB, CIaireaux

    AE

    Cockbum F. London,

    Chapman

    and

    Hall

    1995; 319-338.

    45. SalaIiaCM

    opek

    3.Placenta. Ini Andersons Pathology, loth

    ed.

    Ed. Damjanov

    I,

    Li de r J. St

    Louis

    Masby 1996,231@2353.

    46.

    Altshuler

    G.

    Role

    of

    the placenta in

    perinatal

    pathology

    (revisited). Pediatr Path01 Lab Med 1996, 16: 207-233.