Parenthood Lost
Healing the Pain After
Miscarriage, Stillbirth and Infant Death
Draft
Written and Edited by
By
Michael R. Berman, M.D.
Windows
Gather
every morsel
of hope,
precious gift,
and open your eyes
to its wonder;
common images
earthly sights
hourly routines
that maintain
the equilibrium
of why and how
you live
and lived.
Delight
in what are your joys
and then
for just a brief moment
let them close
to the darkness
and paint
upon the canvass
of your soul
portraits
of secret longings
that come alive
in these minutes
of solitude
called dreaming,
art forms to dance
from the palette
as you revel in
this secret world
of unspoiled vision
and immortal promise.
Table of Contents
Dedication......................................................................... 7
Introduction....................................................................... 8
Part I. Poetry
Poetry: Comforting Through Time................................... 12
Cherished Purposes: A Doctor's Poems............................ 12
Parent's Poems................................................................. 12
Part II: Stories and Views
Parent's Stories of Loss.................................................... 12
Caregiver's Views............................................................ 12
A caregiver's story of her personal pregnancy loss.......................................................................... 12
Emotional care of a perinatal loss and its impact on the labor and delivery nurse............................... 12
A Social Worker's Perspective On Pregnancy Loss.......................................................................... 12
Perspectives of a Newborn Special Care Unit Nurse................................................................. 12
Family Grief And Recovery Process When A Baby Dies................................................................... 12
Perspectives of a genetic counselor.................... 12
A thought from a newborn special care unit nurse.......................................................................... 12
A physician writes of birth and loss................... 12
Part III. Reasons for the Most common perinatal losses
Pregnancy Loss in the First Trimester by Michael R. Berman, M.D................................................ 12
Genetic Disorders by Michael R. Berman, M.D.. 12
The Incompetent Cervix..................................... 12
The Antiphospholipid Syndrome by Sara Marder, M.D................................................................... 12
Pre-Implantation Genetic Diagnosis by Anuja Dokras, M.D., Ph.D........................................... 12
Congenital Heart Disease by Joshua A. Copel, M.D................................................................... 12
Placental Causes of Fetal Loss: Part I by David Lima, M.D......................................................... 12
"Behind Every Healthy Baby is a Healthy Placenta" by Harvey J. Kliman, M.D., Ph.D....... 12
Intrauterine Growth Retardation by Giancarlo Mari, M.D......................................................... 12
Molar Pregnancy: Gestational Trophoplastic Disease by Adina Chelouche, MD...................... 12
Ectopic Pregnancy by Steven J. Fleischman, M.D........................................................................... 12
Premature Rupture of the Fetal Membranes by Kunle Odunsi M.D., Ph.D., and Paolo Rinaudo, M.D................................................................... 12
Substance Abuse During Pregnancy by Ashley Wivel................................................................. 12
Hypertensive Disorders in Pregnancy by Tanja Pejovic, M.D., Ph.D........................................... 12
Loss and Multi-fetal Pregnancies by David Jones, M.D................................................................... 12
Infection and Pregnancy Loss by Jacob Tangir, M.D................................................................... 12
Renal Agenesis and Hypoplastic Lung Syndrome by Ande L. Karimu, M.D., Ph.D........................ 12
Post Term Pregnancy by Rotimi Odutayo, MD MRCOG and Kunle Odunsi, MD PhD MRCOG. 12
Reflections...................................................................... 12
Appendix A: A database of perinatal loss......................... 12
Appendix B: Fetal, Perinatal and Infant Mortality Data.... 12
Appendix C: Leading Categories of Birth Defects............ 12
Appendix D: Ten Leading Causes of Infant Mortality in the United States in 1995....................................................... 12
Glossary.......................................................................... 12
Selected Bibliography...................................................... 12
Contributors.................................................................... 12
This book has materially developed over a period of years; the content and thought has been gleaned over my professional lifetime. Its inspiration and thus its being has come from my patients who were thrust into the tumult of sorrow when their child died. I wish this book were not needed, but humankind's history dictates otherwise. I therefore first dedicate this book to my patients and all families, worldwide, who have endured these unspeakable losses.
My love for poetry was nurtured by my high school English teacher, Donald Fenton Hamingson, who died this year at the age of sixty-nine. Donald Hamingson was an extraordinary individual and a role model for every one of his students. When I last saw him five years ago he was still immersed in teaching the wonders and beauty and reason for poetry. It is my honor to recognize his effect on my life in this dedication.
Dearest expressions of gratitude must go to my wife Nancy and daughters, Stephanie and Annie, who have so genuously understood and critiqued the writing of this book. I would also like to acknowledge my colleagues and mentors, Martin E. Gordon, M.D., Clinical Professor of Medicine, Yale University School of Medicine, Richard Seltzer, M.D., Clinical Professor of Surgery, Sherwin Newland, M.D., Clinical Professor of Surgery, Yale University School of Medicine, and Frederick Naftolin, M.D., D.PHil. Professor and Chairman, Department of Obstetrics and Gynecology, Yale University School of Medicine for their support and encouragement during this process; my students who have provided constant intellectual stimulation and feedback; my partners in medical practice at County Obstetrics and Gynecology Group, and my editor, Jane Garry, who approached me with the idea of this book, and without whose support, its publication might not have been a reality.
Michael R. Berman, M.D.
1998
Countless mothers and fathers and those close to them silently grieve with little resolution over the loss of their pregnancies, newborns and children. Seeking reprieve from their sorrow, they cry and yearn for solace and hope, many times for years following their loss; cries that are but a muted weeping of despair as a child so longed for is not born, or is not born alive, or cannot be conceived. Pained by these losses, their lives seem devoid of hope. Yet they prevail, for within each of us is a timeless, enduring spark of divine hope, a uniquely human greatness that permits us to challenge adversity and courageously face the unexplainable suffering of our souls and bodies. To realize the existence of this divine hope is a most cherished purpose, for with it our lives have promise and reason.
Infertility, pregnancy loss, neonatal illness and subsequent death are among the most painful losses we can experience, for they deny us a family and leave sightless our vision for immortality through generations of the future. Moreover, a child not born is likewise denied the delight to revel in the simple beauty and endless wonder of this divine hope.
Early in my obstetrical training in the 1970's, I was exposed to the trauma of fetal demise. I was taught by repsected and caring mentors that if a baby were to be stillborn or born with a serious, "unsightly" birth defect, we as their physicans should attempt to protect the parents from the "shock" of seeing their dead child by covering them over with a blanket and quickly removing them from the delivery area and sending the body to the morgue to be buried in unmarked graves. It was thought that this was helping the parents. We were unaware of the necessity of allowing them to bond, grieve and have closure. Then, one delivery changed my views. A patient of mine delivered a preterm baby, stillborn, with anencephaly. Anencephaly is a condition where there is incomplete development of the fetal cranium and forebrain. It is not compatible with life. I was familiar with this condition and felt it might be too devestating for the parents to see, much less, to hold their child. However, as I spent time with them during their labor, I realized it was going to be very important for them to do just that; hold, kiss, hug and form a union with their son. When he was born, I covered over the top of his head with a hat and placed him on his mother's abdomen. She held him as if he was alive, related how beautiful he was and how much she loved him. She did not see any birth defects; she saw only her child. This experience affected my management of the stillborn forever.
Recently, a patient of mine had a twin demise at 24 weeks into her pregnancy. Like so many, she had difficulty conceiving and this was her first pregnancy. Her twins shared a common circulation and developed very early problems with this “twin to twin” transfusion syndrome. She received ‘high tech’ state- of- the -art care at our hospital's maternal special care-high risk pregnancy unit, weekly ultrasound examinations and theraputic amniocentesis. She phoned me at 9pm the day following her last amniocentesis stating that she had not felt the babies move. I met her at the hospital and confirmed the worst. Her sons had died. Immediately her reaction was, “oh my God, this cannot be…my life will never be the same…how can I go on? Take the babies now…don't make me go through labor…don't send me home" With convulsive-like tremors, she wailed in despair. Her husband gave her much comfort. I cried with her. With a nurse from the labor floor (who coincidently was the co-director of our perinatal bereavement program), we spent hours counseling her and her husband. I explained what I felt was to be the best for her medically and emotionally: to go home that night, alone, together, cry, gather strength and plan for the induction of labor and delivery the next day. The patient and her husband agreed and the next day she delivered her twin sons. She held them for hours. Afterwards, although filled with sorrow, she and her husband seemed at peace. She talked about her sons, clutched their memento box with their son's pictures, and talked about their funeral and memorial service plans. At the memorial service, prayers were said and poems were read. . She buried seeds of the morning glory flower at the graveside. Closure was accomplished. I do not think I have ever seen a patient demonstrate such extremes in attitudes and emotions as the reality and circumstances of the day evolved, and I attribute this to the counseling she received and the way her children’s death was approached.
In the last few years, awareness, compassion, intervention and counseling have become the paradigm for the management of perinatal demise, yet even in this last decade of the century, concern lingers that such mourning for a pregnancy loss is not fully accepted.( "There are no prayers for the matter of miscarriage, nor do we feel there should be".[1] ) It is my hope that this book, rich with its poems, stories and insights into the impact of lost parenthood will increase the awareness of and sensitivity to those who desparately need to assuage their profundity of sorrow; a sorrow of the ages, felt daily, world-wide, as we now enter the new millenium.
Like strands of DNA, the very essence of life itself, the mourning of the demised unborn or newly born has traveled spiriled peaks and valleys.
My professional career has involved a striving to bring comfort and healing to children, born and yet to be born, and to mothers through their years of childbearing and beyond; it has been the cause in my life. I have been uplifted by the triumphs of birth and healing and depressed by the failures. Yet I have always tried to look beyond the failures in search of the triumphs. Parenthood Lost: A Gathering of Hope is a journey and a journal of my feelings as an obstetrician. Here the reader will find uninhibited expressions of my encounters with the emotions and mystical spirit of my participation in the processes of birth, of life, and of death and testimony to my hopeful optimism shared and encountered with my patients through the years.
The stories of pregnancy and childhood losses are recalled from my earliest contact with patients, some are written by my patients themselves, and others come from correspondence with parents I have never met. To preserve anonymity of the patient-contributors, I have omitted or changed identifications.
I have also included poems which I have written for children, mothers, fathers, and friends many with whom I have shared a part of their lives, or they, a part of mine. I have given or sent many of these poems to them or their families and when appropriate have recited them as eulogies at their funerals and memorial services. The poems are original, unless otherwise noted, and have been written over a period of time corresponding to my years as a practicing Obstetrician. I have written notes as brief summaries and explanations of the inspirations for many of the poems. Others are simply defined by their title.
I have also included thoughts, poems, stories and prayers from other “caregivers” as they have tried to reach out to their patients and families.
The last part of the book gives the most common reasons for stillbirth and infant mortality, written by practicing physicians.
Though our spirits may fade and our viscera bleed,
we are enabled by the agents of our humanity
empowered by ancestral song and promise.
A child is not expected to die before his or her parents. The natural processes of birth, life and death should follow in an orderly and rational sequence through one’s lifetime. Any death other than one from old-age after a rich and fulfilling life is premature. Yet when parents see their child die, or carry the burden of an unborn demise, they live with this disruption of natural order forever. The value placed on the unborn and newly born has differed through generations and periods in human history, yet as value systems and moral codes evolved, in spite of rhetoric and practices of populations with regards to infanticide and population control, the profundity of a parent's grief has remained incontrovertible through the ages. There has not been nor is there now one common and standardized way to manage the recovery from such grief, for it’s shadow has been and will be indelibly imprinted in the minds and souls of these parents. Yet forms of expression implicit in symbolic language; poetry and verse, song, prayer and ritual, have served a role in all cultures and societies to dispel the tears and foster the healing of death and human loss.[2] Adult funeral services can talk of the accomplishments of the deceased, and describe joys and loves and relationships through eulogies and memories. Yet when a newborn or young child dies or a child is not born alive, there is no personal history, seldom a long-standing relationship, few accomplishments and barely a discernible personality to recount. However, a bond between mother and father and child or expectant child occurs and must be recognized. Death tears this apart. The issues of mourning, of lost promises, of sadness and above all, of maintaining faith must be addressed.
Why poetry? What forces are implicit in its form and function that move us and arouse our most inner yearnings and emotions? Why does the poetry of death triumph as a source of enduring inspiration and hope?
“…Poetry{sic}gives the patient a voice for his or her suffering. It may not alter the activity of the disease, but in merely providing a voice it comforts the patient in ways that no medication can.[3]
If “ medicine protects life then(sic) literature interprets it.”[4]
"Art, poetry(sic) is human intelligence playing over the natural scene, ingeniously affecting it toward the fulfillment of human purpose."[5]
"The Poet's gift… awakens in a special way the emotions of those who feel wordless in the face of loss."[6]
"By making us stop for a moment, poetry gives us an opportunity to think about ourselves as human beings on this planet and what we mean to each other." [7]
Comfort may be achieved through the transfer of the poet's feelings into the reader or listener's mind. It transports the reader from the distractions and influences of the outside world inward to the internal rhythms and solace of the personal soul. The poet becomes a healer and his poetry his staff. Through verse and meter, free of inhibition yet full with expression, the poet may articulate a sensitivity and empathy and provoke this introspection and inner peace. A poem is transformed into a message of hope. There is wonderment and magic in the words of a poem. Each word is selected for its individual meaning within the context of the entire poem. A few properly selected words can move the reader to tears and awaken the primal emotions of joy, promise, despair and hope. A poet should evoke emotion in his work and write as if each poem is written with the poet’s last words.[8]
The language of poetry, within the broader context of its 'parent body’ (literature,) has always had as its great themes, love, loss and death.[9] The inclusion of hope to these thematic elements is worthwhile if not essential for, (as humans) we have the capacity to bring hope to a despair that is uniquely created by our humanity and our human conditions.
Bereavement over the loss of a pregnancy, newborn or young child is as old as mankind. My search into the origins of the use of a poem’s graceful yet penetrating ability to soothe, into the essence of what its fragile words can create through symbolism, metaphor and rhythm[10] has led me to the portal of pre-civilization, more than 35,000 years ago. Here began this understanding of the primitive, even primal urges for solace and consolation for grieving parents.
"In the dust where we have buried the silent races...
we have buried so much of the delicate magic of life."[11]
Human culture from which we are today descended emerged between 35,000 years and 32,000 years ago (BP-before the present) within an archeological period known as the upper Paleolithic or late Ice Age. This was marked by the biological evolution of modern human beings, sub-species Homo sapiens sapiens. With this evolution into modernity from the Mousterian Period [12] and from our ancestral Neanderthal species, Homo sapiens neanderthalensis (100,000 and 35,000 years BP) came a "cultural explosion” marked by “symbolic behavior and language and the capacity to imagine.” [13] (It is of interest to note that even prior to this period of “modernity” (80,000-50,000 BP), there is archeological evidence of “purposeful and ritualized” burials. Such activity demonstrated that the Neanderthal Mousterians were able to conceptualize death in such a way as to establish conventions to deal with death’s disruptive forces and externalize the emotional responses to it[14]. This “cultural coding”[15] is not dissimilar from what has been described of poetry today. With poetry "the world of external reality recedes and the world of instinct, the effective emotional linkage behind the words, rises to the view and becomes the world of reality.”[16] Primative humans needed to survive the perils of their environment before they could learn to "live beautifully or create beautiful things."[17] However, a "primitive imagination flourished in the midst of this peril"[18] and out of their concern for their physical suffering and disability, they developed religious rites which focused upon the origins of their disease and pain. Their sickbed became their cradle of religious myths and superstitions. The fear of death invoked many of these rituals and burial customs in order to repel the spirits of the deceased.[19] Yet from from such thought also developed behavior, rituals and symbols to safeguard the females from the perils of childbirth and memorialize their dead children.[20] One might consider that these death rituals of the Moustarians were the precursors to our contemporary poetry and prayers of grieving although no written record exists which could prove this hypothesis.
Remains of a Neanderthal child were found in Siberia. The grave was surrounded by goat horns, deliberately placed in a symbolic pattern which demonstrated a very early expression of "animistic beliefs" that nature is personal and filled with the spirits which behave like human beings.[21]
Caves at Shanidar, in Northeastern Iraq, were a rich source of Neanderthal excavations. This region of the world was considered by some to be the cradle of mankind and there was found was evidence of purposeful burials including the inclusion of small, brightly colored wildflowers. The remains of the Shanidar Man was found on a bed of woven, pinelike woody branches. Within the soil were discovered pollen from several non-indiginous flowers such as grape hyacinth, hollyhock and yellow flowering groundsel. This has been 'poetically' interpreted as evidence for the capacity for ‘human feelings’ in pre-human species. The inhabitants of Shanidar buried their dead among natures beautiful foliage after searching "the mountainside in the mournful task of collecting flowers"[22]. One might imagine the recitation of a psalm or song, prayer or poem in the manner which we inter our loved ones today into the death rituals of the Neanderthal's as they buried their dead children accompanied by the natural beauty of wildflowers.
This culture of the newly evolving Homo sapiens sapiens brought with it the cerebral attributes of “knowledge, belief, art, morals, custom and …other capabilities and habits acquired by man as a member of society.”[23] A system of values developed along with the establishment of a moral code, and the value placed on fertility and birth in this period was among the most revered. This is well documented by the abundant discoveries of fertility rituals and symbols, displayed in cave drawings and portable art (pottery, stones, etc.). Birth, life, fertility and transformation into death (regeneration), akin to the cycles of nature, predominate in Paleolithic and Neolithic images, and are particularly thematic in the image of the goddess and the symbolism contained within her language.[24] Richly painted artifacts displayed with a wonderment of color and images have been found, emblazoned with their depiction of life. The goddess in all her manifestations was a symbol of the unity of all life in nature.[25] This makes us believe that the loss of a child whether in-utero or shortly thereafter was a great loss and evoked a grief response and need which are evident through modernity. The enduring beliefs of fertility, sterility and "the fragility of life” are rooted to these neolithic, agricultural populations.[26] The egg, symbolic of birth and rebirth, was among the most ubiquitous symbols during this era. Its form abounds on vases and frescos of prehistoric periods.[27]
Discovery of wind instruments in Southern France some 32000 years ago and the finding of small objects with parallel markings were early evidence of rythmic arrangements and interval scales (Chatelperronian Period-35000-30000). Furthermore, evidence of recurrent patterns and structures of Magdalenian period (18,000-11000 BP) showed complex conceptualizations consistent with oral communication and development[28]. From this we might infer that symbolic representations recorded as a primitive language along with the use of rhythm and music may be considered ancestral to the emotional responses inherent in what we consider poetry today.
The Chinchorro people of ancient Chile lived from 7000 BC to 5000 BC. They revered their dead, particularly their children and their stillborn, and they put special effort in funerary rites and preservation by mummification. The process of such mummification is beyond the scope of our discussion, but the Chinchorro’s commitment to this process was evident by this purposeful, artifical mummification, turning the simple body of a dead child into a complex work of art.[29] Generally, artificial mumification of dead children and fetuses was rare, for many primative cultures did not consider them full members of society, yet it is evident this was not true for the Chinchorro indians. The Chinchorro’s had no written language, and an accurate account of their rituals is not possible. The mummification process of the Chinchorro's was performed with the intent to preserve indefinitely the dead for an "afterlife and ancestral worship."[30] Chinchorro mummies were buried with food and implements for the afterlife. With the effort expended in this process of mummification, one is led to believe that great value was placed on the lives and therefore the deaths of these fetuses and children.[31]
The development of written language documented the rites and rituals which were celebrated upon the death of a child. Much has been written and studied of the Egyptian funeary practices of mummification. Their belief in life after death defined different spheres of a post mortum existence. Their spiritual being flurished after death. Early in the Egyptian civilization, the Egyptians planted their dead adults and children beneath the desert sand. When they were exhumed, intentially or by wild animals, their bodies were discovered in a state of natural mummification, dessicated by the sun before they had began to decompose. Artifical mummification is a purposeful dessicating or drying process. The Egyptian's further utilized oils and wrapped the bodies to provide clothing. Funerary texts descibing the relationships between the deceased and the gods were receited during the embalming and entombing. Such text, a collection of magic spells and formulas, hymns and prayers, was written on papyrus, bound together and collectively called The Egyptian Book of the Dead. It was thought that recitation of this text by the deceased at time of their death and entombing assured their glorification in an afterlife. It began to appear in Egyptian tombs around 1600 BC. The text was intended to be spoken by the deceased during their journey into the underworld, enabling the deceased to overcome obstacles in the afterlife. One pertinent allusion contained in the Egyptian Book of the Dead was to Hathor, the goddess of joy, motherhood, and love. She was rendered the "protectress of pregnant women", a midwife, a fertility goddess and the patron of all women. She welcomed the arrival of the deceased to the underworld, dispensing water to the souls of the dead from the branches of a sycamore and offering them food. "Hathor was also represented as a cow suckling the soul of the dead, thus giving them sustenance during their mummification, their journey to the judgement hall, and the weighing of their soul." In later periods, dead women identified themselves with Hathor.[32]
To better understand the use of poetics in the Egyptian Book of the the Dead, I cite the following which was recited to secure for the deceased the affection of men, gods, and the Spirit-souls.
O my father Osiris, thou hast done for me that which thy father Ra did for thee. Let me abide upon the earth permanently. Let me keep possession of my throne. Let my heir be strong. Let my tomb, and my friends who are upon the earth, flourish. Let my enemies be given over to destruction, and to the shackles of the goddess Serq. I am thy son. Ra is my father. On me likewise thou hast conferred life, strength, and health. Horus is established upon his tomb. Grant thou that the days of my life may come unto worship and honour. [33]
Ancient Greek and Roman cultures held diverse and sometimes conflicting attitudes with regards to the values placed on the worth of a child or a fetus. This is well documented, for their culture was rich in literature and in particular poetics. Pregnant women in ancient Rome made a sacrafice of flowers to the goddess Juno, who was thought to have the power to prevent miscarriages.[34]
Yet the paradox of infanticide or “exposure” existed, not only for ‘defective’ newborns but also for healthy ones. Infanticide, an old and almost universal custom was commonly practiced in imperial Rome by Pegan worshippers for reasons of poverty, vanity, malformations, population control and other less defined social reasons. Many newborns-mostly female- were brought to the columns in Rome and left to perish.[35] It was felt by some that humanity was not endowed or given at birth and a higher value was placed on an ability to contribute rather than the inherent value of just being human[36], and that failure to contribute rendered man "worthless". Likewise, children, according to the Greek philosopher, Aristotle were considered natural slaves of limited potential.[37] Plato and Aristotle accepted the morality of exposed infants and supposed that “value” and worth is not intrinsic but acquired.[38] The third century writer, Heliodorus, likewise felt, contrary to these ancient classical values, that it was not permissible to disregard an “imperiled soul” once it has taken on human form[39]. Within the early centuries of the Roman Empire, inspired by Constantine, there developed a growing humanitarianism, a medical ethic of respect for human life, which condemned abortion and active euthanasia. Christians held that "the immortal soul rested in the unborn fetus as truely as in the newborn"[40] and revered and mourned their death. Thus, flourished a sentiment of altruism and philanthropy with regards to the value of a person and thus a capacity for compassion.
Subsequent to the primative and ancient times, there has been shown reverence for the fetus and newborn accompanied by the appropriate processes of bereavement , yet there has also been irreverence; contrasts of beliefs and rituals abound. At one extreme, the aforementioned infanticide; at the other, a desire for large families and the blessings of fertility.[41] The Dark Ages, Medieval times and even the Renaissance were among the darkest periods in the history of women and child bearing. Obsterical practices were filled with cruel and hideous atrocities. So many fetus' and newborns died from disease and obstetrical disasters that to mourn them was felt too burdensome and overwhelming for the families. Evidence of high rates of mortality among children can be seen by observing those buried in Medieval England cemetaries. Among two such cemetaries, more than fifty percent of those buried were children and the largest single category was children aged 0-5.[42] Found there also was evidence of the burial of fetuses.[43] Contrary to these formalized burials, there existed religious and cultural customs in which funeary rites were not observed for the miscarried fetus, stillborn or newly born infant. There were "secret (Christian) burials of un-baptized infants…excluded from the confines of the church cemetary".[44] Early Jewish law, in an effort to spare parents the "pain" of mourning, restricted acknowledgement of the demise of a fetus or newborn to thiry-one days or more and these children were not "accorded full human status". [45] The Yoruba tribe in Nigeria would thow a dead baby or stillborn in to the bushes fearing that if the dead baby was to be buried in the ground, it would offend the earth shrines of fertility.[46] Paradoxically, Hindu newborns and stillborns were buried so they may return to an "earthly life".[47]
"Just as despair can be given to me only by another human being,
Hope too can be given to me only by another human being." [48]
Perinatal loss entails a "unique bereavement" and is an "exceptional" type of loss. While "the death of a baby is a catastrophe and a tragedy which shatters the good, secure and confident life in a matter of moments," the sharing of feelings of such profound loss with others undergoing similar losses, a "community of loss" ,can actually beget a healing experience. Healing must take from the despair of our grief its thoughts, memories and tears and within a framework of inspiration, introspection and time, transform this grief into promise and hope. My approach to healing this penetrating perinatal and neonatal loss with my patients is by the use of three modalities:
Healing the spirit through language that is poetry.
Healing the "loneliness" through communication
Healing the body and mind through medical care and information.
What follows are thoughts gleaned from the roots of my soul written on occasions of death, futility and desperation, words and poems of dark themes written with embers of hope amid fires of love-love for my profession and for what I really care; an attempt to strive for the “happiness of others”[49], even in the darkest of their hours. "To know the worst and write in spite of that, that must be love.[50] Poetry and words written from such love in a muddle of frustration and despair, “gathers up hope” in the art-form of language just as the physician with stethoscope, scalpel and pharmacopia does in the art form of medicine. Healing thus springs from the complementary remedies of poetry and medicine. Exposing the soul to clear view, the poet speaks by acknowledging weakness. He writes what he feels when he can do no more.
Poems become “words against death.”[51] "The poet exploits the cadence of our language [sic]"[52] to feed the soul with beauty. The words of the poem not only must "sound" but must speak."[53] Y’haudi Amachi, the great Israeli poet feels "that every poem should be the last poem, written as if it contained the last thing the poet would ever say, shaped to contain the condensation of all the messages of his or her life. It should be a virtual will."[54]
As a physician-poet I write my words -for myself and for my patients-when I have been left void of other means of expression. As a collection, I have entitled my work, “Cherished Purposes" and these poems are presented in their entirety, encompassing nearly a decade of work.” I have lived by these two words, "cherished purposes" from the time I was a college student in Philadelphia, searching for meaning, for a purpose in my life. Chiseled in a statue memorializing the bravery and the spirit of the soldiers of the Civil War, they were chiseled in my mind:
Each for himself gathered up
the cherished purposes of life;
its aims and ambitions;
its dearest affections;
and flung all with life itself
into the scale of battle.
Anonymous
I choose to interpret these beautiful words freely and have applied them to my life as standard-bearer for my resolve and commitment to search for meaning. They have been a watchtower for me and in turn are meant as a watchtower to those who must grieve these tragic losses.
Poems are not just feathers drifting into the Grand Canyon;
They can make a real connection with another mind and heart.[55]
Netzah
[Eternity]
Could I have died so soon,
So soon that my cries
Were silenced in your womb?
So soon that I'll never touch
Your breast nor feel
Your hands caress
My brow?
So soon that you never got
To sigh and cry
Sweet tears of joy,
For your first child,
Your first born boy?
Could I have died so soon?
I suspect not,
For I felt the passion
Of your love around me
As my heartbeats slowed,
Then stopped.
As I lay motionless,
I heard the misery
In your cries that
I would not be born alive
And wondered, why?
Yesterday father, you fathered me.
Today dear mother, you birthed me.
I was there, You were there.
We all stood witness.
I heard your whispers,
That you love me.
I heard you tell each other
How beautiful I was viewed
In my eternal quietude.
I even felt your soft caress
As you held me to your breast.
On this morn, mourn not for me.
With ethereal grace I have a name.
I have a home, I have a life...
To live through all eternity.
Netzah, one of ten fundamental forces or Sefirot of Jewish Mysticism , means eternity and represents the conquest or capacity for overcoming. Alexander died in utero one day before his birth. The cause of his death was from a true knot in his umbilical cord. After the birth, his mother and father and family held him for hours, in love. I read this poem at Alexander's memorial service.
Hope
When roses lose their loveliness
When rivers cease to flow;
When sunlight fails to warm the air,
When stars no longer glow.
When birds cannot take to flight,
When a ruby's luster fades;
When leaves refuse to fall from boughs,
When trees cannot give shade.
When fields of flowers wither,
When clouds cease making rain;
When mountain ranges cast no shadows,
When prairies cannot grow grain.
When these natural wonders end,
When there's no dusk or dawn;
When all life's miracles cease to be....
...Only then will my hope be gone.
This expectant mother had a miscarriage in her fourth month of her pregnancy, after five years of
infertility and several cycles of in-vitro fertilization. She has no children at home and is determined to continue her quest for a child.
Aurora
Part lost is my soul,
But not lost my hope.
My strength still remains;
I am able cope.
For on this day
When my child has been taken,
I look towards the heavens.
I've not been forsaken.
The sun darts back
And forth in between
Clusters of clouds,
Yet few shadows are seen.
For there shining through
Is a hope which will brighten,
And fade all the sorrow;
My burden's to lighten.
The indelible trauma of the demise of fetal life. If this happened one time it would be too much. This patient endured two unexplained fetal deaths and felt she would not surrender her faith. She had a healthy son one year after this last loss.
Gemini
Behold my body cares for a
wondrous
Harvest grand and full.
Two beings longing for birth
With one singular purpose,
To reveal their soul.
With delight in my womb
I yearn to touch and cry.
And when birth arrives,
A passion I'll consume
And behold my Gemini.
Gemini , twins in Latin, and in
classical mythology "great twin brethren." This mother
was exposed to DES and had multiple miscarriages
because of a weakened cervix[incompetent cervix.} When
she was pregnant with this twin pregnancy, she had a
suture placed like a purse string around her cervix to keep
it from dilating prematurely. She remained at bedrest
throughout her entire pregnancy and delivered twin
girls at full term.
Betrayed
Liquor about my child
Entombed,
confined within
My faltered womb
How you betrayed all my
Life's hope.
Yet it is hope
That will befriend and bath
her primal soul
With sweetness to
Eternity's end.
All too often a mother will have a disorder of the
amniotic fluid leading to perinatal loss. These
unexpected and disastrous events led me to write
these lines.
Brook
Summer breezes sway the poplar,
As I walk the banks with my new daughter.
Recalling summers spent in sorrow,
In fear I'll forever walk without her.
But through the seasons of this year,
New hope was born, without that fear;
My body pregnant, filled with life;
No more sadness, no more strife.
And in awe, my eyes did see
Her image as she was born of me;
Ruby cheeks, down-like hair,
Eyes aglow, skin so fair.
Thus I turn to thoughts of Summer,
When breezes blow and sway the poplar
When I walk and talk and look
At my beloved daughter, Brooke.
This mother had multiple pregnancy losses as a result of the antiphospholipid syndrome and no living children. She was at very high risk for another loss, but delivered Brook, healthy and beautiful.
Jordan
Listen all to the music of trumpets,
Of harps; of lutes.
With harmony they announce a joyous birth.
Her namesake a river whose banks
Of fertile soil caress the ripples of its
Vital waters. Her life full of wonder,
to flow endlessly, yet willingly,
Into larger seas with unknown boundaries
And infinite depths.
For as the river flows out from the wilderness,
So from our bodies her life began;
With love and hope,
Our angelic daughter, Jordan.
This beautiful baby girl was born with Down's syndrome. Her brother, born one year earlier died of
congenital heart disease. (See Cameron) Her mother is the epitome of courage and strength.
Tralee
Not far from where the Shannon flows
Lies the village of Tralee,
Rejoicing the birth of Emily Rose,
With simple serenity.
A beautiful being born this day,
A traveler who's traveled the journey of birth;
A miraculous Odyssey for which we have prayed,
Greater than any on all the Earth.
So with a passion that cannot be rivaled,
We hold dear to our hearts,
This young child of ours,
And bless her for life, our very beloved,
For one full of song, sunshine and flowers.
Dedicated to Emily Rose, born after many years of her mother's infertility. Tralee is a small village in Ireland that each year holds a majestic Rose festival.
Madeline
Alabaster columns of sunlight, gleaming,
Illumine the darkness of this day.
Nightmares turn to peaceful dreaming.
Awesome fears fade far away.
Though now my soul no longer dwells,
Upon the world as I have known,
Still I live beyond the pastel
Elysian fields, are now my home.
Weep no more for me, beloved,
For I can sense no pain.
At one with God in heaven above
You; I'm at peace, and at peace shall I remain.
Commencement
I bear today
A countenance of promised dreams;
Sanguine visions sweetened with
May-time baskets
Of floral scents and sights
To smile upon the face of
Spring's delights. And while
The frosted tears of winter's cry
Melt and flood the
Mountain streams,
I pause to wipe the joyful tears
I've cried
For my daughter's life and being,
And her countenance of promised dreams.
A poem for a daughter
Futility
With caring hands he touches mine,
And tells of my lost dreams.
Melancholy surrounds me.
No longer lives the love
Which I've proclaimed.
No longer lives the dream
My mind has seen as
Misfortune now comes to my
Heart where only Joy should
Rest.
This young women had just endured her third consecutive, unexplained pregnancy loss.
Dawn
The body in anguish to create,
And the soul, cry out for birth.
Then, you're born; not yet of age
But whole. You cannot speak but your
cries are heard as your mother wipes
her tears and smiles.
After many years of infertility and pregnancy losses, Dawn was born. Her birth was complicated by premature labor and fetal distress, and she was born emergently by Cesarean section. She weighed but four pounds at birth and is now ten years old.
The Rain
Around me falls the silent rain,
Dark clouds sound the thunder.
My body's failed me once again
Can I endure much more? I wonder.
A weakened mind cries out for mercy,
A stronger heart...it quests for hope.
There is no sun- today is dreary,
A shroud of mourning does envelope.
The wrath I sense cannot be stated
In words that one can understand.
All good feelings have now abated,
My tears I wipe with weakened hand.
Fields of lilies grow this spring
They bloom in all their glory...
Yet for me there is no life to bring
My child is but a memory.
Only despair was felt by this patient whom after two earlier miscarriages and one ectopic{tubal} pregnancy, carried this pregnancy into the twenty -second week and without warning, was found at her routine visit to my office to have a fetal death.
Hymettus
Softer than the softest rose
are the clouds on which I sleep.
Sweeter than the springtime honey
are the thoughts that I now keep.
Farther than the farthest star
is the home where I shall live,
Deeper than the greatest love
is the love I've yet to give.
A love that is immortal
and will grow with each new dawn.
What in our lives we shared together
will remain to be reborn.
So grieve no longer upon my death,
my soul is still; at peace.
I suffer not upon this journey;
my ascent to ethereal grace.
Hymettus is a mountain in Attica, famous for the sweetness of its honey. This poem is for a husband whose young wife and mother suddenly and unexpectedly died.
Colleen
Two spirits flood
My mind and soul
With abundant passion.
A legacy willed to me
Eternally, to bestow
An inner sense that I belong.
I possess a gift,
Grand and sweet like the
Gentle sound of the dulcimer's song.
Perfect, yet simple:
The blessed beauty
Of my parents' love
To endure forever.
1992
Just prior to Colleen's birth, her two grandparents died.
Cameron
I no longer see the stars; I am the stars.
I no longer breathe the wind; I am the wind.
I am the sweet smell of honeysuckle after an
Evening rain.
I am the dew on the rose petals in early
Morning.
I am harmony and I am peace.
I am love.
In sorrow, my mother and father cry,
But they need not fear. For I am strong.
My heart is whole and in union with my soul.
I understand my fate and I smile.
For nature's will is my destiny
And my guide through eternity.
After years of infertility, Cameron was born only to die soon after birth of congenital heart disease. Unlike most forms of congenital heart disease, Cameron's was inoperable and fatal. His courageous parents were with him every moment of his short but love- filled life. (see Jordan)
Pax
Far above the obscure shore
The sky cast forth a" darkness visible"
That speaks your sadness forever more,
Of a loss that's ever so insensible.
But above these clouds where the sun beams glow
With no shadows to cast or eclipse,
My soul lives on; I feel no sorrow
For in my world, I still exist.
To those who love me, I feel your love.
There is no pain, I am at rest.
I have my peace in this heaven above,
And with your prayers I am forever blessed.
Written for parents upon the loss of their son, David.
Ventose
The chilling winds of March do blow,
As on this day we mourn.
And from our eyes fresh tears do flow,
...our child will not be born.
With God's consent did she ascend,
To his Empyrean throne,
A refuge surely to transcend,
This grief we feel at home.
So as the 'Ventose' winds abate
And springtime flowers bloom,
We know her soul is incarnate
In Heaven's immortal womb.
Empyrean is the highest abode of God. Ventose in French represents the March winds. This pregnancy terminated in the fourth months after an infection developed in the uterus.
Megan
Every cell in my body cries.
I want to reach out, embrace you and
tell you I care.
I feel your pain, I know your needs,
but I cannot find a way to comfort you.
I watch the sun at dusk and sense
its strength, And know it will rise again.
For a patient whose child was ill at birth and survived.
Immortality
Arise from behind your shadowy cloaks,
Sinuous branches of olden oaks,
Reveal thy life and thy glory;
Your luminescence of immortality.
Forever have you shown yourself
Upon this earth where mortals dwell,
To remind us we live for eternity,
If not on earth then heavenly.
With lenity and grace you comfort,
When from our loved ones we must part.
You give us all the strength to bear
The formidable burdens of our despair.
And a lessening of our sorrow,
As we live, love and delight... beyond tomorrow.
Written for a young mother who died of ovarian cancer.
Silence
No longer do I fear my death,
For my weakened body now reborn,
Will witness every dawn of every morn
That is yet to cast itself upon
The remnants of my past.
And thus the light above me now,
With rays aglow in silent symmetry,
Will forever shine far into that eternity
Where I will be
At peace.
Sidney
Clothed in winter's vale of lace,
Stands an aged tree.
Awaiting springtime's youthful face,
To birth its hues of green.
Yet here upon this winter eve,
A birth did not await.
A daughter whom from love conceived,
Born pure and delicate.
Her father's hands were first to touch,
This soft and graceful form.
A special being to love so much,
And rejoice with each new morn.
So as the snow drapes on the boughs,
Of olden elms and oaks.
Know well this child of winter now,
Is blessed with spring's new hopes.
After having a pregnancy loss, this mother conceived. She went into labor at home and did not have time to get to the hospital. Her husband delivered his daughter Sydney by himself at home.
The Vow
Sapphire waves besieged the shore,
With fury calling at my door,
For me to join them in retreat.
But not yet ready for defeat,
I spurned their request
And went onwards with my quest:
To live and love with you.
With my life at last fulfilled,
I have succumbed to natures will.
Now tranquil as the ocean's depths,
I feel a peace here after death.
My spirit's strong and remains whole,
For I vowed this vow within my soul:
To live and love with you.
Amaurot
"All we know
Of what they do above,
Is that they happy are,
and that they love."
Edmund Waller
If I could wish myself a dream,
It would be to retreat for a lifetime and hide
From a world of unjust suffering
Where mankind's afflictions and pains reside.
I'd labor to quarry limestone and granite
To fashion for my very own
A sanctuary to spend infinite years;
Eternity would now be my home.
I'd cultivate gardens of forsythia and violets,
Plant olive trees and harvest grains;
Grow apple orchards and grape vineyards,
From their full bounty would I be sustained.
Of lyres and harps there'd come splendid music,
Beautiful children would dance and be gay.
Sadness and crying would never bear witness,
Illness and sorrow would remain far away.
You'd be the first to visit my home,
Sweet child whose earthly life has been taken.
For here you would live and love and be blessed,
With God at your side, your eternal beacon.
Amaurot is the fictional capital of Utopia. I wrote this poem in memory of a child born with a most
devastating birth defect and died shortly after birth. I have dedicated this poem to her and all children who have died.
Sonnet of Faith
Appareled in a veil of grace,
Angst and despair showed its face.
Yet from your eyes a gleam did shine,
A hint of nature's grand design.
To teach us all that we must cope,
And never lose our faith and hope.
That all things bad and all things sad
Will be eclipsed by what makes us glad:
Love and trust in one another.
Wholesome values as father, mother.
Embracing our children sweet and fair,
Holding their hands, combing their hair.
These are the flames that within us burn,
The passions strong for which we yearn.
So while today your loss brings drear,
The morrow's sunshine will again appear.
Written for a young couple who
underwent a termination of pregnancy for a lethal genetic
anomaly. They had a wonderful understanding of each
other and a devotion to their three old daughter
that allowed them to face their bereavement with
strength and hope
Saline
I grasped his strong hand
weeping edema beneath
mottled skin and
pulsed coded messages.
Then with a kiss
placed gently upon his brow,
withdrew, and said good-bye.
Around us, aprons of sand
embroidered shores of saline oceans.
Inland, grasses wove their tapestries.
Grains, blades and salted pools mingle;
reservoirs for creation,
repositories for death.
Silent is our morning's song,
lost our morning's glory.
The grasses, stilled by quiet winds sleep
day-long now. Rays of crimson sunbeams
like thorns, pierce
the clouds of our despair
as our dissonant cries fade
into nothingness.
Windows
Gather
every morsel
of hope,
precious gift,
and open your eyes
to its wonder;
common images
earthly sights
hourly routines
that maintain
the equilibrium
of why and how
you live
and lived.
Delight
in what are your joys
and then
for just a brief moment
let them close
to the darkness
and paint
upon the canvass
of your soul
portraits
of secret longings
that come alive
in these minutes
of solitude
called dreaming,
art forms to dance
from the palette
as you revel in
this secret world
of unspoiled vision
and immortal promise
Obsidian
My shrouded body
lies interred in frigid
caverns of blackness,
as you mourn and fear
the coldness of my death
and the abyss
of my nothingness.
But neither barren
nor alone nor pained
am I, or will I be
for as the midnight
at full moon, I'll gleam
God's light
through all eternity.
The Tree
Be free
Imprisoned one,
Last remains
Of a fallen tree
Fractured by an
August storm,
Sapped and devoured,
Hollowed from decay,
Destitute of life's
Precious humors.
Debris encrusts your
Body like a death shroud,
Yet the poet knows your
spirit,
The artist your beauty.
Be free.
Rhapsody
Gone are ten thousand days
of perfumed winds
bellowed from the
lungs of God with
gusts and drafts that
scattered wandering seeds
of despair, craving
earthen roots to anchor
their promise of reborn
hope.
Sorrow Fades
Your cries sing of
past sorrows,
Sing no songs for me.
For my heart lusts to
live... tomorrow, And my
soul longs to be free.
No longer will angst
befall you
When at my birth you hear
The cries I sing of life anew,
And you kiss away my tears.
The Morning Dove
By reason unexplained
came the wrath of nature's
will and pain upon an olive tree,
to cleave unequal its fair soul
and hurl each fracture into
stormy destiny. And as time
and hope and prayer
within an earthen womb
nurtured tendril branches
where buds and blossoms bloom,
I cried, for I was first to
see a morning dove bear a leaflet
in the Spring and fly
homewards... for eternity.
For a mother and newborn both critically ill at birth but in time were healed. The newborn was delivered
at twenty- four weeks gestation and weighed one and one half pounds at birth. I witnessed his growth to four
pounds when he left the hospital for home.
Sean
The moon's thin crescent
casts dim spears
of speckled light upon the
path I walked this night
with your hands in mine.
And although darkness
hovers close above our bodies,
warmed with dew's sweet tears,
you turn you eyes to mine
to see the embers shine
and burn to ash all despair
within the abyss of my soul
and praise tomorrow's scented air
I breath, for now my body's whole.
Spire
From oblivion to infinity
without origin or finality,
our minds petrify like fossils
ancestral passions
to consummate all life's promises,
while above us windsongs cleave
one cloud in two,
two to four, four to eight
and create
infinite dispersions
so we may see
stars flicker,
moonbeams' shadow
sentinels for sunlight's travel,
...and watchtowers for the treasures
of eternal hope.
Divus
I loved
the quiet time I spent
when every heart beat
you had sent
to my flesh
and to my skin
flowed forth to bring
me peace within
your silent womb,
...I loved the silent time.
And even as
my tiny heart
labored at death's call
before my start
at birth and life,
and as I ailed,
soon no longer
to inhale
or feel your pulse to mine,
...I loved the quiet time.
My body now
apart from yours,
still lives, yet not
upon your shores,
and suffers not
nor is in pain
for within
its new domain
I can love the quiet time.
...I loved the quiet time.
Divus is the Latin expression for a Godlike, blessed memory. This poem was written for and given to a patient whom I had not met- until she came into labor and was found to have fetal demise.
Yekhida
Thee,
I've touched
and kissed,
and loved you...
... now I
float in
clouds
above you.
Memories
please me
from my
past
transparent shadows
purely
cast.
Though my
corpse
on earth
remains
My spirit lives
in this
domain...
...And like a rose
in desert's
sun.
A miracle
is what
I have
become.
A prayer of hope for immortality. In the Kabballah or study of Jewish Mysticism, Yekhida is the ultimate union of the soul with the essence of the Divine.
The Mist
When winter's gloom succumbs,
and grief melts in the sun,
warm currents on my breast will stream,
and turn frosted tears to sunbeams...
Sadness moistens my brow like
mist.
Silent tears coalesce upon my cheeks.
Petrified by the cold of winter,
Forgotten by the spring thaw,
I shiver and feel lost in this the season of my sorrow.
Loss has embraced me more than
once, yet it has never seized me.
Hope has been my reclamation,
My emancipation,
From the bondage of despair.
Hope exists in the swelter
Of summer and persists
As the leaves fall in November.
Hope thaws the snows of winter.
Hope does not forget.
Six pregnancies, one child. This poem is written for a wonderful and courageous mother and father, desperate
to have another child in face of overwhelming, medical problems.
Birth
I have seen the caul
like honey glazed
contain and bathe
in sweet succor,
kept watch as
mother's wombs
tear in pain to
bear their child
and then
as if my first,
stood aside and
cried with awe at
the birth,
that quiescent harbor
where life sings
“psalmic” verses
of calms and storms
rains and draughts
sun lights and dark nights,
agendas to live on forever.
1993
This states best as I can the overwhelming emotion I feel, day by day as I attend births.
Courage
"Until the day of his death,
no man can be sure of his courage"
Jean Anouilh, Becket
He was a being in search of his destiny,
And with abundant virtues and dignities,
He filled his days with endeavors of selfless devotion.
A sage with a love for mankind,
He cared for the needy with reverence.
Though the sorrow we feel is deep,
We must not share in his suffering, but
Triumph over his death by committing our
Hearts, our bosoms, and our most visceral spirits
To profound purpose.
Yes, stand tall, thy men of courage,
For a leader amongst us has fallen.
With gallant humanism, and valiant resolve,
He leaves Our mortal plains and hills of despair
To ascend his mountain peaks of glory.
With his inspirations of vitality and hope,
Everything was beautiful and good.
We lament his short life, yet find comfort that
His mortal being was but "a fleeting gleam"
Between two eternity's of tranquil salvation;
Be comforted; for now, His soul is at rest,
Cradled in peace.
Written for a friend and colleague upon his death. I consider this man an ultimate caregiver and healer.
Andira
Beneath their feet the parched leaves crack.
Lifeless, fallen branches fracture.
Wearily fathers hunt and search
To mend the pains of endless thirst.
A mother cradles to her chest,
The newborn child upon her breast,
And while gazing towards the cloudless sky.
Asks why be born if now to die?
Wasted by their arid land,
Children beg with outstretched hand
Their feeble voices impotent,
To cry; A Death-Watch all too silent.
Hunger cries but finds no ears,
None to help their doleful tears.
Impoverished people bearing sorrow.
Starved today; entombed tomorrow.
Andira is a genus of tropical tree found in Africa known as a "rain tree". This poem is written in memory of all children who have died and are dying from the ugliness of starvation.
The Din
a clamor.
louder
than the searing noise of
jackhammers,
trucks, motorcycles
and the like,
pains my ears:
gunshots and sirens,
screaming mother's tears.
murdered teens-
just children you know,
dead now over some drug deal
or gangland ego.
a disordered, senseless waste
of human life and vigor,
granted to every person of every
race,
by god's decree
of just equality.
yet of those who escape
the leaded missiles
from wanton guns,
or needles
infected with contagion;
of those not starved
for food or love
or for learning;
nor for clothes
or shelter or for yearning
to have a solitary chance
to breathe
per chance.
the fresh air of a country
morning,
i ask:
"what is it you fear,
what clamor do you hear?"
For those who can see and feel and fear the horror calling at our doorsteps.
Asclepidae
From Hippocrates
On whom we swore
And Aesculapius
Who thus bore
Hygeia, we now
With dutiful dedication
Somehow
Must manage to transcend
A myriad of extrinsic forces
With one purpose: to mend
The bleeding and the cries
Of our diverse patients' lives.
We birth their children,
Curette their wombs,
Remove their tumors,
And for those whom
Maladies cause pain,
We set upon a course of healing
So that once again
Their being is restored.
But there is much more,
So very much more.
For the primal core
Of what we dedicate
Our time and strength
Is not just to operate,
Or to "stand before" and facilitate
The births of tomorrow's children,
But rather to provide
True counsel;
To advise and to guide
Through the darkest paths
In the deepest forests
Of our patients lives.
For when they face us,
Stare, eye to eye
And mourn their loss
Of health, of parent or of child;
When marriage dissolves into divorce,
And depressive thoughts of suicide
Bring them to us
And us to their bedside,
We must be skilled with more
Than laser or with knife.
We must be filled
With integrity and
compassion,
The moral virtues
of our life,
And bring to the ill
Comfort, sympathy and
hope.
1993
The Asclepidae was the Greek Priest-Physician family of which Hippocrates was a member physician and surgeon. This is written as a plea for those medical students and residents who have chosen Obstetrics and Gynecology as their profession.
Aoide
The first song on earth
Was a child's cry,
A canticle of absolute beauty.
Each note a bequest for eternity; Ageless
music of heart-sounds
And first-breath sighs
To immortalize
The promise of humankind.
Aoide is the Greek Muse of Song. These lines are a dedication to the labor and delivery suite of Yale- New Haven Hospital where I practice.
The Harvester
I am a planter in the garden of life
where seeds and seedlings struggle
to dance to songs of the wind and
hide tears in rainfalls of the morning
yet reach afar to embrace the trellace of humannity
and become a harvest of eternal renewal.
Evening's Song
I know the scents of evening's-light,
The sweetness of its songs,
And its taste of honeyed-dew
That fills me as I watch it greet
The fresh first light of dawn.
I feel the silks of evening's-clouds
Caress my weakened frame,
To the music of a symphony;
Resounding, ringing, beating, singing
Tearing at my pain.
Beyond meadows, valleys, mountain-crests,
River banks and streams,
I've known the joys of giving;
Touching, caring, loving,
For this is what I've dreamed.
As landscape's margins meld together
As dusk seams itself with night,
My body mends without it fearing:
...From the deepest darkness
Comes the brightest light.
Longer Days
Today, my senses are paralyzed
In frozen chambers of dismay
As in solitude I chant
Silent notes of prayer.
Like a leafless tree writhing,
I long for blossoms
At spring's first dawn
When the brightest days
Are longer than
The darkest nights,
When the breezes are warm,
And the air is fresh
With the scent of laurel,
When climbs of roses
Bring new hopes to bear
And tears of time
Drown my despair...
...When oblivion is home
To all my dismay.
The Covenant
I am an artisan,
A painter of hues unfading
To blend upon my pallet Infinite promise
And emblazon on my soul
A landscaped canvas
Stretched to infinity
Between pillars of prayer.
Neither stalked nor
Conspired against am I.
Only Fate has been my betrayer.
And although the defenses
Of my mortal flesh have weakened,
The borders of my body
And the cisterns of my soul
Are strong, alive
With pulses of blood
And liquors of hope.
I will not lament
Nor ask of this from you.
I will not know defeat
Or the wrath of any pain
For I, like a solitary seedling
That yearns to taste the falling rain,
Know well that God's eyes alone
Will shed but triumphant tears...
...Upon my brow for me
And for my covenant of victory.
Courtney
A wind rushes about me
fueled by earth and sky
to purify stagnant basins
where thrives the praise
of autumn's last remains,
its gentle rain,
its moonlit frost,
the falling ocher leaves
that cluster in brittle piles
to blanket earthen roots
whose petals now are lost... .
..and I, confined and desperate
to smell the scent of pine
adrift in winter's frigid winds
in darkening December skies,
about to touch the promise gleaned.
Suri
Earthen trails confuse in
Lost loneliness of nightfall,
Darkness that blinds
My path is like shadows
That fleet with the sun
Rising and falling
Appearing and disappearing.
Yet in those aged fortressed forests
Where loneliness and fear
Bring profound blackness
And where despair shivers
Have I found my way
For Oliver, Born of the Sun
Our senses light ephmeral
Like a mist whose song is sung
Upon the glory of the dawn,
And then moments,
Even hours later
Stretches towards
The silvered profiles
Of slivered moons
To watch as scars
Crevice the substance
Of your heart
And mark its passage
To our love;
...And now we dream
As tiny angel breaths,
Warm with endless promise,
Melt to spawn
Infinite acts of faith.
Return
Return home
Upon the long and winding road,
Where etched is your pathos.
You empowered the breeze
To make shadows sway,
Silent voices speak,
And all grace rejoice.
Return home
Upon the long and winding road,
Conjoined with faith,
To dance among the boughs of spring.
..My Heart Be Yours Forever
I make you both a promise In these my infant days,
Half my heart be yours forever,
The other for God- in praise.
For he has blessed me with abundance,
Granted more than I can give,
Never will I feel dismay, ...Your love is why I live.
When you hold me very close,
Your pulse feels slow and sure
Which calms the flutters of my heart
And gives me hope that's pure.
As my parents you are frightened
That my tiny heart is frail
That my body cannot endure assaults
Fate to it assails.
So I must tell you mother, father,
I implore you...be assured
Spirit transcends my adversities
Horizons harbor my cure.
For a baby, Sydney, born for a serious congenital heart defect and who survived and is thriving today.
The Passing Tides
I loved the river:
Enchanting.
I loved the wind:
Caressing.
I loved the daylight:
Soothing.
I loved the starlight:
Haunting.
I loved my ‘dear ones’:
Being.
I am now all I loved:
Blessing.
Butterfly Breaths
Every day awakens
With kisses on your brow;
With mist that veils the early light
And hides the morning clouds.
With butterfly breaths of longer days
Where heard are fewer sighs,
And echoes from a mountain's song,
Dissolving plaintive cries.
No longer will the seasons part
The year; dividing into four.
Now hours blend to days and weeks,
Weeks to months, forever more.
Every day awakens
With visions of what's to be:
Spheres full of joy and wonder,
Timeless moments of Infinity.
This poem was written for a young girl undergoing therapy for cancer of the kidney.
Soraque
(A Primitive Philipine Song)
Winds drift on ephemeral wings
To watch the sun's veil lift.
Distant, darkened skies crack clouds.
Humans cry outloud.
As I kneel to meet my death
Mortal and frail, I fall
With ravaged mind abused
And hide in temples
Of immortal winter sequestered
From one life's end
To the end of all and wait
As infinity becomes my soul.
Obstare
I have stood here before
When birth deceived and
Surrendered to my hands
The very spirit and soul of humanity;
The essence of life, save life itself .
And I have touched before
The angle hair and silken skin;
A child lay bare, still and silent
In these outstretched hands
As my will cried out
To scream a breath of life
Into his pale lips
Now frozen in the mist
Of endless dreams.
Yet today I smile
As I have smiled before,
For from such drear
Comes a voice ;
A voice, so serene
That it transforms
The searing pain felt in
Our hearts into song;
Melting stones of sorrow
Into liquors of love,
Forever a memory
of our dear Child.
Obstare is the Latin root for Obstetrics and means "to stand before"
Love Contained
Music floats on streams
Of summer’s final breath
As rains of hope
Wash famine from my lips.
And now love contained
Within my marrow sleeps
And I am left to dream and wonder
While angst becomes my silent partner,
Dueling with the rain.
I love the music
Which floats on streams
Of summers final breath
And hear it even as
Sadness mutes its song.
For its rhythm is certain
As the pulse of my heart;
Its voice everlasting,
As my memory is long.
This poem was written for twin boys, Andrew and Joseph, who died before birth. It was recited by their courageous parents at their sons' memorial service.
Return
For Anne
Return home
Upon the long and winding road ,
Where etched is your pathos.
Empowerig the breeze
To make shadows sway,
Silent voices speak
And all grace rejoice
Return home
Upon the long and winding road,
Conjoined with faith,
To dance among the boughs of spring.
Zachary
Where golden swans and princes dance,
.My prince has danced.and dances still
As my heart with fire burns the pain
And turns its acrid char
To sweet and boundless faith
Which love cements from flesh to flesh to soul,
Dear prince who danced and dances still.
For a newborn who died of multuple congential anomalies.
Decent...Ascent
My face droops, chiseled
with furrows of sadness.
Eden is no longer.
Trust teeters
tenuously in anonymity.
Ignorance,
Poverty,
Desperation,
Cohabit; irrational and violent.
Sickness lusts. Death waits.
I tremble
Yet, steadfastly will I climb,
season to season,
for a lifetime,
amidst tendril roots and ragged
crevices,
in search of reason,
and when weary and my flesh aches, and
heart hypoxic hungrily palpitates,
my sight dims
and body falls painfully sick,
I'll travel obscure atmospheres
glancing back to see
past images appear
of life's fine threads and
loves unspooled, with
unimagined clarity
and pause, alone
upon the threshold
of my empyrean home,
and whisper prayerful
thoughts
to heal my wounded soul.
Despite anguish, pessimism and oppressions , there can be discovered wonderment and hopeful optimism throughout the course of our lives.
Gone
Everything was beginning to seem so perfect.
Just him and me
And Baby makes three.
Had a lifetime of dreams and plans
Wrapped up in this little one.
But, suddenly, all hope was gone.
One morning it was clear,
No kicks, no heartbeat.
Nothing,
So Still.
Silent, she would come into the world
Taken without a sound.
Never to live on the outside,
Her crib - the ground.
The doctors said
There was northing I could have done.
There were no tell-tale signs
Of something wrong.
A bad heart all along.
She seemed so healthy and strong one day
But, the next day, all hope slipped away,
Without warning, she was gone.
Sarah
I miss her.
Why isn't she with me?
Wish she were here,
Or I was there,
Wherever that might be.
SARAH,
With hair so black,
Tiny hands and long nails,
Skin too pale,
And lips too red.
Sarah,
Where is she now?
My pretty baby girl.
I never got to hear her cry.
Why is my baby forever silent?
Why did my daughter die?
Sarah,
Am I so terrible?
Did you not want to be with me?
Did you think I didn't care?
Are you somehwere safe and sound?
Is there a Heaven?
Or are you nowhere?
Sarah,
When I remember her,
I see nothing worth what I endured.
Nothing that I'd wished for,
Nothing to love,
I close my eyes hoping,
Praying to see black,
Instead, I see Sarah.
Did I do something?
Two Poems for Sara by Jennifer Goins-Caufman
To the Child in My Heart
Precious, tiny, sweet little one
You will always be to me
So perfect, pure, and innocent
Just as you were meant to be.
We dreamed of you and your life
And all that it would be
We waited and longed for you to come
And join our family.
We never had the chance to play,
To laugh, to rock, to wiggle.
We long to hold you, touch you now
And listen to you giggle.
I'll always be your mother.
He'll always be your dad.
You will always be our child,
The child that we had.
But now you're gone...but yet you're here.
We'll sense you everywhere.
You are our sorrow and our joy.
There's love in every tear.
Just know our love goes deep and strong.
We'll forget you never-
The child we had, but never had,
And yet will have forever.
Author Unknown
For Eric
Hello my precious baby boy,
How little did I know,
I would never get to hold you,
Or the chance to see you grow.
You see my son, we bonded,
Those six short months of time,
I carried your life, I felt you move,
That humming yhou heard…was mine.
I guess I never told a soul,
How much it hurt inside,
Or that I walked around the block,
Ten-twelve times…how I cried
Within my heart, a special place
Meant for you alone,
A memory of love-Eric,
The son I wish I'd known.
Laura Mc Donald
My Angels
I have cried from the depths of my soul for you my lost children
There have been days when all I wanted to do was die
I re-call your memory more than ten times in a day
And still I do not fully understand why we had to part
I questioned time and again every move I made
Did I so something wrong to cause you to go?
Were there things I should have done that I didn't?
Would you still be here now had I not worn those clothes?
Before your leaving caused me great pain,
The knowledge of your being brought me hope.
I looked to the future with optimism for a change
And bounced round the house like a fool!
You are always with me deep in my heart
You memory, never will it fad
There are still tears that I cry for you both
But I know you are now somewhere safe
My two little angels of joy
No more can we be together
I still feel the pain of our parting
But your memory lives on forever.
Sheryl McMahon
My Precious Baby
I’ve watched many trees blow in the breeze
since you were taken from me
I’ll never know how you would have looked
had you had the chance to grow
To be a child, a teenager, an adult
Untimely taken to a greater place
The reasons I’ll never understand or truly accept
But my love for you will never end
the yearning, aching still here in my heart
Yet you blessed me so much
Just to know you were once alive
Now resting in peace some place else
Sheryl McMahon
For Baby Coxon who left us at 10 weeks into my pregnancy 17
December 1996
If Only…..
Quietly I remember you
The tears still come
I can’t leave you back there in the past
I’ve carried you in my heart all these years
Wanting you to be back in my arms again
My baby girl
Life changed so much once you had gone
If only you could have stayed
Shared more days and had more cuddles
Watched the flowers grow
If only…….
Sheryl McMahon
For Alison Hannah Born 4 May 1985, died 5 May 1985
My heart still beats, but am I alive?
My heart it still beats, but am I alive?
Did not my soul go with you when you died?
Silence, tears and a broken heart
Are what was left for me
I never heard you cry, you were too ill
Unable to breathe unassisted
A machine was your lifeline for the few hours of your life
Everyone tried to console me
But all I wanted was you back in my arms
How could they understand, they couldn’t feel my despair
Seen my world come crashing down
There has never been a day without you on my mind
How tall would you be now?
How pretty? The colour of your hair and eyes?
My little girl you will always be
There will never be a day without you on my mind
Sheryl McMahon
For Alison Hannah
Written in 1998 after the birth of my son Jacob. I still feel the pain .
Baby Alison
When the words were spoken
Words not wanting to believe
We had to say goodbye to joy
We were left alone to grieve
Our baby’s life was ended
Our love, our pain just grew
The anguish, tears and disbelief
Could this agony be true?
One day we had a treasure gift
Her suffering came to an end
A brave little angel, a memory now
A lost, beloved friend
Take away the tears from my eyes
Give me back part of my soul
A life, a treasured part of me
Until then I will not feel whole
In memory of my second born daughter, Alison Hannah McMahon. This poem was
published in the Autumn 1997 issue of the Miscarriage Association’s
Newsletter along with my story.
…..
My Pretty Little Girl
Since your birth twelve years ago
There has never been a day when I haven’t thought of you
I have hurt every day for the loss of you
And still I cannot let you go
I want to have you back in my arms
There are so many things I have wanted to share with you
teach you, laugh or cry about with you
Sadly I have lived through these years still grieving
I ache so much to have lost you
I was so happy and proud to have brought you into the world
Then I had to let you go
I thought I would die the pain was so raw and deep
It always seems like yesterday to me
Even now I can feel you in my arms
That small, beautiful girl I longed to bring home to love
My love is always yours, Today, Tomorrow, Forever
Sheryl McMahon
For Alison Hannah . Written 1997
For Alison Hannah
When the words we spoken,
Words not wanting to believe
We had to say goodbye to joy
We were left alone to grieve
Our baby's life was ended
Our love, our pain just grew
The anguish, tears and disbelief
Could this agony be true.
One day we had a treasured gift
Here suffering came to an end
A brave little angel, a memory now
A lost, beloved friend
Take away the tears from my eyes,
Give me back part of my soul
A life, a treasured part of me
Until the I will not feel whole.
Sheryl McMahon
Still Life
To those women who have lost a child,
May your sorrow fade and your courage grow.
There is something missed tonight
a lost presence among us
a wail that winds down all halls
the air waits to fill you
someone silently counts your fingers and toes
We whispered for you
swimming in that dark pool
you must have heard us
the chant rising in our throats like thunder
building before a storm
rumbling over quiet houses
praying for light
You left without a sound
before the ache of loss
the joy of a full belly
without being kissed and tucked into bed
I picture you as a child
giggling into summer grass
your fingers sink pleasantly into dirt
and your laughter is bubbling and deep
hurled into the sky like a baseball
I will watch for you in the blind of the sun
and in the rippling of a quiet lake.
Lisabeth Marie Smith
Don't go there
"Don't go there,"
I warn myself.
But it is too late.
Even after all these years
My eyes well up with
Tears much too easily when
I travel to that part of my
Self which has been
Scarred by the pain and hurt of
Infertility.
I take comfort in the fact
That I am now only a
Visitor to this place of
Profound sadness;
A witness to a time that has,
At once, challenged my very being,
And, in the end,
Changed me
Forever.
Debra Kasowitz-Sachs
Sometimes
Sometimes,
In the quiet cool of an Autumn day,
I journey
Deep within myself
The ticking of a mantel
Clock keeps pace
No map or compass
To guide me
I wander cautiously
Through layer after
Fleshy layer of
My self
Each determined footstep
Conjuring up the Vulnerability of life
And the sweet soft sadness
Of my season.
Suddenly,
Abruptly
I retreat from this
Panorama of pain
No longer wishing to be
Part of its scenery.
Debra Kasowitz-Sachs
"…Sorrow which is never spoken
Is the heaviest load to bear." [56]
When I read all the stories about all the pain and heartache that is felt worldwide it saddens me but in a way comforts me knowing I am not alone. Strangers we may be, but yet we are connected by a common thread, the loss of a child, and that makes us all soulmates.[57]
This poignant expression of the value of sharing loss comes from a visitor to my internet program, Hygeia®. Before electronic mail became available; before bereavement support groups became international foundations[58], the only means for a sharing of feelings was through the personal contact with friends and family members, medical personel, clergy and bereavement counselors, either alone or in a group setting. Electronic communications, in form of internet e-mail, has established itself as an important medium if not the paradigm for contemporary communications in that it enables its users to communicate and share world wide, irrespective of geographic borders and demographic differences.
Communications is the web of human society. The structure of a communication system with its more or less well defined channels is in a sense the skeleton of the social body which envelops it. The content of communications is of course the very substance of human intercourse. The flow of communications determines the direction and the pace of dynamic social development.[59]
Although some might argue that communication and conferencing online might disrupt the "socialization and non-verbal cues which accompany face to face conversation-i.e. body language, facial oral expression",[60] I feel that Hygeia and similar online support sites have demonstrated not only the value of electronic communication, but a newly acquired and growing interest in the search of such communication.
We who have lost children are all connected in that way... I never received any counseling, I never read books, I grieve mostly alone and in private, and only in the last month or so have I begun to search the Internet for information/support to help me deal with my loss. [61]
What follows are poems and stories and feelings; poignant and personal reflections from parents with whom I have had contact. Some are my patients; some are my friends and others are visitors to Hygeia®. I have chosen not to indentify the sources or my relationship to the parents in order to emphacize the universality of the bereavemnt process and protect their privacy. The selctions I have chosen reflect most passionately the sense of sorrow which accompanies the devestation of parenthood lost as well as entrails of hope which thankfully follow. I have edited the "stories" so to concentrate on the feelings behind the losses rather than a narritive of the pregnancy history and details. For the most part I have omitted the actual diagnosis of the loss from the narritive (although it might appear evident) but have included all diagnoses, medical definitions, explanations and insights into the etiologies in the appendix and glossary. Many other works about pregnancy loss, mostly written by parents who have incurred these losses and caregivers; i.e. bereavment counselors, nurses, social workers and some physicians, have used stories of loss to "tell a story." I have chosen to explore the "feeling" of the stories so the reader may grasp the universality of emotions inherent in these untimely deaths, no matter the cause or medical history. Although I did not set a finite number of stories to include, my intent is to emcompass most kinds of perinatal and neonatal loss which have experienced by parents. The reader who has lost a pregnancy or child will most likely find a story and/or a feeling very similar, if not identical to their own. As the stories are read and re-read, they appear to become as one, expressing common thoughts and common feelings, sharing common words, phrases and sentiments all which trumpet the pain of each author-parent. Herein rests their value.
The candor which parents have expressed and which I bring to this book is painful, yet cathartic. I am grateful to every parent with whom I have had contact and who have contributed to the true foundation of this book. Although not indentified in this book by name (parent or child), each parent and child carries their identity in my thoughts and in this following poem which I dedicate to all children (and their parents) who have died in utero, at birth, or soon therafter.
Martyr for Desire
You are my quiet darling.
Your eyes, like morning burn
The minutes of futility
To contrite hours, turn
Eastward where begins the dance
Of ocean tides, and slumbers still
The famine of our grief, to hide
So deep within my wounded will.
A promise, poisoned from the start
So brief without reply or song
Did graze your spirit in my field.
"Return to me" I cry, I long.
As chaos prods my anguish, yet
Neglecting fortunes in my soul,
Tinted hues of destiny
Are tender thoughts which sorrow stole
From me when first I heard your voice;
Each murmur on your breath that sang
Like harps converging as a choir,
And chimes afar, with passion, rang.
You are my quiet darling
Within a cold and flawless fire,
And I, a prism in the shadows;
A silent martyr for desire.
Jack and Kyle
We became pregnant in October 1996 and were very excited. In November we were told that we would be having twins, which was even more exciting. I was one of six children and we had talked about having a large family. However, we also wanted to be young parents to all our children, so we were happy to get off to a fast start with twins. By late December, Carmen started having some difficulties with her pregnancy. Her doctor instructed her to rest and reduce her activities due to a blood clot in her uterus. While we were concerned, the condition did not seem too serious, and we hoped rest would cause the clot to dissipate.
Subsequent ultrasounds showed the clot getting smaller so Carmen’s doctor allowed her to move around a little more; dinner and a movie would be alright once and a while. Then in early March, Carmen called her doctor because she noticed some discharge. An ultrasound showed a little funneling of her cervix, but since there was no apparent contracting, she was told to maintain strict bed rest and have a follow-up ultrasound in four days. The follow-up ultrasound showed increased dilation of her cervix. Carmen was admitted to the hospital immediately. The date was March 10, 1997 and she was 22 weeks pregnant.
In the Hospital:
At the hospital, we were told Carmen was fully dilated and that birth could occur at anytime. We also were told that at 22 weeks pregnant, the babies were not viable. However, an ultrasound showed good growth for one of the fetuses and that if they had any chance for survival, Carmen would have to be transported to a level III hospital.
Despite being pregnant with twins and enduring some minor difficulties along the way, it never occurred to us that our babies could possibly be born this early, let alone with little chance for survival. Jack Michael was born on March 13, 1997 and the three days leading up to his birth were the longest three days of our lives.
At the tertiary care hospital, we were awake almost twenty-four hours a day. The daily routine involved meeting with doctors to discuss what would happen if the babies were born this day. As each day passed, their chances for survival would increase, but we were told that their best chance for survival would be after twenty-four weeks gestation. With two weeks to get there, it seemed like a lifetime to us. I was distraught thinking that Carmen would have to lie flat on her back with her feet elevated and be subjected to all these different medications for two weeks, or longer. At the beginning of each shift, the new team of doctors would meet with us. They would provide us with all sorts of statistics regarding probability for survival. Based on this information, which was totally foreign to us, we had to decide what we wanted the doctors to do if our babies were delivered. I remember saying to myself that I could never imagine that by age thirty we would have to be making these kinds of life and death decisions about our own children. It was like an entire lifetime was condensed in to these three days.
Since this was our first pregnancy, we did not know what to expect. At first we felt anxious but optimistic. We figured that since Carmen was in the hospital under 24-hour care, that delivery could be delayed. Initially, we still even had thoughts that she might make it to term. As reality set in over the next several hours, we realized there was only so much doctors could do. Most measures for delaying delivery at this stage are designed to buy you days, maybe weeks, not months. We were now just hoping that they would make it past 24 weeks, or as close to 24 weeks as possible since all the statistics showed the likelihood of survival jumped exponentially after 24 weeks. It became apparent to us that there was a sort of cross over point, maybe toward the end of 23 weeks gestation, after which the doctors would recommend increased intervention once the babies are delivered. Before which, however, they were primarily recommending comfort and convalescence. This was very hard for us to understand. As lay people, we could not understand how a few more days in the womb could make such a difference in our babies’ chances. To us, it was like, if you recommend increased intervention “tomorrow”, why not today? I remember feeling so angry and frustrated over not knowing what was the best thing to do. The doctors were talking about all these statistics and probabilities, and all I could think about was, this is our child we are talking about.
During the three days leading up to Jack’s delivery, which seemed like weeks, all sorts of friends and relatives were coming out of nowhere with information and advice on what to do. Not only had we never contemplated the possibility of premature delivery for ourselves, we never realized that many friends, or a friend of a friend, had similar experiences to share. While the support was a blessing, all the different stories we were hearing about this baby or that baby that had been born at 22 or 23 weeks and was supposedly doing fine, only complicated our daily decision of what intervention to request from the doctors. I remember just praying that our babies would make it past 24 weeks gestation, so that we would never have to make the decision of what to do if they were born sooner.
Our first son was born on March 13, 1997, 22 weeks and 6 days gestation. We were praying for the best but expecting the worst. What became important to us as we entered the delivery room was that we be able to baptize him immediately in case he does not survive. Baptism materials were set up right in the delivery room. However, when he was delivered, the team of neonatalogts whisked him away for examination and assessment. The initial assessment offered hope but only time would tell how he reacted to the oxygen treatment.
Amazingly, Carmen stopped contracting after he was delivered. Earlier that day, we discussed the possibility of this happening with our doctor. We sat there in the operating room for a very anxious fifteen minutes or so to confirm that the contractions had stopped. Once things calmed down, we wheeled Carmen back to her room. It was like we were in a dream. We could not believe how surreal this all was. We just went through delivery of a child and now Carmen was back in her room resting and still pregnant.
We had names picked out for both girls and boys. We did not know the sexes ahead of time. The first choice for a boy was Jack Michael. We both loved the name Jack and Carmen could not wait to call our son by that name. We did not tell the hospital our name choice right away, he was known as Baby A. We considered giving him a different name than Jack. Given the circumstances of his delivery we considered naming after Carmen’s younger brother who had died a few years ago. After thinking about it some more, we decided that Jack was the name that we had chosen for our first son, and that we should stick with that decision. We felt that if we gave him a different name, it would be like admitting that we did not think he would survive. We could not bear to give up hope yet.
Our families had been in the waiting room awaiting news on Jack. When I went to tell them of Jack’s delivery and to explain how we had to wait and see how he responds to the oxygen, this feeling of love and pride rushed through me as I was talking about my own son. I was a father. We were new parents, and despite all the trauma in getting to that point and all the uncertainty ahead of us, we felt some happiness in having a son. We thought that as each hour passed, his chances for survival would increase. No news was good news. Then, several hours later, Jack’s doctors told us that he was not responding to his medications and that X-rays showed that his lungs were not developed enough. We were faced with the news that our son would not survive. He was basically living on the oxygen machine.
We had decided earlier not to exert any extraordinary measures to keep him alive, deciding that he had been through enough. As much as we wanted him to survive, we did not want him to suffer anymore with all the machines and wires hooked up to him. The hardest thing for me that day was to tell our families the news. After describing to them how Jack’s condition worsened throughout the day, the hardest part was when I told them that Carmen and I decided to have the doctors turn off the machines. I could barely get the words out. After all we had been through over the past three days in the hospital; it was only now that we had the full realization that we would not be bringing our son home. I could not remember a sadder moment in my life.
The doctors and nurses, who were incredibly caring and gracious, wrapped Jack in a blanket and brought him to us to hold before he died. Jack was only 12 ½ inches long and weighed 1 pound 5 ½ ounces at birth, but he was the most beautiful little boy with perfect features just as if he were full term. His fingers, toes, ears and nose were perfectly shaped despite his size and age. It was incredible. We were so happy, for lack of a better word, to be able to hold him and to tell him we loved him and to say goodbye before he died.
Carmen and I held each other and cried. We could not believe that at our young age, we were grieving the loss of our son.
The grieving could not last long, at least for now. Carmen was still pregnant and we had to focus all our energy on Carmen and our second twin. It was a miracle to us that the second baby did not deliver with Jack and it gave us hope that maybe we could make it past 24 weeks. We were told that delayed birth does not happen often and that delivery could occur at any time. But as each hour passed, our spirits were lifted. As we got closer to 24 weeks gestation, we just prayed for one more day, one more day, since we now understood what a difference each day could make to the survival chances for our baby. In addition to the emotional strain on us both, the physical strain on Carmen was enormous. She was subjected to all kinds of medicines designed to delay labor as well as having to lie in bed all day with the foot of her bed tilted up. To find some humor in this, we talked about how despite all the medical training and technology, we were relying primarily on gravity to keep our baby inside his mother for as long as possible. But the strain on Carmen was immense and I hated to see her in such discomfort.
After enduring the side effects of all the medicine for a few days, Carmen was worn out. We decided that it could not possibly be good for our baby if his mother was feeling so lousy. So Carmen stopped taking any medicine designed to stop labor, except for small doses of nyphedapine, and we were resolved to accept the fact that whatever happens was meant to happen. Almost immediately, Carmen felt much better. She continued her bed rest and we again began a game of wait and see. Since the baby was now past 24 weeks gestation, and therefore considered viable by our doctors, we were relieved that at least we did not have to decide whether or not to intervene and support the baby’s life after delivery. However, an ultrasound indicated the baby was breech. Now we had to decide whether to risk a natural delivery, or do a caesarean section, as the doctor’s recommended. Given the gestational age, the caesarean would have to be a classical cut, which is more intrusive and destructive to the mother and would have to be repeated on all future pregnancies. With Jack’s death weighing on our minds, our optimism over the outcome of his sibling’s delivery, if anytime soon, was weakened. Without really knowing what to do, we decided that this is in God’s hands and if this baby is meant to survive, it will. And if it’s not, then we can accept that, but we did not want to subject Carmen’s body to a classical cut caesarean in the process. The next thing that happened can only be described as a miracle and I still tell the story with amazement almost two years later.
Carmen went into labor on March 26, 1997 in the early evening, 13 days after Jack had been delivered. While only the second delivery that I have witnessed, it started out as being pretty routine, push-relax, and push-relax. Being breech, the primary concern was that the head might get stuck as the baby passed through the canal, which would have cut off oxygen to the baby. Once Carmen’s water broke, the canal might then collapse onto the baby, causing its head to get stuck. I won’t gore you with the details, but the miracle was that the water sack did not break until the baby was literally halfway outside Carmen’s body. When it finally did break, the baby just shot out into the doctor’s arm from the force of the water breaking. Our second son, Kyle Mark, was born on March 26, 1997, at nearly 25 weeks gestation. The sack provided a lifesaving protective shield throughout the entire delivery so there was no loss of oxygen to Kyle. When we remember that day we are reminded that Kyle is truly a miracle baby to us.
The preliminary prognosis for Kyle was positive, so we were cautiously optimistic. Kyle was in the Newborn Special Care Unit (NICU) for fifteen weeks. He was released on July 11, 1997, his scheduled due date. Kyle’s stay in the NICU was a rollercoaster for him and us. After Carmen’s own release from the hospital, which was delayed one week due to an infection in her uterus, she would spend almost every day at Kyle’s side. We lived one hour from the hospital and I would visit most night and on weekends. At first, while Kyle was in an incubator, we could hardly touch him for risk of infection. We prayed, sang songs and read books to Kyle just so he could hear our voice. It was the most helpless feeling knowing that your child was struggling for life, and feeling like you could do so little to help him. We did not really feel like parents, because even though we visited Kyle whenever we could, at the end of the visit, we would return home without him. Even though Kyle survived his delivery, he was still so small and premature, that he was not out of the woods yet. All the while, our son Jack was still in the morgue at the hospital. We wanted to have a burial service for Jack, but knowing that we could not go through that twice, we could not do it until we were sure that Kyle was going to make it. As time passed, and the chances of Kyle’s survival increased, we were still concerned about how he would grow developmentally.
All we wanted was a happy and healthy baby and while he seemed fine in the hospital, there was really no way for us to no for sure what problems might become apparent as he got older. Being in the NICU for so long, fifteen weeks, there are so many ups and downs, not only regarding your own child, but just what you see with other families around you. You are there so often, you can’t help bonding with others experiencing the same heartache. The worst experience was witnessing the loss of a child by a fellow parent and, while grieving for them, you are also being reminded that your child is not out of the woods yet. We have formed friendships with other parents that I am sure will last forever. Strong bonds are made when you are sharing such a difficult part of your lives together. I know those bonds helped us endure through some long nights at the hospital.
As Kyle’s conditioned improved steadily, we were allowed to hold him more and eventually became more involved with his daily care including bathing, feeding and holding him while he slept. We became so excited by each little milestone whether it was drinking a full bottle, which for him was less than an ounce, or the day he was moved from the incubator to an open bassinet. We could finally touch him without reaching through holes. The struggle was so long and hard, that even little accomplishments were major events for us.
Another emotional struggle was our wanting to remember our son Jack. All our energy was focused on Kyle while he was in the hospital, that we did not have a chance to just stop and remember Jack. Our friends and family did not always know what to say or do either. It was a strange circumstance, saddened over the loss of a son, while happy over the birth of another, but still concerned that he to may not survive, or if he does, with what ailments. We finally had a burial service for Jack in May 1997. We never thought that at age thirty, we would be picking out burial sites for our son.
Finally, on July 11, 1997, his expected due date, Kyle was discharged from the hospital. We were so excited to finally be taking him home, but at the same time incredibly nervous about not having the support of the nurses and heart rate monitors around. We became so reliant on the monitors, that I was seriously concerned that I would not be able to tell if he was breathing while he slept. He weighed about 4 ½ pounds when he came home. He was so fragile, we were afraid to let anyone touch him. Also, his lungs were still premature and we had to be careful about exposure to others to avoid even minor colds.
Kyle is almost two years old now and doing beautifully. But the hardest thing to deal with since he came home and even today is having to treat him differently since he was so premature. For the first year we could barely take him out in public for fear of getting sick. As parents, it is frustrating to see other kids that are the same age as Kyle and are bigger and more developed. While we are truly blessed by his progress, you want so much for your child to fit in unnoticed with his same age group so that he does not grow up thinking he is different in any negative way.
We talk to Kyle about his brother Jack and someday hope to share with him the whole story. We worry that he might feel guilty that his brother died and that he lived. Seeing Kyle grow and develop into a toddler has been a wonderful experience. Now that we are approaching his second birthday, we look at Kyle and wonder what life would have been like had Jack also survived. Would they look alike? Would they have similar personalities? Would they play well together and grow up being best friends? While Kyle gives us so much joy, it saddens us to know that they won’t know each other. We bring Kyle to the cemetery, which is just down the street from our house, to visit his brother Jack. And when we drive by, which is often, we wave and blow kisses to Jack and say, “Hi Jack, we love you!”
We want to keep Jack’s memory alive for our sake and for Kyle’s. It is sometimes difficult to do. Our families and friends pay so much attention to Kyle and give him so much love, that they sometimes don’t remember or acknowledge that he had a brother. We have to remember that just because he did not live a very long life, does not mean that he is any less loved or missed.
We certainly never hope to go through an experience like this again. But remembering that it was Kyle who has had to endure the most through all this causes our love for him to be that much stronger. We have been blessed with a beautiful son here on earth and a beautiful son watching over us from Heaven. While we would give anything to have both of them here with us, we still, in many ways, consider ourselves to be the luckiest parents in the world.
As of December 1998, Kyle weighs about 23 pounds and is 31 ± inches tall. Kyle is a very happy baby. He loves meeting new people, especially other children, and listening (and dancing) to music. He also loves animals, especially dogs. His pediatrician is very pleased with his progress, and so are we.
A mother's loss; found
The pain, the pain that can't be seen, the pain that never leaves me, the cut that never heals. This is what I feel when I think back to that time, the time my son was born. There is a lot of pain associated with this event of this birth and death, feelings never dealt with, feeling never validated; worthlessness.
It was not bad enough that I was not worth anything to anyone or myself in the earliest years of my life, or so I was made to feel, but this loss of my son and the way I was treated instilled that belief that I was worthless for many years. So many years until I was much older and wiser and worked at my worth within myself without the validation of others.
They just took him from me. I know I heard a cry. They said it was my imagination. I begged he baptized. I still don't know if they did that. I begged them to keep him warm. I still don't know if then even heard me. I told them to tell him I loved him. I don't know if he was told. They covered my eyes. I wanted to see, but the drugs took the fight out of me. I gave in to the bliss of the painless drug induced blackness and wanted it to all go away.
But it didn't go away. It still hasn't. I awoke to the face of a doctor I did not know who standing over me and said "… can you hear me."? How strange, I thought, he calling me by first name and didn't know me, but came only to tell me that "your son expired shortly after 6pm tonight, would you or your husband like to go down and see him? How personal I thought him calling me by name and how cold to tell me my son "expired". I was so confused at this mixture of warm personalization missed with a pinch of detachment. How it got me, in the pit of my empty spot where he used to be. I didn't go. My husband went and came back and told me how beautiful he was, that he looked like me. I wanted to hold my son. I was never told I could. I was crying after everyone left that night only to be told by the nurse that saw me: "don't be so hard on yourself honey, it could be worse. The woman down the hall lost twins last night." Then I was given a sedative and that was it. Oh, so I guess losing two made it worse somehow, and I should be ashamed that I had only lost one child!
I hurt all over, even inside where no one could see. The core of me, the one that held secrets even then, the secret that that my husband beat me just two days before I lost my son and I didn't dare blame him, no I couldn't I would get hit again, so I stuffed the hurt of the loss and my resentment towards my husband.
The social worker came and gave me me some papers to sign the next morning. I said "I want to wait for someone to read these with me." She said "oh that's not necessary they are just saying that you don't want an autopsy on the baby." I said "ok" and signed. To this very day I don't know what I signed. I just believed and trusted her. I went home the next day with breasts on fire and my body sore, the physical reminder that I had given birth but with nothing to show for it but only an empty place in my heart and soul never to be filled again. They said they would bury him for us but I could never know where. I didn't question. I was scared to question. I don't know why and I had a four-year old to go home to that needed me. I made the mistake of thinking they would put some worth on my son's body and would treat it with dignity, again I trusted.
It has been twenty-four years now and I've grown strong as a person and a women. I have found out where my son is buried. With the love and support of a lot of wonderful generous people I have had a memorial stone put in place of his burial and the burial of all the babies that never had a chance at life, maybe even those twins the nurse told me about. This memorial can serve for all children, not just there, but the abused, forgotten children all over the world that need to be validated as worthwhile human beings. I have come full circle and I feel joy, not sorrow, at the site of this beautiful place where he rests. It is a place to come and celebrate his coming into the world and leaving so quickly. It reminds me daily that I will see him again when my time comes and I can tell him then, what I know he feels from my heart today, face to face that I loved him then and I love him now.
The grief I felt at the moment…was beyond words. …I sobbed until my heart could cry no more. For years I carried this saddness deep inside…
Sarah
My name is Jennifer and my daughter, Sarah, was stillborn. If anyone had told me that I would be writing these words two years ago, I would not have believed them. The death of a child is such an unbelievable event that I know you, too, are in shock that it has happened to you. I have written a book, Letters to Sarah, with the hope of easing some of the pain and informing others of what lies ahead.
In my ninth month of pregnancy, my friends from college threw a baby shower for me. About two hours before the shower, Sarah kicked over a hundred times. This was unusual. I had never done fetal movement counts but this one time, I stopped to count because I knew the baby was kicking more than ever before. Daniel felt the kicks as well. Throughout the shower, we commented to our friends on how strong this baby was. Those were the last kicks I ever felt.
During the first twenty-four hours without movement, I figured "Well, he/she is just worn out from earlier". But by the second day, I was getting worried. I dug out a stethoscope to listen for a heartbeat. I had always been able to find it before but, this time, I could only hear the echo of my own heart. I said nothing to Daniel. We went shopping and made plans. The same night I pulled out the stethoscope once again with no result. The following morning I told Daniel that I believed the baby had died. He then got out the stethoscope and "found" a heartbeat. I wanted so badly for him to be right that I allowed myself to be comforted for the time being.
The baby appeared to have dropped so I told myself he/she is too crowded to move. When I mentioned a lack of movement to others, they supplied the same hope. Finally, I went to the doctor. He had difficulty locating a heartbeat, but he did eventually "find" one. He then sent me to the main hospital. The nurses searched for a heartbeat and did not find one. My panic was rising and when the doctor arrived with a portable ultrasound, he confirmed my worst fear. The baby had been dead for several days.
I chose to induce labor but requested to wait until Daniel could arrive. I had to call him from the hospital to utter those horrible words "The baby died but I still have to go through labor and delivery". Sitting in the hospital room waiting to get this over with was the worst experience of my life. The hospital was, at least, a four hour drive for Daniel.
When he finally arrived, we cried together and prepared for the long night ahead. I was given painkillers on request and spent much of the time "out of it". Sarah was delivered after twenty-one hours of labor. I chose to see the baby before consenting to drugs. I will never regret this decision. I was able to hold her, but Daniel only got to see her, kiss her forehead and say "I love you, Sarah". He then left the room.
I partially unwrapped the blanket to look at her but I felt as if I was being watched and that this was inappropriate. I never thought to ask to be alone with her or for Daniel to return before sending her away. She was perfect looking, lots of black hair, a round face and long, beautiful fingernails. She weighed 7 pounds, 1 ounce and looked normal.
The funeral was planned by my parents and the nursery was dismantled while I was away. Sarah was buried in my hometown with a graveside service. Friends from college attended or sent flowers. I was numb, amazed that any of this was taking place. I felt I just wanted to be strong and get on with my life. I felt that this was what was expected of me.
It was not until the day Daniel had to return to work, as well as my mother and twin sister that I was alone to think. Then it hit me how much I loved her and how much I had lost. I cried uncontrollably all day. I could not understand "Why?" "What did I do to deserve this?" "What is wrong with me?" and "Why didn't she love me enough to stay?". Two weeks later, I returned to classes and was treated like a glass doll. I felt as if everyone was looking at me and saying "She's the one with the dead baby". I faced people who tried to help, but whose comments were hurtful things, as if they had not even spoken. I tried to turn off my pain, appear strong and "get over it", but, deep inside, I was hurting more and more each day. I eventually realized that denying my grief was only going to prolong it.
Difficult Decisions
They told us our baby had 2 cysts on the brain, thickening of the neck and only 3 chambers of the heart; an amniocentesis revealed Trisomy 18;…It was a very hard decision but we had to be strong and supportive in the decision we made to interrupt the pregnancy when I was 20 weeks. It was the hardest decision to make because we have waited so long and tried so hard to become pregnant. When our daughter was born we weren't sure if we wanted to see her, hold her or anything. I was so scared. When she was born, I knew then I had to be strong to see what had be kicking me from the inside. We held her, named her, got photos of her, hand and foot prints. I cherish everything I have. I now that I look back, I would have regret it by not doing the things I did. We then had to bury her so we got her the best headstone we could find. We love her dearly.
Our son died last year. We chose, in a decision filled with horror, anguish, pain, and love, to have an abortion after learning that our son had defective kidneys and was in the early stages of congestive heart failure. I was just shy of 20 weeks pregnant. I still miss him every day. I started out this grieving process feeling mostly sad, missing my baby, and have progressed through many other feelings, including anger, helplessness, fear. I have played around with acceptance, but I don't think I'm there yet! In addition to our sorrow over our lost baby, we learned not long after the abortion that the disease he had is a hereditary one. I really want to be a mother, and to carry our own child, but it is beyond frightening to think of having to have a second or third abortion of a baby that I want; that I love and cherish. I have had an early miscarriage since the abortion and while this loss caused some sadness and frustration, it was nothing at all like having to make the decision to end the baby's life.
Our Son
Our Son was born on February 11, 1993 and died 2 hours and 27 minutes later. He was beautiful. He was 3 lbs, 2 and 3/4 oz and took a deep breath and cried a loud cry when he was born. I think when he cried, both myself and my husband thought he would be OK. He died in my arms a peaceful death. People ask me how I could have him die in my arms and that it would be too difficult for them to do but my answer to that was that I was his mother and he knew I was holding him. He could feel my heart beating and I certainly wasn't going to let him die in a stranger's arms or in a little cot in a corner of a room by himself. This was going to be the only and last thing I could ever do for my child and I was determined not to let him down. Two days later we buried our Son. I think that out of all of this, this was the hardest thing I had to do both emotionally and physically. You are suppose to bring your child home to a warm cozy crib, not a casket in a cold ground. For some reason, I have a hard time dealing with this. The night he was buried I took a hot bath. Lying in the tub that night, my breast milk started to come in. It was so ironic. Tthere was no baby to nurse. How could God be so cruel I thought. Some people abuse their children and don't want to become pregnant and I on the other hand wanted another child to be a part of our family and I couldn't have him. Of course there has been alot of feelings and emotions in the last 4 years and I think that it's only now that I have the emotional strength to talk about him. I long to hold him in my arms just one more time but I have to think that he is our little angel in Heaven. We openly talk about him now and even sign cards with his name on it. I got a Mother's day card yesterday and his name was included. I think to survive this, keeping your child a part of your family helps in the grief.
My son
I would like to share my feelings, hoping that it will give me some peace. I awoke to realize that my baby wasn't moving like he usually did in the morning. Somehow I just knew my baby was gone. An ultrasound revealed our worst fears. I will never forget seeing that little, still heart on the ultrasound screen. We went home and held each other and cried. The next morning I told our other children and we began the awful process of trying to induce our baby to leave my womb. Finally I delivered my son with his umbilical cord tightly wrapped around his little neck twice. I held him and cried for all that we had lost and for this precious little life that had been cut short before it ever began. We buried him under a beautiful tree with chimes blowing in the wind, two days later.
My Drecious Daughter
My precious daughter was born during the 19th week of my pregnancy. She had spina bifida. We were devastated and heartbroken beyond imagination. She would be paralyzed from the waist down and would most likely have bowel and bladder problems, hydrocephalus and unknown mental disabilities. Although we were in total shock, we pulled ourselves together and tried to figure out what we should do and try to learn as much about spina bifida as we could. What was the best thing for our baby? I don't think I'll ever know for sure what the right thing was - there is no "right" answer in a situation like this. No one wins. There is no happy ending. With much sadness, my husband and I decided to end the pregnancy. Although this was the most traumatic thing I have ever gone through, some good came out of it. The nurses and doctors were absolutely wonderful and compassionate, especially, the genetic counselor who helped us through it all. She convinced me that I might want to see my baby. I treasure the few moments I had with my daughter after the delivery and am so thankful for having the chance to see and hold her. That moment is etched in my memory forever.
The hospital prepared a "birth" certificate, took footprints and 2 photographs. These items, along with my daughter's blanket and cap are kept in a special keepsake bag. I felt so very sad for our poor little girl. She was so ill. My arms ached for her as they wheeled me out of the hospital. It felt so strange. I was pregnant, and now I'm not. There is no baby to take home and care for, love and hold. She was buried in the baby section of a beautiful cemetery the following Monday. We had a short memorial service and several family members attended. She was buried with a stuffed animal my sister gave me when she found out I was pregnant, a picture of my husband and I, and a picture of our two dogs. My husband and I visit the grave often. It has now been 9 months and my husband and I have been up and down emotionally for months. As I've told others who have asked we will never ever forget our baby, the pain just eases as time goes by, and the good days start to outnumber the bad as you pass through the stages of grief. We have thought about having another baby, but we've lost our "innocence" and realize that another pregnancy right now would be wrought with fear and worry about it happening again (our chance of recurrence is about 5%). We haven't given up on the idea completely, we just want to wait a while longer.
Journeys
My husband and I lost our 3rd pregnancy at 16 weeks. (The first two were 1st trimester losses). This pregnancy loss has affected me much more deeply than the first two. I feel a true physical loss and emptiness. I feel so terriby alone, inadequate, un-womanly, desperate... I wrote the following poem for our little boy. I will always love him.
Journeys
My grandmother died in my arms.
Many years ago.
I held on tight.
I didn't want her to be alone.
On her journey.
My baby died in me.
Just a few days ago.
I tried to hold on tight.
I didn't want to be alone.
On my journey.
My granmother left a hole.
I patched it with pieces of her house.
Her cakes. Her laughs.
When I think of her I smile.
I'm glad I didn't let go.
My baby left a hole.
The patches do not hold.
They slide away in the night.
When I think of him I cry.
I didn't want to let go.
This journey will be long.
The pathway will curve.
The bramble will catch.
The ocean will rise.
At my shore.
And the birds will still sing.
Every day.
Every. Day.
The body will Heal.
The mind will Accept.
The feet will Walk. Run. Dance. Skip. Skip. Skip.
One. Day.
The heart will pump.
Not as hard.
Not as fast.
For one.
And the journey will cease.
It will end in a bed.
I hope someone holds me.
And doesn't let go.
I love you, little baby.
Rose Bud
… I realized I hadn't felt movement. I had two separate dreams that my baby had died, so when I went into the hospital I wasn't surprised when no heartbeat could be found. I was induced and gave birth to a beautiful perfect daughter. There is no indication to why she died (even after the autopsy). We brought her home with us for the weekend, and she was buried on a bed of rose petals with the casket surrounded by white rose buds, which people who came to the funeral had brought. She is our little rosebud blooming in heaven. Now five months later, our life has hardly changed (outwardly) since before I became pregnant. Inwardly our life has changed considerably, and for the better. The experience has enabled us to get close to our families, and to God, It has strengthened our love for each other, and for the world we live in, It has given us more confidence in ourselves, we've survived a very traumatic event intact. We can survive anything. Most people probably find our philoshophy strange, (I do) but I've found that my faith that this is part of Gods great plan, which we can't understand but can trust, has helped me heal. My faith does not heal the pain in my arms at not having a baby to hold, or the pain in my heart when I see my friends babies, or the pain at being back at work when I want to be at home with a baby. But it does help with the questions, Why us?
A Lasting Pain
I have not been able to write down my experiences until now because it is just too raw and too painful. I have not wanted to dig so deeply into myself and re-visit the most painful experience of my life again. Even to begin writing it just cuts me to the core, yet there has not been a day since this happened that I do not, think about it. There is constant pain. Even as I write this, I feel the tears coming and my chest hurts and my belly hurts. Prior to this I did not know that grief physically hurts.
I did not grieve after the 1st miscarriage. I just told myself that it is one of those things and because the relationship I was in at that time was not sound that it was not meant to be. I got on with my life and was back at work within a week.
My princess, was born breathing alone and alive. I heard her whimper as the staff rushed her to the corner of the room and began working on her. It was to be the only time I heard her voice. She weighed 1lb 70z. She was beautiful. Tiny but perfectly formed. She had black curly hair peeping out from the hat she had on. She was wired up to machines and tubes and monitors and was on a ventilator. We held her hand and welcomed her to the world.
The next morning we went into see her and it hit me just how tiny she was. Her whole arm was the size of my big finger, her chest was the size of my hand. We saw the doctors and they told that she was doing well her chances were good. They told us the black girls had the greatest survival records. I began expressing breast milk and she was been feed by a tube through her nose; 1ml at first and then she got up to 5ml every 3 hours within the first few days. By that weekend I began to feel robbed as if the womb snatchers had struck. I felt empty and hollow, I had my baby but I did not have her. I could not hold her feed her or anything but I was grateful that she was alive. The levels of oxygen she was recieving was reduced. Then she developed an infection. They did not know what it was but started a treatment. Her oxygen was increased again. Then there seemed to be some improvement. She was started again on breast milk. They weighed her after a week she had gone up to 1lb 13 oz and she looked bigger to us. Her condition begun to fluctuate. She would be ok for a few days then something would happen. I could not leave her for I was afraid that if I left her she would feel abandoned and die. So I stayed with her.
I would sit with her all day every day and sing to her and talk to her and wash her and change her nappy and just love her. I told her secrets, I told her of our plans for her and our dreams. I told her about her family. I fed her through the tube. I washed her body with a cotton ball. I oiled her skin. I kissed her fingers. I believe she knew I was her mommy and I was there. Her Daddy would come and sing to her and talk to her. She knew him and always opened her eyes when he spoke. They needed to transfer my daughter to another hospital. She became much sicker. I prayed so hard, please don't let her die, please don't let me have known her for 5 weeks just for her to be taken away now. Just dont let her die. I prayed if there is really a God, grant me this one thing and I would never again ask for anything in life. We refused to except that she was going to die. I whispered in her ears: "baby, mommy and daddy love you, when you have had enough, you stop, I want you here with me, but if it hurts too much you stop, I will understand"
I could not watch her suffer any more. The Doctors told us there was nothing else they could do for her and that we should consider switching off the ventillator. We spoke with our families and loved ones in the waiting room (there must have been about twelve family members there) and together we made the decision that enough was enough. I was so glad they were there to help us make that decision because I could not have made the decision alone. We agreed to switch off the machines.
We had a naming ceremony for her. Everyone held her and kissed her and wept. Then her dad and I took her into the parents room where we had been staying, and I held her to my chest and for the first and last time I felt her naked skin against my naked skin. We took pictures and hugged together for about 15 minutes. My precious baby girl died on my chest and my world fell apart and I changed forever. She had a beautiful burial ceromony with about 150 people (family, friends and loved ones) in attendance. We were fortunate that we were able to bring her body home for two nights. We kept her on ice. Maybe some people will think that is morbid, but to me there is nothing morbid about my baby. She was ours. We wanted her to know where home would have been. I carried her around the house and showed her her room and the things I had prepared for her. I made her a beautiful outfit to be buried in and my sister and her dad made the casket and lined it in yellow satin. In the casket with her we put gifts from her aunties and uncles and toys and photographs.
Now 8 months on it hurts as much as it did on the night she died. It does not go away. I am not the same person any more. I feel like such a failure, it is the most natural thing in the world to have a child. Yet I could not carry my baby to term and she was born only to suffer and die.
Who feels it knows it. Nothing can compare to your child dying. Sometimes I wish I had died with her. It is only now that I can go to the cemetary and not feel like digging up the grave with my bare hands just so that I can see her again. I know I have changed and I long to feel normal again.
How can something that is supposed to bring such joy just bring so much pain and sorrow? I feel jealously when I see happy young mothers with babies…I feel so angry when I hear moms complaining that their baby kept them awake that night. Oh for that pleasure I would give everything. … People don't want to hear about this all the time but I still want to talk about her. They don't understand what it feels like to know I never heard her call mommy. I never heard her crying or laughing…I'll never comb her hair or comfort her. Yes I am a mother! But my baby is not here with me.
My Grief
I was 22 weeks pregnant with a baby boy when a routine ultrasound revealed two major congenital heart defects. All of our previous genetic and ultrasound exams had been completely normal, so I was not expecting any problems of this magnitude. To my shock, the Pediatric Cardiologist began discussing the possibility of teminating the pregnancy. After long and tearful discussions with my husband and our families and friends, we decided to terminate the pregancy. I had an abortion in my 23rd week of pregancy. It has been almost two years since our baby died. I still cry easily and often. In thinking more about our baby recently, I realized that a good deal of the ongoing pain comes from the way our baby died. I feel as though I abandoned him at the moment of his death. One moment I was pregnant and the next I wasn't. It was an unbelievable shock. There is a huge disconnection between my experience of time and emotion. I grieve that I was not with him at the time of his death. I could not see him or hold him in my arms. I was unconcious at the time my son, who I had loved and nurtured for months, died. At the time no one offered me the option of inducing labor and allowing my son to die after birth. I thought about it but did not ask anyone if this was an option, the thought was just too painful. I wish I could have held him as he died. I wish I could have seen him, and spoken to him, and comforted him.
My Twins
After two previous miscarriages, when I became pregnant again I was worried I'd miscarry again, but I began to relax after the first trimester. Then at 20 weeks we found out I was having identical twin boys. We were very excited and things were going well until 36 weeks when one baby showed signs of distress. I was monitored closely and they decided to induce labor the next week. I showed up at the hospital for the induction and they could only find one heartbeat and it was confirmed by ultrasound that one baby had died (only about 2 hours earlier). Later that afternoon I delivered twin boys. My first was stilborn and my second was very ill and transferred to another hospital. They were later diagnosed with a CMV infection. He eventually got better although we are still dealing with the long-term effects of the infection. I suffered a lot of guilt and depressioon after his death almost to the point of being suicidal. But eventually I learned to accept his death and to try to go on with my life. Now it's been almost 2 years and I'm expecting another baby soon.
My Son
In the seventh month of my pregnancy I went to the doctor, as I did every month. I had always looked forward to my doctor's appointment to be sure the baby was doing well. I was scheduled for an ultrasound that day and I was excited to get a glimpse of my baby. While on the table, the radiologist began to observe the baby checking for all his little baby parts and to see if he were growing well. As he proceeded with the test he began to hesitate. Something was wrong! He had found an absence of amniotic fluid around the baby and my heart crushed as he searched again and again for the baby's kidneys. There were none! My husband drove me to the university hospital center. My daughter stayed at her grandma's house, not knowing what was wrong with her baby brother. Upon arrival to the University Medical Center, I felt assured that if anything could possibly be done, it could be done there. I was admitted at once and taken to the maternity ward. The nurses seemed to know we were coming. They appeared to be nervous around me and I could feel their tension. I sensed that they knew more than I had been told. After repeated ultrasounds and other tests, we were told the words we hoped we would never hear. Our baby was going to die! He was given a five percent chance of survival. I wanted to collapse. I became totally immobilized. I just knew my heart had shattered and I was too weak to pick up the pieces. I began to analyze my life for anything I had done wrong that could have caused this to happen. The questions became repetitive. Why me? Why? Our choice's were to carry him to full term, giving him his five percent chance of survival, or to induce labor right then. To us there was only one choice, we knew we had to give him a chance. In the month ahead, we were still in a state of shock. My husband and I prayed constantly. We wanted to mourn, but felt it would cause us to lose hope. We were not going to give up and just accept the obvious.
Then on the last day of May, eight months into the pregnancy I delivered a four pound, eleven ounce baby boy. He was taken immediately to intensive care where they proceeded to resuscitate him. My husband was allowed to visit him shortly after his birth while I was taken to the recovery room to await his diagnosis.
Then the news came. My son was born with Potter's Syndrome, a rare disease that causes the kidneys to not develop. He was not going to survive. I was transported to intensive care on a stretcher to say hello and good-bye to my son. He was beautiful, he looked normal, and I wanted to pick him up and take him home. He looked like his father. He was now being kept alive by machines, only to allow my husband and I more time with him. He had already begun to suffer and we were soon asked for our permission to disconnect the machines. We were told that once his life support was discontinued he would die within moments. We were given a private room and baby's respirator was removed. We held him in our arms and rocked him. We begged and pleaded with God to let him survive. My husband and I were willing to sacrifice our own life to let this little one live. For two hours my son gasped for breath. He tried to cry but couldn't because the respirator had damaged his throat. I had never felt more helpless in my life. It felt as though my insides were ripped to shreds as I watched my son take his last breath. The pain is still felt when I think of my beautiful son. All we have left are pictures, a lock of his hair, and the little tee shirt he wore that day. But I learned something through this difficult time. I wasn't angry with God because of my son's death, but thankful for the time he had given us together. Most of all I was especially proud to be his Mother. He was too good for this old world and he is much better off where he is.
Two years after I buried my son, I gave birth to boy and girl twins. God knew I would never forget my first son, but he found a way to ease my pain. We now have 5 healthy and beautiful children.
My Daughter
Our daughter, beautiful and precious, was born in August 1998. She was only 21 weeks gestation. After having a level 2 ultrasound and an amnio she was diagnosed with Trisomy 18. We went to genetic counseling and were told that her disorder was incompatible with life. We were told that if she were to make it to term she would have had a life full of pain and suffering. As much as we wanted her we put aside our feelings and decided to interrupt the pregnancy. I went through 18 hours of labor and she was born at 1:52 a.m. Thursday morning. She was perfect and beautiful. We held her and just looked and wished that she could stay with us. Our arms hurt to hold her again. Although she was perfect to us she had overlapping fingers, clubfeet, low set ears, and an elongated head. Her internal anomalies were also numerous. She had large, bilateral choroid plexus cysts, small left heart, brainstem disorder, a hole in the main ventricle, etc. It was amazing to us how much we loved this little girl, however she would be in a better place than us and she would indeed be perfect and beautiful and healthy. We constantly tell ourselves this although it does not make us feel any better yet. We want to have more children but we don't think it will be the same. It is funny most people think that your grief should be measured by the size of your baby, that we should think of it as a miscarriage and move on. Oh how these people are sorely mistaken. We cherish the memories we have of our daughter! We are sure the choice we made to see her, hold her, name her, have momentous of her, was the best thing we could have ever done to make sure she would never be replaced or forgotten! We look forward to our next pregnancy, but our hearts are sore from the loss of our sweet daughter!
Prayer and Hope
First, may I offer prayers and blessings to all of you who have experienced the loss of a child. There is no darker or longer time in your life, but at the end of my story, I hope some of you will find a fraction of the joy that now abounds in my life. My son was born at 42 weeks. We had a trouble free pregnancy. He was our first child. He was perfect, but for one small problem: he had a huge hole in his diaphragm. This is not deadly, so we are told, but his abdominal organs including a portion of his liver had migrated to his chest cavity. Therefore, his lungs could never develop. We made the decision to have him transferred to a hospital an hour away so that surgery could be performed in an attempt to save his life. I arrived at the hospital shortly before he died. My husband swears he was waiting for me, as his vital signs (never good, but stable) dropped as soon as I arrived at the hospital. We talked with the neonatologist and asked him the prognosis he responded, head bowed and voice soft; "We do not aggressively resuctate an infant in this condition." What to do? I wanted to remove the life support. Surprisingly I did not need time to think about this. Enough is enough. It was so hard to look my husband in the eye and tell him I wanted to let his first born son go. But when I did look at him, I saw the same love and pain struggle. We bathed our son, removed all the tubes, monitors and finally the respirator. I held him in my arms for the first and last time. What a bitter-sweet memory. He lived only 18 hours. It is our belief that God had a small soul that needed a lifetime of love in a very short period of time, and we were there to give it.
At our baby's memorial service, we decided to try for another baby as soon as medically possible. What surprised us both was the year it took my body to be ready. Six infertility doctors later, two surgeries, drugs, sperm counts etc. we were blessed with another son. We were told to come back when we were ready to conceive again. Well, they have turned me on, and can't turn me off! We now have three healthy boys, ages six, four and two. A very wise women said to me once "If God did not want you to have children, he would take away your desire for children. It is just in his time & his way." Infertility treatments, adoption or reaching troubled kids. All kids are a gift, no matter how long you have them with you on earth, you will always carry the gift in your heart. It will strengthen you, define your future decisions and if you allow it, bathe you warmth like no other.
Anna
We just gave birth to our beautiful daughter Anna. She lived 15 hours and they were the most wonderful in my life. She had potter's syndrome and her kidneys shrank to nothing. We knew that she had just a slim chance of coming out with adequate lung development. My amniotic fluid was found to be low at 18 weeks and just went down from there. I went into labor at 35.5 weeks. We had planned a c-section to give her every chance we could. I guess it was not enough. I remember laying there, unable to see over the screen and asking my husband over and over if he could see her yet. I remember hearing a little cry- the only sound that I would ever hear her make. I thought that that meant she had good lungs. I was so happy for those few minutes. I knew that her kidneys were bad, but we were so prepared to go the long haul! We were ready for peritoneal dialysis and then a kidney transplant. I would not give up on her. They took me into the NICU on a stretcher and let me see her. Soon, I got up and, in a wheelchair, spent the rest of her life in the NICU touching her. They finally told me her vital signs were dipping down and that I should hold her, perhaps for the last time. My husband got a children's book and read to her. Her vital signs would improve for a while at the sound of his voice. We had been reading to her in my stomach for the whole pregnancy, and I pray that she was comforted in the end by his voice. Her hair was so soft.
My Boy
I write this message 27 days after the loss of my son. Everyone says it gets better. It does, really. I haven't cried in days and I can even laugh and smile. (Sometimes I feel guilty when I do, though. How can I smile so soon after having lost my baby just weeks ago?) I have returned to work and life in general. The distraction of doing everyday things helps although it is so difficult to go back to having a "normal" life. My husband summed it up best by saying, "How can our lives change so much, but still change so little?
Time is creeping by. I remember how it seemed to fly by during my pregnancy. I still have two months to wait before we can try again. Then nine more months before we can bring home a baby. I am frustrated. I know how many weeks pregnant I should be; 25 weeks. I obviously cancelled the prenatal visit I had scheduled for today. I think I have started to move into the "anger" phase of greiving. I'm not mad at anyone in particular, just mad at the world for being so cruel. Although I know I'll never have the answers I can't help asking "why us?" Why did my perfect little boy have to die?
I have learned how to walk down the baby aisle in the grocery store. I can't look at the products on the shelves, but it's a start. I can look at pregnant women, but I can't smile at them yet. I can see babies, but I can't touch them yet. I have stopped envisioning a car seat in the rear view mirror. I am learning that my hand doesn't belong on my stomach. I have stopped calling my husband "Dad" and my mom "Grandma". I quit planning for maternity leave. I still pass off wanting chocolate as a "craving", though! This is the hardest time of my life, but I'm making it through with the help of a loving husband and the support of friends and family.
Sharing
I think I am now ready to share - I need to share. When I felt the baby move - oh it was so amazing like a total flop in my tummy - it had finally happened, I felt I was entering new phase of my pregnancy. On July 10th I went in to see my doctor for my four month checkup, I was 17 weeks pregnant and feeling so good. I wore a cute little dress and felt so smug and delighted in my new tummy and my healthy little baby - it was all about to go very wrong. The baby had no heartbeat…it was not moving…
My husband and I spent the weekend in each others arms crying, talking about what we wanted to happen with the birth of our first child who had died; would we see it? what would it look like? would this hurt physically? how much? As a physician my husband would later tell me he was totally unprepared for the next two days.
Sunday night we went in to the hospital and they put these sponges(laminaria) in my cervix that would dilate overnight so I could be induced Monday morning. The pain was searing as they were put in but it was nothing compared to the pain I experienced as I lay in the hospital bed on the antenatal ward listening to the fetal heart monitors the next room. Luckily I did not have to spend the night with all the healthy pregnant ladies waiting to give birth. They sent me home to a sleepless night with horrible cramping.
Monday morning we arrived at the hospital at 7am (my mom arrived shortly after). Soon my doctor came in to take out the sponges and put prostaglandin in my cervix that would induce me. The perinatal crisis worker came to see us and basically informed us that this was going to be a full labour and an average of 10-12 hours. How would I do this? Then I felt something coming out of me - my water had broken - I felt so sad so cheated my first experience with any of this and it was so dreadfully wrong.
At 5:25 in the evening, our first baby was born. I sit here and I can still feel her coming out of me, the umbilical cord hanging outside of me. We held the baby and cried for what should have been. She was perfect, perfectly formed like a tiny little doll. I felt so calm, so proud of this little baby and yet so awful. The hospital gave me a mahogany box with pictures of the baby, a blanket they wrapped her in, her footprints, the hospital bracelets we would have worn and a crib card. These mementos are so dear to me now when I sit and wonder if this really ever happened at all.
Now I sit here a childless mother. I had a baby. I lactated but no one knows this as I have no prize. I have had two friends in the last week have their first babies, I feel so much pain and anger towards them. Why me? One minute I think I am fine and the next minute I am a total wreck - I am so tired all the time. I have lost my innocence, my faith in life, and only a miracle will bring it back....
My Son
In June 1995, we found out we were pregnant again after a heartbreaking early miscarriage 9 months before. We were so scared but the pregnancy went very well. Because of the miscarriage and the insensitive care we received at the hospital, we had decided to have this second baby at home, barring any complications. It went beautifully and on March 19, 1996 I had an 8 lb. 4 oz. baby boy at 41 weeks after an easy labor. His apgar was low at first but soon he was doing fine. All went well until early morning of the third day, when he became fussy and refused to nurse. He began vomiting and I struggled with feeling like a paranoid first- time mother and panicking. I called and made an appointment with our pediatrician for 8:30 that morning. By the time the doctor saw him, he was gasping for breath and was dusky colored. The doctor had the baby transferred via ambulance to the PICU at the nearest hospital. At the hospital, we were told that he had hypoplastic left heart syndrome and that he needed surgery or a heart transplant to survive the following weeks. Babies have an uphill battle with this type of heart defect. The cardiologist also gave us the option to medicate him to make him more comfortable and let him die naturally. We couldn't believe what he was saying. We went from what we considered the ideal birth situation to facing the death of our dear baby. For six days, while they were getting him stablized, we struggled with what to do and finally agreed to let the doctors try the surgery. Miles only had a 50-50 chance of making it through but we had to go with the choice that we could live with for the rest of our lives. I already felt so badly for not seeing the signs of his illness earlier and taking him to the hospital sooner so he wouldn't have had to suffer. I couldn't take from him the only chance he had. He didn't survive the surgery, which they performed on the eighth day of his life. We were numb. The PICU nurse asked if we wanted to see his body but I felt like we had already had several days of very special boding and I refused. I didn't want to see the wound on his chest, or for that to be my last memory of him, and I don't regret that to this day. I feel so fortunate to have been able to nurse him and hold him in our bed at home for 2 1/2 days. The past year has been rocky. We have lost several friends because they are also having children and the loss of our son probably threatens their rose-colored picture of the way things are supposed to be. I have my son's ashes at home and still cannot bear to part with them. Maybe I never will. I feel lucky that my relationship with my husband has stayed strong throughout this tragedy. We had another early miscarriage three months after his death, which was very hard to take. I think I lost the last shred of my innocence and hopeful assumptions about childbearing after that miscarriage. We are now 24 weeks pregnant again and have had a good result with a fetal echocardiogram that was done at 20 weeks. But I still can't imagine having a baby to keep when this is over in July. We found out it is another boy and he kicks vigorously every day, but I know now how fragile a baby's life is and I can't let myself fully enjoy the experience.
Twins
I was diagnosed with Twin to Twin Transfusion Syndrome at 19 weeks and found out that I had been in premature labor for the past month or two. I found out that my identical twin son's placenta was being shared between the two boys. One son was classified as the stuck twin he was getting very little of the nutients from the placenta and my other son was getting it all. The second son had an excesive amount of amniotic fluid and the first had very little so little that he could barely move. I was put on strict bed rest and turbutaline and magnisium sulfate treatment to stop labor.
At 27 weeks. I told the nurses that one son wasn't acting right and they said I was an over worried mother even though my son's heart beat was faint. I was brought down to ultasound an hour later at 1:00pm and my son was dead. The staff than broght me up to the maternity floor and stoped my gurnny next to a newborn baby and left me there with this child crying in my ear. My heart was broken my dreams were shattered and all I could think about was my son who was alive and the one who wasn't. It wasn't fair to him or to me that he shouldn't have to go through life without his brother.
After a week and a half I told the doctors I needed to go home and recover with my family. They told me I could have my twins anytime due to the placenta being damagaged from the uterus, I took my chances.
I went into labor and my first son born and weighed 3lbs. 15oz. My second son was was stillborn shortly thereafter and weighed 2lbs. 14 oz. My first son, who was born alive was rushed off to NICU and they tossed my stillborn son into a cold metal basin and carried him away. They brought him back in hour later dressed in one of the matching outfits I had bought for my boys. He was resting in a wicker basket made for dolls. I never lifted him out of the basket for fear that he would break. He was so perfect in every way. I counted his toes and undressed him to see everything about him. His life may have been over but his love and charm will always remain.
My living son gave his life so that his brother could live. To me he will always be my hero. I have ultra-sound video's of my sons playing together and I have a picture of my son smiling at me. These are the only live memories I have of my son and I hold them as the most treasured memories of my life. I know that Christian is a part of his brother and always will be and for that I am truely thankful.
Three
My husband and I have tried for over 4 years to have a baby. My first pregnancy ended in miscarriage at 6 weeks gestation. We never saw the sac on the ultrasound, only the spot where it had been after the miscarriage started. It was doomed from the start, my progesterone was low and the HCG numbers rose erratically. We waited a few months and then tried intrauterine inseminations again. On our 3rd wedding anniversary, we found out that we were pregnant again. My HCG numbers quadrupled within 48 hours, on February 28th, I had some slight spotting and went in for an ultrasound. We found two sacs. We were having twins. Things seemed fine for a few weeks but then I passed a blood clot. We went to the doctor and we were able to find one heartbeat, the other one was still a bit small. I stayed home and in bed. One week later, I woke up and felt a "pop", and began to hemorrage. I passed one of the twins at home. I was rushed to the doctor. My bleeding became worse and soon I was passing clots the size of baseballs. We were not able to determine if the other baby had a heartbeat, but I was bleeding to death (I lost 1/2 my blood supply in a few hours) They did a D&C and once again, I went home crushed. My greif was so deep that I could only think about getting pregnant again. Two months later, I had another insemination, against my husband's better judgement. I got a positive pregnancy test 12 days after the insemination. The next day I went to the doctor. My HCG numbers were very high, considering I was 5 days away from even supposed to be having my period. My back ached horribly and I began to have sciatic nerve pain. The next week after my HCG numbers had risen exponentially, we had an ultrasound and found that we were having quads! Two days later I had some spotting, I went back to the doctor. One of the sacs has stopped developing and was going to reabsorb. It looked like my triplets were there to stay. On the first day of my 6th week, we had a routine ultrasound and found all three heartbeats! But as I left the office I felt something was wrong, I could not stop crying. As I went home to change for work I started to bleed. Soon I was passing clots. I rushed back to the doctor. All three were still there and my cervix was closed. She put me on bedrest for the next six weeks I would have huge bleeding episodes and passed big clots. Each time I went in they would clean me up, watch me for a while and then send me home. The babies were fine. I had a cervical cerclage in my 12th week, as my cervix seemed short and one of the babies was laying right over it. That baby, (I later found out) was the source of all my bleeding, coming from her placenta at my 13th week I went back to work. Six hours into my day I had another massive bleeding episode, this time, with my cervix tied shut, the clots pressed down and strained to get through, I was in excrutiating pain. I was taken off the blood thinners I had been on to suppress my antibody problems that may have caused my two previous miscarriages. I stayed home in bed. We had our 19 week ultrasound and found that we were carrying two girls and a boy (just as we had thought). We also found out that I was funnelling, my cervix was trying to open up and my uterus was ballooning out at the bottom. The baby over my cervix (we named her Rebecca Nicole) had changed positions. She was engaged; her little head crammed up against the cervix. I was sent home with some indocin and ordered to stay off my feet at all costs. A week later, I woke up at 3 am to use the restroom. I noticed a lot of mucous. I began to have contractions that morning, They were calmed somewhat by the indocin. By that evening the contractions had become painful. I went to the hospital at 8:30 to find out I was dilated 3 cm with the cerclage still in. My doctor removed the cerclage and I was put into bed with the bed tilted backwards. It was certain that Rebecca would come, the Dr. told me that if they all came that day then they would have no hope for survival. I stayed awake all night, feeling them kick and bargaining with God. By the dawn I knew they would all be born. The first daughter was born. She was so perfect, but very red and very small. She was alive for about 45 minutes. Then my second daughter was born. She was the smallest, but still so beautiful. She held on to life for 30 minutes. I was by this time bleeding heavily, having not passed either placenta. The Dr. felt the last sac coming down slowly. She put me on pitocin to induce his birth, or she would have to operate as I was losing so much blood. At 1:23 pm my son was born. He was far bigger than his sisters and he lived for about an hour. My angels were so beautiful, and as I held them I was overjoyed that I was able to hold my children and so devastated that they had died. It has been a long hard road for me and my husband. He seems better than I am, but he has never gone to see their grave (the hospital cremated them and put their ashes in a stone monument at a cemetary along with the ashes of other babies that died there that year.) We will try again, but this time we want to be more financially prepared, my husband wants to have 6 month's worth of bills in the bank so we won't have to worry, as I am sure I will be on bedrest again. My doctor has told me that with my weak cervix I cannot carry more than twins and we cannot afford IVF. We have decided that if I get pregnant with higher order multiples again, we will not reduce, we will take it as far as we can. I still have nightmares and I still cry just about everyday, when I see other pregnant women or other babies. But it will happen. Someday we will have a child to raise.
My Story
My story began with the arrival of my first daughter Angela Katherine on 12 October 1981. After 7 hours in labour and an epidural as well as pethidine, I underwent an emergency caesarean under general anaesthetic. It took some time to recover from the experience, both physically and mentally, but I was thankful to have a healthy daughter and have been grateful ever since that the doctors had the foresight to undertake the operation to save both my daughter's life and my own. It is only now with a lot of hindsight that I realise how lucky I was to come home after a ten day hospital visit with my baby girl in my arms to share with the world!
On 4 May 1985 1 gave birth to my second daughter, Alison Hannah after 9.5 hours labour with an epidural that only worked on one side and a vaginal delivery. I was on a high almost mwnediately following her birth after thinking it would not be possible following the caesarean. Unfortunately, Alison went into distress during labour and swallowed and inhaled meconium. I don't need to explain in detail to you that there was little that could be done once her lungs were filled. All we could do was pray that she would pull through and come home to meet her big sister.
Sadly, after 27 hours, Alison's fight for life was over. She died in my arms on 5 May 1985, a day I will never forget as long as I live. There are no words to explain how I felt deep inside at letting go of the child I had longed to get pregnant with and enjoyed an otherwise textbook pregnancy, planning for the future. My life came to a standstill as I tried hard to retain some normality for the sake of my older daughter. Angela had so wanted a sister. She kept saying she wanted a friend, not a brother.
We buried Alison at a local cemetery where other members of my family are resting. We had a nice funeral for her and involved Angela in everything. How she coped with it all made me feel so proud. If only adults could behave in the way Angela did. So innocent and unaffected by the attitude of older people who wanted me to leave Angela behind as we laid her sister to rest. I feel it made a difference in her life and now she still remembers Alison with affection and love. We take flowers for Alison on her birthday and Christmas and any other time I feel I need to have time alone to share with her quietly. I am lucky in that I have photographs taken of Alison at a time when the last thing I was thinking of was a camera. Without the photographs, I probably would have forgotten with the passing of the years what my little girl looked like; how lucky I was that the nursing staff were so thoughtful.
I was fortunate to have an understanding doctor at the time, who never tired of me asking to look at the record of Alison's birth and death. I stayed in touch for a long time with the student midwife who was carrying out her first delivery with Alison and myself. My family were and always have been very supportive, friends too have been a valuable aide in my grieving process. The grief has never stopped, the memories are still as fresh today, 12 years on. I suppose I have just had to learn to live with my feelings, because I know I can't change what happened. I'm just grateful for the experience of having two little girls. I had very different birth experiences with both of them and I am thankful I was able to experience a vaginal delivery, which at one time was only thought to be an ambition. Sadly, I may never be able to experience it again because of medical problems, but I have the satisfaction of having brought my daughter's into the world, albeit in very different ways. I have known the desperation at wanting to be pregnant. I have carried my children and seen them arrive into this world. I am one of the lucky ones. After a lot of soul searching, I decided the time was right to try for another child. I had divorced and am now with my new husband who has been very supportive in my darkest moments. He has been my rock when things have got just a little too hard to bear. We've been together for four and one half years now and Angela sees him as her father.
It took only a very short time to conceive and our elation was obvious. We only told close family and friends, wanting to wait until we had reached 12 weeks, just to be on the safe side. Not for a moment did we think anything would go wrong, we just wanted to be cautious.
On 17 December 1996 I had an appointment with the hospital consultant. We discussed the birth, which would undoubtedly be an elective caesarean, but he told me not to worry about it as I was only 10 weeks and there was plenty of time to organize things. I asked if I could have a scan just to put my mind at rest, as I had been feeling slightly different during that day. I was sent for a scan within minutes just to confirm everything was all right.
As my husband, my sister and I sat in the scan waiting room, I felt as if I was bleeding. I went to the ladies to check, and I was. Andrew tried to reassure me that everything was going to be fine, but I knew in my heart that things were not as they should be. As I lay on the bed in the scan room, the operator took what seemed like an age to find our baby. Then the fatal words came: "I'm sorry, but I can't seem to find a fetus, the sac appears to be empty." I knew then that it was all over and that our plans for the future would have to be adjusted. I had so desperately wanted this baby, as with my other two children. The maternal instinct was very strong and couldn't be erased. I was only 10 weeks pregnant, but I was carrying a child inside of me for however short a time. l had lost again and no-one seemed able to console me. I still cry and wonder what might have been, but now feel as if things are getting a little easier to bear. I have tried so hard to put thoughts of babies out of my mind, but I am unable to do this. Its at the forefront of my mind all the time, and until I can bring Andrew's baby home, a sister or brother for Angela, I will not feel totally at peace witlain myself.
I used to think that miscarriage was that word that happened to other people, but not to me. I was the one it wouldn't happen to. How wrong I was. My sister has had three miscarriages and each time has been devastated by the pain of it all. She used to say it was worse for me losing Alison as I had gone to full term. But now, having experienced a miscarriage myself, I can say in all honesty that the pain was just as acute, if not a little different. Our grief cannot be measured on a scale of 1-10. We can grieve for what we have never had as well as what we have had and lost.
As far as I am concerned I have had three children, of which I am very proud. The excitement of being pregnant and anticipating the arrival of a new life into the world is something that cannot be explained. I am deeply grateful for being able to live the excitement, some are not so lucky. I cannot imagine what my life would have been like had I not been able to be pregnant at all. I suppose in my own way I would have coped, as I have coped with the loss of two of my children. My sister has never pursued things with the medical profession, and may never have the joy of giving birth to her own child.
Loss and grief are very personal emotions. You cannot fully explain to someone exactly how you feel. You can only hope that someone has the compassion to try and understand. Others who have been in a similar position will know the depth of your grief, but your own loss is very personal to you. Some people feel unable to discuss the matter with you, it is only because they do not fully understand your grief and fear for hurting your feelings. People can seem very cruel at times, but only because they do not want to bring up something that they feel may hurt you.
Following Alison's death I was treated very well by the hospital staff. After my miscarriage, I was admitted for a D& C at the hospital, then I came home. I received little support at all and it hurt. Only with time have I learnt to come to terms with things, and felt strong enough to try and do something positive out of my grief. I have arranged to attend a local miscarriage support group in the near future and have already joined the Miscarriage Association. I have often said I would love to write a book and so this may be a starting point for me. I don't know all the answers, I am living my own private grief, but maybe in some small way, I can help others who have had the trauma of loss.
We all came from our mothers. We must continue the search for answers to all the questions we have. Why do so many women miscarry? What if anything can be done to prevent it or reduce the risk? Or is really just nature's way and we must accept that as an explanation from people who do not fully understand what we have endured? Thankfully, since I lost Alison I have never heard of any other children dying from the same fate. So maybe things have improved greatly. In the early 1980's I would never have dreamt that so much could have happened to me. I will never ever know where I've found my strength. I sit with the photographs of Alison and cry my tears. I always keep her memory alive by talking about her, so that people know of her existence. Angela still recalls the memory of her baby sister and still hopes to be blessed one more time. I hope I can give her the chance again to have a sister or brother before she grows up too much and loses interest. I want to give Andrew a child of his own and see the joy it will bring into his life. Most of all I want to be a mother. Bake bread, sing, do all the things I wanted to do but work got in the way.
I have seemed to throw myself deeply into my work over the past 5 years or so. It has been an escape for me, something I have a reasonable amount of control over in my life. Now has come the time to put things into perspective and to realize that we only pass this way once. There are things in life all people want and I am determined to get some of what I want and need. If it doesn't happen, well I'll know there was a reason for it, just as there were reasons for losing Alison and my 10 week old pregnancy.
On December 27, I was told that my baby had spina bifida and hydrocephalus. I was 21 weeks pregnant. My husband is in the Air Force and the military hospital wouldnt do an ultrasound so my mother paid for me to have one done as a Christmas. Mom is a nurse and she really felt at least one ultrasound was necessary. I really took the health of the baby for granted. We were going for the ultrasound for the fun of it, to find out if it was a girl or a boy; how trivial that was. Mom, Dad and my husband were all in the room when we found out our baby had spina bifida. Dad turned his head to the wall so I wouldnt see his tears. It was so horrible. I really didnt know what spina bifida meant but I know mom did. Our baby girl had paralyzed legs, club foot and a very large cyst on her back that was obvious on the ultrasound. It appeared to be a third of the size of her body. I never realized that the reason I had barely felt her move till the last week was because her legs were paralyzed. The doctor who did the ultrasound was a very wonderful woman. She told me that she was sorry, she even cried with us. She told us it would take some soul searching to decide what we would do. She told us that outside influences to our decision were to be avoided since my husband and I would be the ones to forever live with whatever we decide. That was the best advice we got. She told us the name of a neurosurgeon who would talk to us about his experiences with children with spina bifida. She also gave us the name of a doctor who could do a genetic termination if that was what we decided. After going to the neurosurgeon and after his review of the ultrsound tape, he couldnt tell us much. I wanted someone to tell me that my daughter would be ok, other than having to be in a wheelchair. A wheelchair and paralysis could be ok, mental retardation and shunts to survive were another issue. The neurosurgeon told us hydrocephalus of her degree at 21 months was a concern and not a positive indication. No one could tell us the unknown, no one could predict her fate. So, unfortunately this decision was placed on our shoulders. It was very sad. I dont think my heart or soul has ever felt so heavy. I had just began to feel her move Christmas eve. It was her hands moving. It is almost as if it was her way of letting me know she was real and her way communicating with me for the first and last time. She gave me that gift to remember her by. My mother and husband felt her move ever so slightly. When my husband and I decided to have the termination, it was unbearable. We wanted her so badly, but the thought of placing a shunt in her brain for hydrocephalus and other numerous intrusions made this the right thing for her and for us. I cried and cried when I felt her move the last night before the termination. My husband just hugged my belly and cried. Its hard to admit but I hoped the drugs they gave me would cause her to sleep so I wouldnt feel her move. It was so heartwrenching to feel her move inside me. The next day at the clinic I went into the bathroom so I could tell my daughter goodbye in private. I couldnt even look at myself in the mirror because it made it more real. Today, I have a bit more peace about her death. I know she is safe now in the arms of an angel, but I miss her. I know that the termination was a horrible choice to have to make but we did the best we could with the knowledge we had. At this moment I am a little disappointed that all of the medical advances we have today lay these kinds of issues in the hands of women instead of letting things take their natural course. On the other hand I am grateful to have had the chance to meet my baby by the ultrasound. I watch it alone sometimes. My husband won't watch it. Somehow all of this will make sense someday. For now we are still healing and missing her.
My Son
In 1992 I found out at about 20 weeks of pregnancy that my baby was anencephalic. I was told that this was always fatal and that I should terminate the pregnancy as soon as possible. It was not an easy decision, but I wanted this baby for as long as I could have him. I decided to carry him to term. It was a long 5 months of waiting and crying. I can't honestly say there was alot of hoping. I knew that he wasn't going to live. They told me he most likely would not live through birth. I had great support from my doctor, which helped. Most everyone else just chose to pretend I was no longer pregnant. My son was born by c-section. He did live through birth and then for 5 days. He was a beautiful baby, at least in my eyes. We were able to bring him home from the hospital and he spent a day with us there before he died on December 21, 1992. We buried our son on Christmas Eve. I have never regreted my decision to continue my pregnancy. It was a decision made for a lot of reasons. Mostly I think because I felt he was safe there. That no one could take him away when he was still inside of me. I wanted him for as long as I could have him. There is a saying that goes "we hold our childrens hands for a while, their hearts forever." I truly believe this. We don't know how much time we have with our children. It is time to be cherished and enjoyed. I had time with my son, 9 months of pregnancy and 5 precious days of life. I have since had another child, another boy. I am also blessed to have had my older son to help get me through the pain and lonliness of losing my son. I will always be thankful for his gift, and I will forever miss him and wish we had him longer.
My Son
I have a hard time telling this story. I know that everyone else does too, but that doesn't make it easier. After six months of a very complicated pregnancy, my son died in utero. I tried so hard to do everything right, and it wasn't enough. It was one of the first times in my life I found I could not make something happen by shear force of will. I was only twenty-one, married three weeks, when we found out I was pregnant. We were young, scared and poor, but have such loving and supportive families that we finally decided to go ahead with the pregnancy. It never even occurred to me that something could go wrong. I had no risk factors, didn't smoke, didn't drink, and yet something was wrong with the implantation of my uterus that stunted and eventually ceased my baby's life. The experiences I had with the doctors were awful. They were condescending, accusatory; they acted as if they couldn't understand why I couldn't "get with the program" and accept what was happening. They kept talking about next time, but I was still thinking about this time. I had already felt him move, I had seen him kick and hiccup on the ultrasound. My husband told me that during my amniocentesis the baby turned and moved toward the needle when it went into the sac. I already had a happy, inquisitive little soul bouncing around in there. How was I supposed to pick up and go on? In the end, I did find a wonderful doctor who tried very hard to save the pregnancy, but my son died at the beginning of his twenty-sixth week. I went into labor later that day and got to see my beautiful, beautiful son. I am so grateful that I had the chance to see, hold, and name my child. I have an enormous debt of graditude to the nurses who helped me that day, especially the one who broke the sac and cleaned his tiny body, wrapped him in a blanket and took pictures of him. At the time I could not appreciate it, but now it gives me great comfort that she was so strong and kind. My son was so perfect, the neatest blend of my husband and my father--my two favorite men. His tiny blue eyes were open and he looked peaceful and wise, as if his soul had drifted in and out of the womb noiselessly. Seeing his face, I knew he would have been just like my husband: kind, calm, wise and good. I miss him so much.
When we lost our first baby, like so many others, we were utterly crushed to find out that he had died 4 days or so previously. In fact I seemed at some level to know this, because I was strangely frightened of visiting our doctor for the first ultrasound, whilst my husband was so excited about it. The last few days we have gone from hope and joy to despair, and I am lucky to have such a loving and supportive partner but who has gone through agony with me during this heart-breaking time. We did something which brought us comfort and peace - we went down to the sea with flowers and incense. We found some driftwood in the shape of a little boat and placed our offering inside it with a letter of love and farewell to our baby. We said some special words, read out our letter and burned our incense and then set our little boat into the turning tide - which is the metaphor for all of life, both good and bad. The passing of someone so dear and special should not go unnoticed. No one else knows of our loss, but this doesn't matter now, because we were lent our child only briefly and with our farewell we take him back into ourselves for all time. I thought others might like to know that what seemed too hard to do a few days ago, actually helped us immeasurably at a terrible time. It was a release for all three of us and yet also a coming together too and there need be no parting from this union ever again.
We buried our son at a at a very nice place at the cemetary. That small place is only for children so now he´s got some friends, I hope. The whole summer was a long, long mourning period. I was always crying or at least felt very sad. I thought that I was the one to blame. Maybe I did something wrong that caused his death? The most difficult part has been to explain everything for our daughter, but now I think she has understood everything that she can. Even if she is only three years old, she sometimes surprises me by knowing a lot of things that I did not think she would know. Sometimes she says to me: "Mum, cant we go and visit my brother today?" Things like that makes me warm in my heart. We have been talking very much about the loss in the family but a lot of our friends have disappeared. They don't know what to say or say the wrong things and are afraid to make contact with us again.
You feel like you failed at the most precious thing you can do in life.
When I read all the stories about all the pain and heartache that is felt worldwide it saddens me but in a way comforts me knowing I am not alone. Strangers we may be, but yet we are connected by a common thread; the loss of a child and that makes us all soulmates. When our son was born, I thought I have his whole life to hold him. Foolish what we think! Sometimes in my case a whole life-time only lasted 3 days. When our son died, our fairytale turned into a nightmare. I did not care about anything. My husband despite his pain pulled me back from the brink of insanity and my family held me together. If ever a viewing and a funeral could be beautiful well then his funeral was. We picked two songs to be played at the cementary and then we let three blue balloons into the sky and it was as if an angel came right out of the sky and took the ballons with invisible hands into the heavens. It's been almost a year and the pain is still as strong. Zachary is a part of my life forever. He lives in my heart and as his gravestone says, "We Will hold you in heaven".
It's hard not to feel alone and like no one understands when you are experiencing a loss. My husband and I have lost three pregnancies in the last two years. All first trimester - no heartbeat and blighted ovums. I could probably write for hours about the emotional drain and depression I have felt these past two years. I am certainly not the same person I was two years ago, and the sad part is my family and friends notice too - I thought I was hiding it better. If I wouldn't have the unending love and support of my husband, I would probably be a mental vegetable by now. We waited to start a family, I am thirty-three, because I loved my work and was determined to build a successful career. Now I sit here at work and I don't feel like doing a thing. My work used to be my life, now I could care less. The hardest part is watching my friends and family members have successful pregnancies, and watching the children at church, even going to church. It's hard to believe in a God that would put you through this much agony.
It's been almost a year since the birth and death of our beautiful daughter. Like everyone else's stories, ours started the same way. Everything seemed to be fine until an ultrasound revealed some growth abnormalities. I had made up my mind that I could deal with a child with severe abnormalities but my daughter had lethal anomalies and would die at birth. I carried her until my 34th week I went into labor. Throughout my long labor her heartbeat was strong and I prayed that was a sign things were not as grave as I had been told. At 7:42 pm she was born in this world. At 7:43 pm she left it. I was devastated. My sweet little baby girl, the little girl I had dreamed of having my entire life was taken from me as quickly as she was given to me. We kept her with us until almost midnight. We held her and kissed her and gave her as much love as we could during that short period of time. I thought I would die when my husband carried her out of the room to give her to the funeral home. I have a lot of pictures of her, but sometimes I ache from wanting to feel her . We had a funeral and she's buried in our family plot. I visit her often. For Christmas this year I put a little Christmas tree up at her grave. I miss her. The pain has come back greatly since I also suffered a miscarriage in my 7th week within the year. I've lost two babies in one year. Do I dare to try again?
I feel like I have these different voices in my head with conflicting opinions. I hear the one strongly that is saying, "What if something awful happens again? Maybe you should just quit while you're ahead". I believe the desire for another baby is stronger than this voice. This has been a terrible blow to our family. I find myself struggling to find solid ground, a new belief system, because the old one didn't include a "nice" family like ours losing a newborn baby. Someone at a hospice bereavement support group (open to anyone) told me that grief was a very powerful thing and I liked that description, because it doesn't tell you how you should do it or when, or how you should feel. This experience has changed me like an earthquake that has ripped through all of our lives. Perhaps ulitimately the effects can be good. I would like his little life to have brought good somehow.
My Story
I saw you on the monitor today. For the last 16 weeks I've been trying to pretend your not there. Not an easy task when I'm throwing up everything nightly, crying at the drop of a hat, especially when those
sappy commercials come on, and all the hormonal changes that a body goes through when it's creating a new life. As impossible as it is, I've still tried to keep you out of my thoughts, out of my prayers, out of my heart.
It's not that I don't want to love you, but please try to understand, that after losing 4 others, I'm hoping that if I ignore your very existance, and I lose you too, the wound to my heart won't go as deep. Maybe this time it won't hurt so much. But here you are on the ultasound screen, ruining all my well laid plans. I try to see you as the world does, to them your only a fetus, not a baby, just a blur on the screen. If I don't listen I won't hear the beat of your heart. If I keep my eyes from focusing, I can't make out your face, your hands, your tiny feet.
The Doctor leaves the room. I try to turn away. I can't. Instead I reach out and trace your image in front of me. From the bottom of my soul my heart cries out to you. Speaking the feelings I've tried so hard to repress. "Please fight little one, please hold on, I do want you, I do love you. please fight." Hard as I try I can't stop the hope and joy I feel. Maybe this time. Your heart beat is so strong, everything seems fine. Maybe I can let you in.
It's been 4 days since I've seen you, It's 1:00am. Something has awoken me. I lay in bed for a few moments wondering what it might be. Then the feeling comes. Something isn't right. The tears begin to
fall. "No", I tell myself, "I'm just being paranoid, everything is fine".
But the tears won't stop. I slip out of bed and go downstairs. I don't want to wake your father.
Your gone. I know it somehow; and yet I begin to pray in spite of that knowledge, not willing to believe it. There's no proof your gone right? I pray and pray, pleading with Heavenly Father to give me peace,
to let me know that everything is fine. The tears begin to fall faster as the confirmation won't come. Hours later when the tears won't come any more, exhausted I return to bed. Your father asks, "What's wrong?" He's come to trust my feelings,, He knows now I as do that your gone. We hold each other and cry. But still deep down inside I am still hoping against hope that I am wrong. Once again I am seeing you on the monitor. Straining my ears to hear your heartbeat again, not wanting to blink as I stare at the screen, fearing I might miss a slight movement that would prove my worries wrong. The Doctor turns off the screen. "I just don't understand it," he says,"everything was just fine the other day." My mind screams,"try again, turn the monitor back on, maybe your sleeping, maybe we didn't wait long enough." Sobs shake my body. I try to keep you safe by wrapping my arms around my body. Maybe if I hold tight enough you'll be okay.
I know the next steps well. The hospital, the nurses, the Doctors, all the preparations for removing you from my body. As I watch the hospital staff move around me, a silent war rages in my mind. "What if their wrong? What if they are planning to take you from me, and your still alive? Should I ask them to try again?" The fight continues even as they wheel me into surgery. My fears are never voiced as I fall into deep sleep. I awaken, your gone. They tell me you weren't really real. This is for the best. Maybe you weren't forming right. It's much easier to lose you now than later. I never really knew you. I know their trying to help. And I try to belive what they say. But if you were so unreal, then why does it seem I can smell your sweet soft skin? Feel your downy head on my cheek? If you weren't real, why is my heart breaking in two?
I don't know if I will ever find the words to explain the void I feel now that your gone. How I long to touch your tiny fingers, to count each little toe. To hold your warm body next to mine. My arms ache from not holding you.
They say that time heals all wounds. I know this is true. You'll be forgotten quickly by the world. They never saw you on the screen as I did. They never heard your heart beat with life. I'm not sure what you were to them. But you were my hopes and dreams, you were my future, and by me, you will not be forgotten.
Through all the pain I have experienced, there is
always been hope. I never really gave up hoping that there would be more joy in
my life, though at times I struggled to believe I would ever feel the joy again
of holding
another child of my own in my arms. The grief process is ongoing and there will
never be an end to the pain I feel from losing my children. I still ache and
cry regularly for my daughter and have found it very difficult to
accept her death, even after 13 years.
How precious and fragile life is. Something I’ve come to appreciate
much more since my son arrived into the world. I hold him close and shed a tear
sometimes for what might have been with my daughter and my baby I miscarried.
If not for them, I wouldn’t have this lively, energetic, happy, bouncing baby
boy. What greater gift could I wish for. I am grateful that I had the chance to
try again and that feeling I had when my son was lifted aloft
by my pyhsician, in the first seconds of his life outside of the womb, cannot
be compared to any other feeling I have had before or will have again. Through
my contact with the bereavement services, I am healing better than in the past.
I was never offered any form of counselling back in 1985 and so a lot of what I
felt back then, came back
in my recent pregnancy. I have made several new contacts and am touched by
the way others want to share their experiences with me and the way they let me
share my babies with them. I’ve cried many a tear for
others in their sorrow and now I want to give something back to them.
Brief Thoughts
" We are struggling with our loss and each day seems to be a battle. We are sure in time this pain will get less."
"I am still unable to talk to anyone without bursting into tears. It has helped to read others stories. By reading the stories and poems, it has helped me not to feel I am the only one who is still hurting. My grief is real."
"I know the empty feeling. It is especially frustrating that most people discount how it feels to lose a baby when you are pregnant. …It has been so much harder than I thought. Recently I have gotten the feeling that my friends don't understand why I am still not over this."
"I feel like time has helped even though this will never go away. I miss her terribly but have learned to live with her in my heart instead of in my arms."
"The sadness will always be there, but my life is full and happy. The loss of my child helped me appreciate all children more. The loss also gives me courage to face other difficult things. After all if I survived the loss of my child I can survive anything!"
"I felt so empty when we left the hospital, and so sad for my husband, who stood strong for me and tried to show everyone he was okay. I think that it is harder for the fathers of these losses, because at least for the first few months I had the chance to feel the life growing inside of me."
"It seems that everyone around me has completely forgotten my baby girl! I was actually told that I should just forget her because she wasn't a baby and didn't matter. ...I cannot do that. I am completely consumed with the thought of my baby girl."
"I found that I was all the time battling between trying to maintain what is expected of me as employee, a spouse, a bread winner of the family, etc, while at the same time trying to move on from the grief that was at times all I could take. It seems everyone tries to get you to move on & not think about it, not realizing that you really don't choose to be weighted down, it's just the way it is. Grief is both emotional & physical. And it takes time."
"I find that there is no escaping the grief… I have realized, however, how much I have changed my life (career decisions, housing, future dreams) because I've expected to be a mother…Now I am dealing with the fact that it may not happen. I think about this often. Giving up on the dreams is like giving up hope that I will ever be a mother. Keeping the dreams alive means forcing myself to deal with the pain of the loss every single disappointing month."
The difficulty that all caregivers of grieving parents (e.g., physicians, nurses, medical students, social service workers, counselors, hospital and office personnel and family members) have in dealing with parents who have lost pregnancies and newborn children is well documented. Recognizing their needs, I have asked several of my colleagues and family members to contribute to this volume. By doing so, it has aroused an increased awareness of their feelings towards this most difficult of situations.
In memory of our son, Joseph Michael
By Karen Aresco
It was Friday when I knew something was very wrong. Actually, not much had gone right in my pregnancy; bed rest, bleeding, hyperemesis. But this was different. I felt an overwhelming sense of doom. I couldn't explain it, but I knew. I tried to believe everyone I spoke with that it would be ok as long as I kept doing what I was doing, which was really nothing, just lyinh in bed and obsessing what my baby would look like, sound like, who he would grow up to be and what he would do in his lifetime. But, my thooughts and dreams were always interrupted by a sense of anxiety that something would go wrong.
On this particular morning, I felt an unusal flutter of activity. Then, as the day wore on, the movements decreased. By the time my husband came home, I was in full panic. I han't felt the baby move all afternoon. I knew there was a problem; my five years experience as a labor and delivery nurse taught me that. But as my husband tried to calm me and talk to my son through my stomach, he began to move. My fears were quited for the time.
On Saturday, I didn't feel much movement at all. On Sunday, nothing. It seemed odd and I still feel somewhat guilty over this but, as I called my doctor, I felt a sense of calmness come over me, almost relief. I had spoken with him several times over the past twenty-seven weeks of my pregnancy, and daily for the last three days. This call was different. He tried to reassure me that is would probably be alright and I belive he really thought it would be, but I knew when I got the office and walked into the ultrasound room, I had already accepted that me baby had died. The ultrasound confirmed it. My doctor did not have to say a word. I saw that there was nolonger a heartbeat.
Telling my family was so very difficult. They had all taken shifts being with me over the last six and one-half months. This was really more our baby than just mine. We had all invested so much into this baby. I felt so guilty, like I had let all of them down.
Arrangements were made and I went into the hospital where the horror continued. I think the hardest thiong about it was seeing the looks on the faces of my co-workers. They really were more like family to me. No one knew what to say or do. I felt like it was my job as their friend to make it easier for them by being tough. And I tried, but the look in their eyes over the next few days is what I remember most. I became very ill and ultimately ended up needing a cesarean section. Iwas hardly conscious when the deciosn was made, but I remember again feeling releif; it would finally be over.
I din't awake for several hours after surgery. I am not surprised, really. I hadn't slept much over the last several days. I think my body had just given in the the exhauistion. I awoke to see my husband sitting next to me. He looked so sad yet at the same time I could see the love and relief in his eyes as I awoke. My mother was there too. She looked so worried, as did my dad when he came in. I remember feeling badly that I had caused so much touble and worry for everyone.
Once I had washed my face, I felt a little better and wanted to see my son. I can vaguely recall the details. My vision was at the time still blurry, but I remember thinking he looked so much like my husband. I looked him over from head to toe. To me he looked perfect and that is how I will alwys remember him. I handed him back to my husband, closed my eyes and went back to sleep. My co-workers took pictures, handprints and footprints of our son and put them in a memory book for us. I treasure this book and look at it ofter. It helps me feel closer to my son.
I stayed in the hospital little over a week while my body began to recover physically. My emotions on the other hand were like a roller coaster. I went from sad to angry to guilty and back and forth in aq matter of seconds. I kept asking why? Why did this happan? I did everything I was supposed to do and still this happaned. Why? There were no answers to my questions. Many of my fellow co-workers, family and friends came to see me and lend their support. For them, I am so grateful. They will never know how much I appreciated all that they had done for me, especially when I was being difficult. You see, mostly I was angy and I took out my anger on those closest to me. I wanted them to hurt as much a s I did. In my own grief, I couldn't see the pain that they too were in. I was angry at myself and my body. I felt like a failure. I felt like I must have done something wrong to have caused this. I felt like less of a women becauswe I could not do this right.
The day I left the hospital, I felt like I was aboandoning my child. Although he wasn't physically with me any longer, I felt better knowing we were in the same building. It was so hard to leave him behind. I was glad to be home once I got there but at the same time, the reminders of what might have been were so hard to deal with. The book of names by my bedside, magazines on raising children, the needlepoint picture I was working on for his room; all things that helped pass the time while I was on bedrest now were a sign of what never would be. The hardest thing was looking into what would have been our son's room. I just closed the door, couldn't deal with that emotion yet. My arms felt empty. I was longing to hold my precious baby. I was so very sad and lonely.
My mother helped us with the planning of the services and the buriel for our son. My mother and husband picked out his casket. I couldn't. My mother went out to purchase an outfit for him to wear. I pinned the guardian angel on the clothes. It was gift from a friend during the pregnancy and it seemed only fitting that I give it to my son as I viewed him now as my special angel. I also gave to my mother to put into hjis a casket, a stuffed musical elephant, a gift from my sister. I used to play it to my son. I remember how he would move to the sound. My brother put into the casket his alter boy cross from when he was a child. My mom and I picked out flowers and made an arrangement for on top of his casket. It wqas a small gaveside service in the cemetary down the road from our house. I chose this cemetrary because I knew I would be spending a lot of time there and also because I felt better knowing that he was so close to home. I went to cemetary almost daily. I would sit at my son's grave and just talk to him, tell him how I was feeling. Sometimes, I would just cry. I was still trying to find an answer to the question why.
Over the next several months, I tried to process all of what had happaned. I tried to find a pplace to balance all the sorrow while still living. It took a very long time to believe I ever would find peace again. Some days were harder than others. I never knew what would trigger the emotions. As time passed, I finally allowed myself to smile again. I remember the first time I laughed. It was about two months after our son had died. I was surpirised that almost immediately after laughing, I was overcome with guilt. How could I allow myself to be happy after this happaned? What kind of person was I? I felt I was being disrespectful to my son.
Getting past my due date was especially challenging. I was consumed by thoughts of what should have been. The holidays too were difficult, but I kept trying to put my life back together. I knew that I had to for my sanity.
I went back to work. This was especially difficult because I was around laboring women and babies all day, reminding me of what I had lost. But I loved my work and couldn't imagine doing any other kind of nursing. Looking back, I think that it was this that helped me deal with all of the pain. It forced me to deal with my emotions on a daily basis and not just bury them.
Soon the good days out numbered the bad. I remember enjoying the seasons, fall winter and then spring; you see I had missed all of them the year before when I was on bed rest. For some reason, I felt much better when spring started, like the fog had finally lifted. I felt like I had finally gotten back to "normal". But I was definitely a changed person. This experience forced me to realize the uncertainty of life. It helped me to reprioritize my life. I appreciate more today my family, friends, and life itself. I never take anything or anyone for granted. Don't get me wrong. It's not all roses. Some days are still very hard; some days I want to wallow in self-pity. And I think this is ok. I can feel sad about what happened, but I can also look beyond this and remember the good that happened. You see, it helps me to remember the good things like the feeling when I first found out I was pregnant, the look in my husbands eyes when I told him I was going to be a father, the first time I felt my baby move, the hopes and dreams I had for him, the love and support from my family and friends. These are the things that help me heal and I think I am a better person and nurse today because of what I have experienced.
Healing is an ongoing process; one that I am not sure will ever end. There are many bad things that I could choose to remember, but there are also good things to remember. I feel I owe it to my son to remember him with a smile for, as I learned, he brought me so much. And maybe, just maybe, that is the answer to the question of why.
Brenda Whiting Beard, R.N., B.S.N.
Louise Ward, R.N., M.S.N.
"Oh, you're a labor and delivery nurse? ... That must be so much fun!" is the usual comment gushed with great enthusiasm when people find out what kind of nursing I do. They might be envisioning loving Madonna's with their angelic babes all pink and healthy with the nurse present for surrogate mothering when the mum's needed to rest. What a great job that would be.
The reality is that nursing at a level 3, tertiary care center is a mixture of emergency nursing, operating room nursing, an Intensive Care Unit, some basic maternity and a large portion of teaching. My college education prepared me for that and much more. What the best education in the world cannot prepare one for is a perinatal loss- a stillborn infant, or a premature delivery where all efforts fail to save the neonate's little life.
I have been enabled through education and empowered by experience, to manage the clinical aspects of caring for a family facing a perinatal loss, but what do I do with my own sense of grief? No one ever told me that as a nurse I would grieve so deeply and sometimes so often with families that were until recently strangers to me. As a professional, my head knows to stay focused so I can help start the family on the right path for grieving. A complex and perhaps never-ending process at a time that should be filled with great joy. Also as a parent, my heart tells me many other things. This is what a dear friend (and coincidentally, my minister) calls stirring up the 'pot of loss'. When faced with a loss situation, all previous losses are stimulated. They will rise to the surface much like stirring up a soup or stew made of every ingredient one Is kitchen might have. By stirring, this concoction, left so long on the back burner, is seasoned, tasted again and a new seasoning - a new loss - added and put back to simmer. A family experiencing a perinatal loss will have their 'pot of loss' uncovered and all previous losses will surface. They may remember a family member's death, the loss of a friend, loss of a pet or loss of a dream. How they dealt with these events will impact on how they deal with this perinatal loss. Likewise, it is my 'pot of loss' that impacts on how I deal with them as their nurse. It is a very well seasoned pot that provides the sustenance needed to continue in a healthy way. I taste from it briefly, am strengthened and go forward to do the work at hand.
The first thing I do when admitting a family with a loss to Labor & Delivery is to initiate a Perinatal Loss Checklist (PLC). The PLC is documentation of the events that transpire and the support team involved. It is a concise list that helps the nurse stay focused while providing care. It also insures that all team members are notified that their services may be required. The team includes the doctors (obstetrician and pediatrician), the nurses, social worker, religious ministry and frequently the genetics department. We work as a team, one service complimenting and adding to the others contributions. The end goal to be facilitating the family to grieve. Depending on circumstances, the family may not see all members of the team while on Labor & Delivery, so the PLC also acts a guide to the team. What is not documented at delivery will be attended to at another time prior to discharge. A copy of this form is forwarded to the attending physician's office so that the repetition of painful questions can be decreased and accurate communication of helpful information will be increased.
The PLC's most important function is to stimulate the collection of memorabilia for the families, The time spent on the labor and delivery floor after birth is often the only time the family may have with this child. Whether the loss is a stillborn, a severely premature infant or a baby born with anomalies that are incompatible to life, it is important to emphasize the act of making memories. I will often make suggestions to the family to help them plan for the delivery of their baby in order to make the most of this encounter.
In the best of circumstances, I take the time to discuss with the families their desires for after the baby is born. They may not have any concrete plans beyond deciding whether to see their baby or not. This issue alone can be of great importance. Those who are sure they would like to see their baby, make my job that much easier. The ones who are unsure, I will advise to see the baby, offering to hold the infant for them while they look on, if that might make it easier for them. My most difficult task is working with a family that chooses not to see the baby at all. I respect their decision, (albeit with a heavy heart that I keep to myself), and inform them that some families feel this way often as a result of fear. I can only assure them that reality is very often less frightening than imagination. I usually take this opportunity to share some of my previous experiences. First of all, I state that their decision is not irrevocable, leaving the door open for them to change their minds. Until they are discharged or the baby is picked up by the designated funeral home, there is always an opportunity to retrieve the baby and see it in our morgue's family area. While I know that the most optimal time is soon after birth due to the baby's condition, all attempts are made to make the viewing as easy as possible. I also give them the benefit of my previous experiences with families that have contacted me expressing regret over having not seen their baby. I feel comfortable that I am doing this in a very non-judgmental way. When a family opts not to see their baby, I take extra time holding this baby in private. This is one of the ways I help myself to heal after caring for a loss.
I take opportunities to inquire about their faith and their desires for a chance to meet with a member of our clergy staff. Some families have strong desires while others may not have even thought of having the baby blessed or a prayer said. This is just one more of the ways in which I as the nurse can help to guide the family through an event in which they have no prior experience.
During the delivery, I try to keep the room a safe, quiet place while providing physical comfort and facilitating the birth process. I will have informed the physician or midwife of the wishes of the family during the labor so that all of us are aware and sensitive to their needs.
I position myself on one side of the bed and encourage the father (or significant other) to be at the other side. If the father has expressed fear of watching the birth, I suggest that he look into his partner' s eyes towards the top of the bed. I often see them glancing at the delivery. I usually am ready with a blanket to take the baby from the midwife and place it gently in the prepared crib. I preheat the crib and have baby blankets and towels lining it as I would do for any infant. I cover the baby completely or partially as to the predetermined plan. I often note that if a grandparent is in the room at this time, they venture over for a closer look in the crib. once the physical aspects of the delivery are completed, such as the delivery of the placenta, repair of the perineum and mother's vital signs are stable, I am then able to turn my attentions to the baby.
I will wipe the baby dry taking care not to damage the skin which may be very fragile. I do the baby care in the room of the patient as often as possible. By having the families watch this process, they are able to see how I handle their baby with gentle and respectful touches. I think it also helps them to see that it is acceptable to touch these babies. I am tearful at the deliveries that I attend. I cannot help but be saddened by the loss of potential life and love that this family is experiencing. I believe that my tears help to validate that this is a life worth grieving for.
I encourage the family in the room to touch the baby as I prepare the baby for presentation to the mother. Sometimes I will hear them comment about features that resemble family members. Even in babies with anomalies, there is often a trait they notice to be familiar. When I hand the baby to the mother, I will introduce the baby as "your son or daughter". I make every attempt to place this baby into the family. When the families discuss naming, I suggest that they can either go with the name that they had originally chosen or they may wish to save that name for another child and chose something different. The point is to encourage naming this baby to help give him or her an identity within the family.
Protocol requires taking pictures of the baby both clothed and unclothed. The parents are informed that this will be done and that they may choose to take the pictures home with them. If they opt not to take them home, they are kept on file with the social worker. There has been an incident of a family returning to claim them seven years after delivery. Most likely these may be the only pictures of this child as many families are not prepared to bring cameras with them.
I try to take pictures that I would want of my own family. The Polaroid camera at work allows me to take multiple shots to achieve the best pictures possible within the limitations of the camera. In recent years, I have begun to photograph the actual deliveries, the blessings and the family members with the baby. These are unopposed pictures and I am careful to be as unobtrusive as possible. I also take pictures of the baby alone using a background frame that I developed to eliminate the hospital equipment from the scene. By using stuffed animals donated from the labor and delivery staff, I can add a nursery atmosphere as well as use the animals to prop and pose the baby. These pictures have been very well received.
The rest of the memorabilia packet contains foot and hand prints, locks of hair, the hospital identification bands, the actual blanket, tee shirt and hat that the baby wore during the pictures and while being held by the family. I also enclose a copy of When Hello Means Goodbye and a baby memory booklet filled in with the time and date of delivery, weight, length and the persons who have been involved with the patient's care.
In the future, our perinatal loss care will include but not be limited to: follow up phone calls - at 2 weeks, 6 months, 1 year; an invitation to an annual memorial service; encouraging involvement with community support groups; providing in-services for our co-workers; and continued evaluation and improvements to our memory package based on input from families, co-workers and professional journals.
The care of these special families is rewarding and extremely satisfying work. I choose to care for them as often as I can or to precept a less experienced nurse to allow her to grow in a nursing skill that is not always covered in a text book. I am very fortunate to work alongside a very compassionate team who are dedicated to making this tragic road somewhat easier to travel.
Andrea Seigerman, MSW, LCSW
When I was asked to write about the emotional impact of pregnancy loss I began outlining a rather lengthy, descriptive paper about phases of the grief process, stages of pregnancy, and how they inter-relate, It was to have been objective and informative without being too formal or academic. As I further considered the topic and reflected on my almost twenty years of experience as a clinical social worker in an inner city teaching hospital's obstetrics department my focus and goal changed. I decided to write about the people -- all the people-- who are affected by a pregnancy loss. In this way I hope to convey the deep and far reaching effects, impact and impression of this kind of a loss. The effects are at times unrecognized, at times invisible, and at times denied. This article is not intended to be a "how to cope" manual regarding pregnancy loss, but rather an exploration. of the complex, multifaceted dynamics that occur in pregnancy loss. It is MY hope that this article will serve to inform two different groups of people --- those who have and those who have not experienced a loss. By reading this article, bereaved couples who have suffered a loss will feel less alone, more connected and better able to cope. Readers with no experience of pregnancy loss will have an understanding of the extent to which the that loss affects its survivors.
What is pregnancy loss. and who are the women that experience it? For my purposes, in this paper, pregnancy loss is all inclusive, It is: early first trimester miscarriages, ectopic pregnancies, second trimester genetic terminations and natural losses, the demise of one baby in a multiple gestation, a full term stillborn, the death of a baby soon after it is born. And who are the brave, courageous women who suffer these losses? The group is large, diverse and spares no one. All ages, religions, races, income levels and stages of life are represented. Imagine these women, united in loss, but as different from each other as one could expect: 12 year olds who aren't even clear how they got pregnant, "older" women who are pregnant for the first time, single-or married or divorced women, women with unplanned or unwanted pregnancies, women who have been trying to conceive for years. Each and every one of them utilizing her own life experience, support network, and understanding of the medical problems, will have to cope and move on.
How does one understand the impact of a loss? In part, by assessing the value of what has been lost. The word pregnancy conjures up images of smiling, gurgling babies, tired, bleary-eyed adults and a "glowing pregnant woman". It is a word that epitomizes joy, hope for the future, dreams and relationships yet to be realized, and perhaps, the next step on the ladder of life-- parenthood, For some people, it represents the fulfillment of a lifelong goal. Expectant fathers share and experience this early emotional connection along with their partners. They often take great pride in considering their soon-to-be role, their contribution to society, and the mark their child will leave on the world. In Rogers and Hammerstein's "Carousel", the leading man sings "My Boy Bill', a song anticipating, savoring and worrying about his upcoming new role and responsibilities. Many health care professionals who choose to work in this specialty area do so because it is considered a "happy" job. For everyone involved in "pregnancy", there seems to be an abundance of positive energy invested in it, committed to it, expected of it. Pregnancy, from a non medical, societal perspective, is considered a simple and natural part of life. Getting pregnant, staying pregnant, and then delivering a healthy, bouncing baby is the way it's supposed to be.
Undoubtedly then, we can understand the utter devastation felt by people when there is a pregnancy loss. Parents feel cheated out of a wondrous, natural experience that was to be theirs, Suddenly their dreams are shattered and their hope for a family, is lost, or temporarily put on hold. Instead of planning baby showers and decorating rooms, they are planning funerals and putting baby items away and out of sight. This is not what's supposed to happen., Your baby isn't supposed to pass on before you have had a chance to hold, love, care for it, and share in it's life. Mothers and fathers alike express: shock, numbness, sadness, emptiness, anger (at G-d, at life, at others who have healthy children), and confusion. "I keep thinking this is just a bad dream and when I wake up I'll still be pregnant.". They just don't understand why something so natural, pure, and simple has slipped out of their grasp, Bereaved parents sometimes allude to a loss of focus and direction, an inability to know what to do next. "I got the room ready and quit my job so I could be home with my baby. I was planning to spend my time raising my child. What do I do now?"
Feelings of guilt, blame, and failure may also begin to surface. While these last few reactions have no basis in reality, mothers often feel ultimately responsible for the well being of their unborn child and therefore culpable. They review events leading up to the loss, seeking an answer, a cause, a reason. Sometimes they unfortunately settle on an action or lack of action of their own as the causative factor. Women often think: "If only I hadn't carried those heavy grocery bags." "If only I had rested more". "If I had eaten better and gotten more exercise." "If I hadn't been so nervous and worried so much." All these ruminations lead to the same conclusion-"I didn't take good enough care of my baby." Feelings of failure can arise out of comparisons--"None of my friends had any problems with their pregnancies. We went to the same doctor and exercise classes. She works too, and probably doesn't sleep any more than I do." All of which leads to-"What's the matter with me? How come I can't do this simple thing?" It is not uncommon for their partners to go through a similar process. Many men have shared these comments with me: "If I'd helped more around the house, she could have rested." "Maybe we should have waited longer. Maybe I shouldn't have pushed for a baby so soon."
The context in which the loss is perceived by the mother and her ability to freely communicate how she is feeling may contribute to her long term adjustment. A not uncommon, although rarely discussed response to the ending of a pregnancy is a sense of relief Women don't readily share such "unacceptable" thoughts as: "This just wasn't the right time for me to have a baby, but I never considered abortion or adoption as alternative." For some women, now that a baby won't be coming, life can continue on it's originally intended course--a continuation of school, beginning a new job, getting out of a bad relationship, struggling to balance existing parental and child care stresses. Relief may equally co-exist with feelings of sadness and grief For some women the situation is even more complex. "I used to think about how much easier it would be if I weren't pregnant, if somehow it would just disappear and things could go back to normal. Now my wish has come true, and I feel like I killed my baby." It's vitally important for parents to have the opportunity to talk, without hesitation, to their partners and to supportive family, friends and health care providers about their conflicting feelings regarding the loss of their baby.
Parents are not alone at the time of a pregnancy loss. The members of the health care team who are caring for the patient often experience a similar flood of reactions and emotions. After all, isn't it their job and commitment to safely guide a woman from the beginning to the end of a pregnancy, to check and recheck to make sure there aren't any problems, to anticipate problems that might occur and resolve medical complications that do arise? However, sometimes even all their caring, attention and use of modem technology can't stave off the inevitable. We can certainly comprehend why they may not want to be the ones to confirm a bad diagnosis, a poor prognosis or the absence of a fetal heart beat. But it must be done. They have to communicate the news, answer the questions if possible, and watch the looks of shock and despair overtake the faces of their patients. It would be foolhardy to think that this does not take a toll. Caregivers may (and do): cry along with the parents, feel upset, feel responsible, wish they could take away the hurt, review their work to see if there's anything they could have missed, wonder how much longer they can do this kind of work, talk with colleagues for support, or they may busy themselves with work and move on--pushing away the feelings. After all they're only human, For everyone involved --patient, partner, medical provider-- there may be a sense that the situation is out of their control, that in spite of everyone's best effort this pregnancy, this life, was lost.
As time goes on, bereaved parents may be viewed as being at the center of the crisis of pregnancy loss and it's impact on daily life. Just as a pebble dropped into water generates infinite concentric circles, the effect and impact of pregnancy loss spreads out to touch many people in more ways and for longer periods of time than one might imagine. Having already discussed the reactions of the mother and father, I want to look at the first circle. The parents, children, family and close friends of the bereaved come to mind. These are the people who would have been the grandparents, siblings, aunts, uncles, cousins, pals of the baby. They have already shared with the parents in the growth and development of the unborn child, have seen the ultrasound pictures and have felt the baby move and kick. Some may have offered to loan cribs and baby clothes, offered to baby-sit, begun to knit a blanket or sweater, or have offered to share their toys and even their room. Now they have to shift gears and direct their efforts to providing comfort, support, a listening ear, a calming touch--to helping in whatever way they can, While the expectant mother or couple eagerly accepted previous offers of services and goods, how will they now respond to offers of emotional support and to being taken care of? Over the years f have found that people strive to be independent, capable, and self-sufficient and want to be so considered by others especially in times of crisis. Will the bereaved parents accept help from those who want to give it?
What about the children who would have been siblings or cousins? What do you say? How do you explain the passing of a baby to a youngster eagerly awaiting its arrival. If there is a funeral should the older children attend? Is there a way to be clear and truthful about the loss without making it sound too frightening? Although in the midst of their own grief, parents are concerned about the other children at home, who want to know that mommy is OK and when the baby is coming home. Parents have to continue in the role of caregiver while requiring care themselves. Parents generally want to discuss these questions and are open to suggestions. Often the family pediatrician who is familiar with the child can be very helpful in framing answers to the questions children inevitably ask.
Continuing the flow out from the center, you next encounter neighbors, coworkers, classmates, the people from your congregation, local shopkeepers, etc. A whole new set of concerns arises. How many of them knew about the pregnancy, are pregnant themselves, or have young infants? How does one explain what happened to concerned and curious associates? How much should you say and how much do they really want to know? How will you face it when their due date arrives? Should you go to the baby shower you've been invited to next week? Your daily acquaintances are undoubtedly as unsure as you are.. They don't want to upset, ignore, or anger parents by anything they might say or do. These are delicate situations and we all have to act or respond as best we can, There are no simple answers.
On the outer perimeter and on a more global scale, pregnancy and babies are everywhere. So, just when bereaved parents feel composed and ready to face the world, they are bombarded by TV commercials for Pampers, pregnant women in the supermarket, and babies in the park.. One can't escape the realities of birth and death, pregnancy or its loss. Each day women, their partners, and their families move ahead and hopefully grow stronger as they recover from the complexities of pregnancy loss. Many may connect with local support groups. Support groups and books on pregnancy loss are excellent ways to increase one's understanding of the topic and to receive ongoing encouragement, motivation, and strength. A few clinical snapshots dramatically illustrate the depth and breadth of the impact of pregnancy loss:
A young Hispanic couple wants a photo of their anomalous stillborn to send to their parents in Puerto Rico so the family can better understand what happened. A 30 year old woman and her husband softly discuss what to tell Molly, their 3 year old daughter, who is waiting at home with a teddy bear for her baby brother. An oriental man with a stoic, expressionless face sits beside his silent wife whose face is streaked with tears. A 16 year old boy approaches his parents wanting to ask about the family secret-his twin brother who died at birth. A 50 year old only child with ailing, aging parents wonders what things might be like if the losses hadn't occurred and she was now the oldest of three. A labor and delivery floor nurse who has just learned she is pregnant is assigned to care for a woman with a fetal demise. A 25 year old woman, mother of a 5 year old, suffers a second trimester loss and becomes suicidal because she feels she's lot everyone down.
In closing, it would be difficult and unfair to define, catalogue, or quantify, the emotional impact of pregnancy loss in any standardized way. The reactions to loss are as unique and special as are the people themselves. Loss touches people in many different ways and at times for years into the future. There is a fluid process of adjustment, reflection, and acceptance--at times easier, at times more difficult. The child is gone, but never forgotten, and often the subject of continued fantasies about what might have been.
Laurel Jonason, R.N., BSN
What is it like in a Newborn Special Care Unit? It is many things: some of our activities have been featured on TV shows which talk about ethical issues, expensive medical care, and sometimes of the medical miracles which often happen there. For those of us who work in these units our job is multifaceted also. It can be incredibly intense as the staff struggles with all of our combined expertise to save a small life. It can be rewarding when we can watch a baby who was deathly ill finally go home to his or her family. It can also be agonizingly sad when in spite of all our efforts, a baby dies.
All the babies who come to our unit are alive. Those children who are stillborn or are delivered before an age for which any resuscitation can be done are cared for by the staff of Labor and Delivery staff. Often, since we are a tertiary center, we receive babies from other hospitals, sent to us for the type of specialized care that only a few hospitals can provide. The babies that we receive can be premature, or have physical defects, heart problems, experienced a very difficult delivery or have a need for specialized ventilation therapy which is not available at other nearby hospitals.
So what is my job in all of this? The easiest way to describe it is to relate the events the life just one of the many babies I have cared for. This is an actual case which I have disguised to protect the privacy of the family involved. Tom was a full term baby. He was the first born child of a married couple , Luis and Carmen. He was born at an outlying hospital and transported to us for worsening respiratory distress. When I received him, and became Tom’s Primary nurse, I could see that we would have to fight very hard for this child. Tom was diagnosed as having Persistent Pulmonary Hypertension, a situation in which the baby’s lungs remain in their fetal state and do not allow for proper oxygenation of the blood. He had a tube in his windpipe and we began to turn up the settings of his ventilator. Meanwhile, he was in shock and I rapidly prepared and administered the many syringes of fluid and medication to try and support Tom’s blood pressure. The attending physicians and the house staff made the decision to approach the family for consent to use a new study drug, Nitric Oxide which has allowed many babies with this condition to "open up their lungs" and be ventilated. They spoke to the parents as they were leaving the hospital where Tom was born and after explaining Tom’s condition and the treatment they wanted to try, the parents agreed and said they were coming to Yale. As we began the Nitric Oxide and continued the high frequency ventilation, Tom was deteriorating. As I drew and sent each new blood gas, we all hoped for an improvement. Preliminary lab results told us that Tom probably had an infection in his blood. Tom had already been started on antibiotics , and as I prepared his second dose I hoped that this round would help us turn the corner. The doctors ordered and I mixed new drugs to try and help Tom’s heart push against the resistance o f Tom’s stiff lungs. More fluid was pushed. Blood products were given. The doctors talked about ECMO a type of bypass pump which could act as part of Tom’s lungs until they could get better. We needed time - time to get ECMO team together, time to get the parents in to see their baby, time to allow the antibiotics to work, time to call in Social work, time…. And it was running out… and then we knew…what we had feared all along… that we would not save this child…. Perhaps this is the most difficult time for us as staff members… to know that we tried so hard and no matter what we do, it is not enough. Some people would now say, "there is nothing more we can do"… but there is… and in that moment which sometimes comes collectively and sometimes separately we all had to redefine our goals. We needed to try to keep Tom alive until his parents arrived. We needed a little time to prepare the parents as best we could for the death of their child. We needed to find the best way to support a couple who had just had a birth and would now have a death.
Luis and Carmen arrived in time. As gently as they could, all the gathered team explained that we had done all we could but Tom was dying. His heart rate was dropping and he would die soon. We asked them if they wanted Tom baptized and all the staff gathered at Tom’s bedside as the priest baptized Tom , and prayed for support for the parents. The attending and I remained at Tom’s bedside. Together we explained what choices there were for Tom’s final minutes. This is always such a difficult thing to do. We ask parents to choose from options which none of us want Do they want their baby to die in his bed on all the life support? Do they want to hold him while he is still on all the equipment.? Do they want to remove him from the life support and hold him in as he dies ? Do they want to hold him in the ICU or go to a private room? What we try to do is to offer them a "road map" for a territory where they have never been… they can choose which direction to go… we will be there to help and support. Luis and Carmen asked about what would happen when Tom died. We explained that we would give him a small amount of morphine to make him comfortable… that his heart would slow even more… that he might breathe a few times on his own… and them he would be still… and that if they wanted they could hold him as long as they wanted. We asked if there was anyone else they wanted called. They said that Carmen’s parents were on there way. We alerted the secretary to let us know as soon as they arrived. Luis and Carmen wanted a chance to hold Tom before he died. Since we believed that he would die quickly off life support, we curtained off Tom’s section of the nursery and moved all of Tom’s equipment to allow his parents to hold him. Both Luis and Carmen wept as their new son was placed in their arms for the first time. As the monitors showed Tom’s vital signs continuing to dwindle, his parents told us that it was time to remove those last connections which seemed to be merely prolonging their child’s dying. We escorted Luis and Carmen into a private room near the nursery, and all of Tom’ s caregivers worked together to remove all the life support we had placed there. Tom., for once, free of all his tubes and wires was gently wrapped in a warm blanket and a clean shirt and hat and taken to his parents. Tom was still alive as I placed him in his parents arms. At the parents’ request, the priest returned and Tom’s grandparents arrived in time to hear the priest’s blessing. As the parents murmured to Tom , he took a single gasp and was still. Luis asked if Tom was "gone"- the attending physician listened and said "…yes".
We have a protocol in our unit for what to do when a baby dies. It serves as a guideline for our actions, but much of what happens next is determined by the wishes and needs of the family. We offer them our presence but also give them the option of being alone. We allow supporting friends and family to be present if the parents wish but we also give the parents the choice of experiencing the death of their child alone. We encourage the parents to see and hold their child but we respect their right to refuse- some parents find holding their baby at the time of death is just too difficult- we explain to the parents that the staff can hold their baby instead- and if this is what the parents wish, we will hold that child until death has occurred. We often offer the parents the option of bathing and dressing their baby- if they choose not to, their baby is always bathed dressed before it leaves our unit. We prepare a "Bereavement Packet" which has a Memory Book for foot and handprints, locks of hair and mementos. We include several pictures of the baby - the setting and style of the photos are at the choice of the parents- often we take pictures of the parents holding the baby as well as close-ups of their child. The Bereavement Packet also contains literature about grief, lists of support groups, a bibliography and additional materials.
Luis and Carmen held Tom for over an hour. Carmen’s parents held him too, and then left Luis and Carmen alone with Tom. This couple expressed the wish to be alone for a while so we agreed that I would come back when they called me. After this period, I returned to them and explained about the contents of the Bereavement Packet. Our Social Worker had come in and spent some time with them and. had discussed burial options . Although some parents refuse the packet, (and we keep it on file in case they want it later), Carmen and Luis wanted their packet. They wanted to see Tom after I bathed and redressed him so I tenderly washed Tom and put him in clean clothes. I also obtained Tom’s hand and footprints as well as a lock of his hair and I placed these inside the memory book along with his crib card and name sign. After I brought Tom back to his parents, they held him for a few more minutes and said their last good-byes. They had discussed their wishes regarding autopsy with the attending and had signed the necessary paperwork. Luis and Carmen handed Tom back to me- this is always a hard moment for all of us… I hugged them both… and then they left their precious child with me and walked out of the unit . I prepared Tom for his final journey and then he was gone from my care. I returned to his empty bedside . I paused to reflect on his short life and to review all the events that had transpired there. As always, I hoped that I had done my best to meet the needs of his family. I am aware that my efforts to support this family have a cost for me. A death is draining- I would need to "refill my cup". I have experienced so many deaths in our unit and I know how important this personal restoration is- each if us has to replenish our "compassion stores" before we can best care for the next family who needs us. Sometimes this is hard to do. ..
As Bereavement Chairperson for our unit, I do much of the nursing follow-up of our families who have had a baby die in our unit. As I do for all the families, I prepared and sent a sympathy card to Luis and Carmen. I added them to the list that we keep and the following March I sent them and invitation to our Night of Remembrance in which we invite all the families of children who have died at Yale in the last two years. It sometimes overwhelms me as I send out the invitations,… each name is a personal loss to that family… and there are so many that I was there for… and I remember… Luis and Carmen came to our remembrance ceremony. As Tom’s name was read, I handed a flower to Carmen who had come forward to receive it. At the reception afterward, I talked to both of these parents with whom I had shared a short but intense and meaningful experience. They were going to a support group and said that they had good and bad days…the holidays were tough… but they had hope that maybe next year when they were invited again, Carmen might be pregnant. I told them again to call me if they needed me… I shared with them the short life of their child… I would him remember him too.
Leena Väisänen MD, Ph.D.
The Loss of a baby is always traumatic The crisis begins from traumatic experiences. The parents transit into the liminal space between life and death. This stage also underlines the paradoxical quality of grief. A logical thought is followed by another, which contradicts the first, as in: the mother feels she cannot respond at all, because she feels dead herself. She cannot be alive, because her baby is dead. Recovery also seems something impossible and far away, although ideas of recovery appear early on in the process, balancing the mind and necessarily protecting the ego from being split . The subliminal time of grief is shown in the altered way of experiencing things. One lives in an altered time with strange symbols, omens, dreams and unusual psychic and physical experiences. The experience of grief is not only stepwise and processual, but multi-voiced and stratified, like counterpoint in music, and there is reciprocal movement within it like in paradoxical loops. The loss of a baby results in grief that runs counter to the expectations. The parents have invested so much primeval energy in the baby who is no longer alive that they tend to re-create her/him in their minds psychologically or spiritually. Grieving thus involves deep attachment rather than detachment, and the processing of this attachment makes it possible to recover.
The somatic aspect of grief
Family grief requires collective tolerance and sharing. The family members huddle close together and set up a wailing wall around them: it is permissible at home to cry aloud or grieve quietly. The quiet, largely somatic aspect of grief is strongly present after baby loss. The mother, and occasionally also the father, may find themselves in a subliminal space between life and death, where the pain of the loss, emptiness and longing is present as physical pain. The loss of a baby in the symbiotic phase results in grief manifested as physical pain and longing, feelings of emptiness, strange sensations and a phantom baby. Some mothers are able to verbalize this better, but all losses involve feelings of distress, restlessness, pain and anxiety which are due to the fact that the mother, with all her finely tuned physiological systems, was intended to keep her baby alive. Although there is no baby, the mother's psycho-physiological need to care tends to persist. She is still symbiotically dependent on her baby, who no longer exists as a living being. She is constantly preoccupied with the baby, the grave and death. She may even be so intensely dependent on the grave that she cannot leave the locality. Visiting the grave daily may be important, and even when she does not actually visit the grave, she may be conscious of it. Because the baby is in a grave, the mother may feel for a long time that she is in a grave herself. Phantom babies are symbolic representations of grief and continue their nearly physical existence in the family. The alternative religious metaphor is a baby angel, which splits the traumatic experience into two: the disconcerting body of the baby in the grave and a consoling angel. Grief reflects the psychological and spiritual attachment to the baby that was lost physically and strongly resists abandonment of the baby. It is based on the primeval energy of parental attachment, which is used, although there is no baby. Grief of family members
The mother's grief process and recovery are reflected in the family's overall coping. If the mother is able to share her attachment to the future baby early on in the pregnancy, the father is able to support his wife after their bereavement. Fathers are generally the best supporters for their wives. The challenge posed by grief to the father is a need to find his own specific grief beyond the mother's grief. In the light of the present findings, young parents who lose their first child need a lot of support. They may have an inadequate support network, having moved to a new locality as students, for example. They have abundant experiences of being left alone. The families who already had a strong social network were given adequate outside support of many kinds. It is important in these families to be able to be alone from time to time. Children were the active parties who interpreted and commented on their parents, and who used use their energy and imagination to console their parents by all possible means. A child may also assume the role of a therapist in relation to her/his parents. In this study group, latency age girls who had identified with their mother's pregnancy appeared to be at risk, because they also lost symbolically the baby or identified with the baby and began to fear for their own death. Children may also have transient age-appropriate symptoms and therefore need an adult to talk about things that are important for them. The basic attitude of children towards death and dead people is natural and curious. Children are conscious of the paradoxical quality of their parents' grief, because they share a cyclic notion of time and way of reasoning. Children are also able to delay their own grief reaction to help their parents.
Time of grief
Grieving takes a lot of time. Although the restlessness, anxiety and depressive moods disappear, grief continues as a long process. The first year is the worst. Each parent has her/his individual schedule. Grief is not something that becomes linearly alleviated, but rather a circular process that is activated by the intense initial guilt and obsessive need to find out causes and details. This study showed the recovery times to vary, depending on the individual personalities of the parents and the family structure. The family recovery process mostly takes place through dialogue between the family members, which allows them to find new meanings. Their goal is to survive the catastrophe by finding new meanings for the family security system, their identity as a family and their world view. The very short recovery times reported in quantitative studies reflect their short follow-up times and the research setup.In this study the active grief time lasted usually for two or three years. Grief for the death of a baby continues at some level for ever, although it is not pathological or complicated. When time elapses, the feelings of pain alleviate
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Leslie Ciarleglio, MS
Introduction
The prospect of meeting with a genetic counselor can be intimidating for the client. There are often fears associated with the investigation of one’s own make-up in the most basic sense. People also often have misconceptions about what genetic counseling is all about. As technological knowledge expands, and the genetic basis for common disorders is understood, it becomes increasingly likely that the “average” person will have the occasion to speak with a genetic counselor. Ideally, this sneak peek into genetic counseling will help to alleviate the anxiety of the unknown and help clients to prepare for a more productive genetic counseling session.
What is genetic counseling?
The American Society of Human Genetics (ASHG) defines genetic counseling in the following way:
Genetic counseling is a communication process which deals with the human problems associated with the occurrence, or the risk of occurrence, of a genetic disorder in a family. This process involves an attempt by one or more appropriately trained persons to help the individual or family
1. comprehend the medical facts, including the diagnosis, the probable course of the disorder, and the available management;
2. appreciate the way heredity contributes to the disorder, and the risk of recurrence;
3. understand the options for dealing with the risk of recurrence;
4. choose the course of action which seems appropriate to them in view of their risk and their family goals, and act in accordance with that decision; and
5. make the best possible adjustment to the disorder in an affected family member and/or the risk of recurrence of that disorder.
Who are genetic counselors?
Genetic counselors are members of a health care team. They provide information and support to families and serve as patient advocates. They are also educators and a resource to other health professionals and to the public. Genetic counseling has historically been provided by physicians, social workers, and nurses. Currently, the majority of genetic counselors are professionals who are masters prepared through accredited programs focusing on the combination of medical genetics and psychology. Counselors are certified through the American Board of Genetic Counseling which was established in 1993. Previously, certification was through the American Board of Medical Genetics.
Genetic counselors have become highly sub-specialized - there are counselors that specialize in only prenatal genetics, pediatric genetics, or adult genetics. Some counselors work in commercial labs as liaisons with the referring community. Some counselors work only in research settings. Some counselors work only with patients affected with specific disease types, such as inborn errors of metabolism, neuro-genetics, or cancer genetics. Others work in a single disease clinic, such as a cystic fibrosis center. Private practice is also a growing area for genetic counselors. As the Human Genome Project further uncovers the genetic basis for many “common” diseases, genetic counselors will be found more globally throughout medical practice.
General principles of genetic counseling
In the ASHG definition, genetic counseling is described as a communication process. This implies mutual participation between counselor and client. This is a strategy that is often unfamiliar for many patients and this unfamiliarity can create anxiety for them as well. This may also be a new approach for many physicians. With this new role, the patient assumes responsibility for his or her actions. In order for the counselor/client relationship to be effective, and to encourage patient participation, the style and dialogue in a genetic counseling session must be catered to each client’s needs, goals, and perspective. Non-directiveness is a fundamental principle of genetic counseling. This refers to the belief that clients are capable, if thoroughly informed, of making appropriate choices for themselves. Counselors need not and should not make decisions for their patients. Non-directiveness is essential. Ethnicity and socioeconomic background have to be considered. Ideally, a genetic counselor will maintain “unconditional positive regard” towards the patient, as well as maintaining continuous sensitivity to the patient’s varying emotional states. Without these considerations, the counselor cannot elicit all relevant information and, additionally, will not be able to transmit information effectively.
It has been said that genetic counseling is 20% genetics and 80% counseling, and I would agree. The purpose of genetic counseling is education of patients, but also empowerment, advocacy, and support of patients.
Genetic counseling is often crisis intervention. Patients may be asked to deal with or to make decisions with significant and perhaps lifelong implications in a time of emotional upheaval. Issues surrounding medical interventions in pregnancy certainly fall into this category. Deciding whether or not to undergo a particular prenatal test can be very stressful. This pales in comparison, however, to deciding about what to do when faced with abnormal diagnostic test results. Many health care providers have worked with couples in these situations. However, few can truly understand their feelings and their pain. Genetic counselors are trained to appreciate the psychological aspects of these patient dilemmas.
The genetic counseling session
Who are genetic counseling patients?
In this context of prenatal diagnosis and testing, I would like to outline a “typical” genetic counseling session. To touch briefly on an enormous subject, prenatal genetic testing has become an issue that, at some time, almost all pregnant patients face. To review, testing is available in many forms, at different times in gestation. First trimester genetic diagnosis is a relatively new area in obstetrics and represents the cutting edge of prenatal testing. Ultrasound at approximately 10 weeks of gestation (counting from the first day of the last menstrual period) can confirm viability, the number of gestational sacs, and identify certain major structural anomalies, such as fetal anencephaly, in skilled hands. Also, screening for chromosomal abnormalities by looking at the nuchal area at this early gestational age is becoming more widely used. Second trimester genetic testing is more familiar to most patients. This includes maternal blood tests such as the AFP test or the “triple” screen, which is used to determine whether a patient appears to have a relatively high or low risk for certain chromosome abnormalities or other birth defects. Level II ultrasound, also known as targeted fetal ultrasound, provides a detailed look at the fetal anatomy. With advancements in technology, ultrasound has become an increasingly relied-upon tool in pregnancy management. Referrals for fetal echocardiography, a subspecialty of fetal ultrasound, have also increased. Amniocentesis is an invasive diagnostic procedure that can provide information about the fetal chromosome pattern. Additionally, specific hereditary conditions can be tested for through biochemical or DNA analysis.
All of these tests allow for identification of congenital anomalies or syndromes in a pre-viable fetus. In the prenatal setting, parents may seek genetic counseling in consideration of some of this testing in an apparently normal pregnancy. Less commonly, parents may meet with a genetic counselor to help them at a time when this testing has identified a problem in a pregnancy.
Content of a genetic counseling session
For pregnancy related issues, as outlined above, there are, in general, two types of genetic counseling sessions - those where parents are concerned about potential risks and outcomes, and those where patients are concerned about a known problem with the pregnancy. Despite the vastly different nature of these sessions, there are common aspects. Any counseling session has two major components - the provision of information to the client, and a therapeutic dialogue where the counselor listens to, hears and responds to the patient’s reactions to this information.
The structure of a session
Most genetic counseling sessions are scheduled by telephone and conducted in person. It is occasionally necessary to have these discussions over the telephone; however, this is not optimal. Ideally, there is a private room specifically designated for counseling purposes with adequate seating for the genetic counselor, the client(s), and any other people the client feels are appropriate to have there. In a medical center, the genetic counselor may have students or other health care providers that are interested in observing a genetic counseling session. Of course, this should only be done with the patient’s permission. Patients have every right to decline the presence of observers, especially in what can be a very emotionally-charged session.
Initially, the genetic counselor will go through the process of “contracting” with the patient. This refers to outlining the session with the clients to establish common objectives. Parents may be asked how much they know and understand already. Especially in the situation of a known fetal anomaly, patients come to genetic counseling with wide variation in the amount of information they have been given before this session. Patients are often asked what their expectations are of the genetic counseling session and what they hope to achieve in the session. The counselor will provide the patient with a general overview of the session that should take these expectations into account. By establishing common objectives and finding out what the patient knows and wants to know, the counselor helps to ensure that the client’s needs are met and the session is productive for all involved.
Most genetic counseling sessions include gathering family history information from the client. This may be as simple as a few general questions about the patient’s health, family tree, and ethnic background. As the situation dictates, however, obtaining family history information may be much more involved, such as constructing a pedigree (a medical family tree) with detailed medical information about extended family members. Family history information is important in assessing potential risks in healthy patients, as well as for increasing our understanding of a known problem in a pregnancy. Knowing in advance that this information will be discussed, the patient can prepare for the genetic counseling session by gathering relevant family history information in advance. In a prenatal setting, the genetic counselor will also inquire about potential exposures to the pregnancy, including maternal illness, prescription and over the counter medications, recreational drugs, environmental exposures, etc.
Next, most discussions will focus on the issues at hand - concerns about risks, or, counseling about a specific diagnosis. Throughout this part of the discussion, the counselor will often ask the patient if the information is being presented clearly. Important points will often be repeated and written down. If this is not done, ask for it. Many counselors draw diagrams to help illustrate their points. Pamphlets and other patient literature will commonly be provided. A genetic counselor recognizes that it is difficult for families to retain all of the detailed medical information at a time of emotional upheaval. Written materials for the patient to take home can serve as a useful review, as does a follow-up phone call. In some situations, the counselor will provide the patients with a summary letter of their session as a reference for them.
Recognition of and responding to a patient’s feelings are an integral part of the genetic counseling session. All clients present to genetic counseling with some level of anxiety, even in the most routine of circumstances. This seems to be particularly true in the prenatal setting. The risk for a problem, or the diagnosis of a specific anomaly in a pregnancy, is often the realization of any parent’s biggest fear - “something wrong with the baby”. This anxiety can be overwhelming and often has a significant impact on a patient’s self image. Additionally, it is appropriate to include in a genetic counseling session a discussion of “what ifs” regarding different potential outcomes. This allows clients to consider how they might feel in different situations, and to assess their own coping strategies and support mechanisms should a problem be identified.
Lastly, a plan is agreed upon. The goal of any genetic counseling session is to allow the patients to achieve a good enough understanding of their situation to make their own informed decisions. In general, there are no right or wrong answers; patients choose a course of action that is most appropriate for them and for their family goals. Counselors are often asked “what would you do?” in a variety of situations. It is unfair to the patient to answer that question directly, as there is such great variation in every individual’s perspective, needs, and goals. The genetic counselor may instead review issues that would help the patient to come to their own decision. The genetic counselor will act as a facilitator, but should not make a decision for the patient.
To follow up, as mentioned above, the genetic counselor will often telephone a client a few days after a session. At times, patients will often call the counselor first with questions they “forgot to ask” or for clarification of certain points. Patients should be encouraged to write down their questions and concerns. It is especially difficult for clients to remember everything they want to ask during what is often an emotionally charged environment.
Summary:
In summary, genetic counselors provide a wide range of services as members of a health care team. The goals of genetic counseling are to provide patient education, support, advocacy, and continuity. As the availability and range of genetic testing increases, genetic counselors are found in ever expanding roles. Additionally, more and more people will be offered the option of meeting with a genetic counselor. I hope that this option may be looked upon as an opportunity... an opportunity for patients to work with a genetic counselor to gain an understanding of their own genetic issues and concerns, which will empower them to become active participants in their own healthcare.
Julia Bishop-Hahlo,
This poem was written in memory of a very special little boy, Lamar. I was his primary nurse and cared for Lamar during the two and one-half months that he was with us. He was born at 26 weeks to a drug-addicted mom. She visited him just once or twice and was not involved in his care. Because she chose to remain at a distance, I allowed myself to become very attached to Lamar and he became very special to me. He, in turn, was comforted by my voice and my touch. I held him as he died and he continues to hold a special place in my heart.
Startled and fascinated by the beauty and fragility
of your wings, I watch as you move
so gently
so quietly
almost unexpectedly
through my world
And then I watch as you move on,
fluttering softly into the distance.
Pleading silently, I beg you,
please ... don't go.
I haven't yet had the time
to memorize
to remember
to understand
the uniqueness of the beauty that is yours.
I know I cannot hold you for long,
capturing you for my world.
But, rest gently with me
if only for a moment.
That I may treasure the memory
and the beauty of the gift that you are.
Frank H.Boehm, M.D
Like most professions, medicine has its boring and mundane times. But several years ago, as I sat overlooking Niagara Falls, I reflected back on the times when being a physician is exciting and rewarding with moments filled with awe and wonder.
Eleven years ago, I was called to hospital's labor and delivery suite to take care of a patient carrying quintuplets. Although only 24 weeks pregnant, my patient was in premature labor. Despite vigorous attempts to stop her progress, she was about to bring into this world, not one but five new human beings.
Moving her quickly into the delivery room, I knew we were in trouble because these five babies were four months premature and had only a one-in-five chance of survival. If they survived, each child would need intensive and expert care for an extended period of time in our newborn nursery.
Within minutes, I was standing in my place, ready to deliver the first quintuplet. Gazing around the room I noticed the enormous amount of equipment and personnel. Each of the five newborn resuscitation tables brought to our arena of life and death had three newborn personnel waiting for their turn to receive one of the quintuplets. A certain amount of apprehension could easily be seen on their faces.
At the head of the patient's table were three anesthesia personnel prepared to do what was needed to bring this new litter of children into the world. Circulating around our place of birth were two obstetric nurses readying the room for our big event, and standing with me were three obstetric resident physicians.
One resident was constantly monitoring the small and fragile babies within the uterus with an ultrasound machine, while the other two stood fully scrubbed ready to aid me. Standing in the corner were two medical students, eyes wide open in absolute amazement at what they were about to witness. Finally, sitting quietly next to his wife was the father-to-be, staring with disbelief at the spectacle he had helped to create. Despite all of these people, the room was relatively quiet. It was a quiet I had heard before-a quiet that said, "This is it-this is what our job is all about!" One at a time, they began their journey down the birth canal. Head first, Stephen appeared, followed by his siblings-Stephanie, Clinton, Barbara, and Christopher-each taking its turn to follow the next. As each child fell into my waiting arms, I carefully cut the umbilical cord and handed the child to a waiting pediatric team member. Finally, it was over. What seemed like an hour was in reality only a few minutes. I had just delivered five tiny human beings into this world. I was truly filled with awe and wonder.
While very birth can easily be described as awe-inspiring, after delivering more than 4000 babies in my lifetime, there can be a certain amount of routines. But not this time. While I delivered many twins and perhaps a dozen triplets in my career, I had never delivered any quintuplets. Since spontaneous occurrence of quintuplets is approximately one in 15 million pregnancies, it is extraordinarily rare and unique event. After the deliveries, awe and wonder filed the room. We were all a part of nature's wonder. What a privilege and honor for us all. But the human uterus is made for only one child at a time, and multiple births cause problems for both mother and babies. In this case, our excitement was soon followed by disappointment and sorrow as we helplessly watched Stephanie, Clinton, Barbara and Christopher lose their fight for life.
What I felt that night years ago went beyond mere awe and wonder. It included humility. Being a part of such an incredible event of nature can easily bring forth such a feeling. How small and insignificant we humans are in comparison to nature's wonder. When I last saw the one surviving child, Stephen. A healthy, happy and loving child, the feeling of humility quickly returned. It is the same humble feeling I felt while viewing up close the magnificent Niagara Falls in all its incredible splendor.
As extraordinary as it might sound, at least 15% of clinically recognizable pregnancies end in fetal loss. We can separate losses into several different categories but for clarity I will classify them temporally throughout the pregnancy as:
1. First trimester-conception through 13 weeks.
2. Second trimester-14 weeks through 26 weeks.
3. Third Trimester-27 weeks through 40 weeks(term.)
The most frequent losses occur in the first trimester either as spontaneous abortions(miscarriages) or Ectopic Pregnancies. Up to 50 per cent of all tissue from miscarriages demonstrate chromosomal abnormalities. Therefore, chromosomal abnormalities are the primary cause of miscarriages. These aberrations occur early in embryonic development and many times do not even manifest a fetus. Unless one or both parents are carrying an abnormal chromosome, the risks of recurrence for these early miscarriages is low. Implantation (the establishment of a maternal/fetal unit) can be interrupted by a deficiency or imbalance in the production of maternal hormones, most often progesterone from the ovary and thyroxin from the thyroid gland. Maternal bacterial, viral or viral-like infections have also been associated with first trimester pregnancy losses. Three in particular are mycoplasma, chlamydia, and gonorrhea.
Mycoplasma can actually be a cause of recurrent spontaneous abortions while chlamydia and gonorrhea can also infect the uterus and fallopian tubes and damage the very delicate lining of the tubes(called tubal endothelium) and create a hostile environment for the transport of the fertilized egg promoting an increased risk for a tubal or ectopic pregnancy.
Other factors which have been implicated as causes of first trimester losses include auto immune disorders such as the Anti-phospholipid syndromes, substance abuse, cigarette smoking, multiple pregnancies and placental abnormalities such as gestational trophoblastic diseases, the most common being molar pregnancies.
Treatments for imminent miscarriage or first trimester loss are unfortunately usually expectant. Attempts have been made to prescribe strict bed rest, administer hormonal supplements as well as other exogenous therapies. In circumstances where there is a viable pregnancy and significant vaginal bleeding, bed rest might be beneficial to reduce trauma in an already precarious pregnancy. Such is the case with the so called vanishing twin syndrome where conception resulted in a twin gestation but one twin aborts causing bleeding while the remaining twin is viable. Progesterone therapy is thought to be of value in circumstances where it is felt there might be a reduction in progesterone production from the ovary leading to poor embryonic development (inadequate luteal phase.) Aspirin, steroids such as prednisone and heparin have been used with some success in the treatment of immunological causes of pregnancy loss.
The second trimester begins at about 13 weeks and continues until the twenty-seventh week. What make this trimester unique is that it spans a time period where a pre-viable fetus becomes a potentially viable neonate, albeit premature{pre-term.} At exactly what week or day or fetal/neonatal weight this transformation occurs depends on many factors and "unknowns." In current practice, 1995, it is generally felt that a pre-term birth prior to 24 weeks is unlikely to survive, although it is not impossible and without hope. [when I was a Ob-Gyn resident in 1973, 28 weeks was considered the critical gestational age.] The third trimester shares similar etiologies to the mid or second trimester.
Chromosomal abnormalities as they account for nearly 15 per cent of mid-trimester pregnancy losses. Fortunately, there exists for all pregnant women an opportunity for a comprehensive prenatal evaluation of their fetus for the purpose of determining genetic and morphologic[structural] normalcy. Although it is not considered mandatory or routine, women at risk for fetal problems may avail themselves to several testing procedures as well as be offered screening procedures. Because some tests are invasive e.g.. amniocentesis, CVS, fetal blood sampling and direct fetal visualization (fetoscopy,) it is important for the patient and her physician to have a clear understanding of what information is to be ascertained from a particular test, its risks and its limitations. Other tests such as blood screening and high resolution ultrasound are less invasive. With these guidelines well defined, the prenatal diagnosis of fetal abnormalities becomes an important tool in the contemporary care of pregnancy.
Pre-pregnancy counseling is very important, and women should consult their physician or other primary caregiver prior to conception, or at least very early in the first trimester, so as to determine any risk factors for genetic diseases; e.g. familial disorders such as cystic fibrosis, muscular dystrophy, hemophilia, sickle cell anemia, Tay-Sachs Disease or chromosomal disorders, the most common being Down's Syndrome or Trisomy 21.
Carrier states can then be detected prior to conception or early in the pregnancy. Appropriate diagnostic tools may be utilized as described above: blood sampling, chorionic villus sampling, amniocentesis and high resolution ultrasound. For families who have been identified at risk for these or other hereditary diseases, genetic counseling is indicated. Genetic centers are usually integrated in University centers.
For families not at risk for genetic disorders, certain screening tests(non-invasive) are available. The maternal Alpha Feto Protein test(now combined with two other markers-HCG and Estriol) is a screening test primarily for two particular classes of disorders; neural tube defects(NTD) and chromosome abnormalities, the most common being Downs Syndrome or Trisomy 21. If the test should return as "positive," either above or below the limits of the mean, it does not necessarily indicate there is a problem-only that their might be a higher risk for a problem. The next procedural step would be to perform a detailed ultrasound exam, sometimes called a "level 2" scan and possibly an amniocentesis. These second line tests can better define the health of the fetus within the limitations of each test.
Genetic testing today, although available now for many years, is on the cusp of a new frontier-that of very early, embryonic diagnosis via micro-fetal blood sampling and maternal blood sampling for fetal cells and fetal chromosome analysis. Early fetal treatment may also be possible through current and ongoing research in gene manipulation and therapy.
Genetically abnormal embryos that develop and survive the first trimester can be either diagnosed by the aforementioned prenatal tests, or be manifest by spontaneous labors or by the anguish of intrauterine fetal demise. One example of an abnormal chromosomal arrangement which presents with either premature rupture of the fetal membranes, premature labor, or fetal demise is Trisomy 18. Although this can be detected by CVS, amniocentesis and/or ultrasounds, most patients not at risk will not have these procedures. Maternal serum AFP testing can screen low risk populations but it is only a screening tool thus some patients might not avail themselves of it and others might have a false negative report. Trisomy 18 is not compatible with life and early diagnosis can offer affected parents the option for elective termination.
Voluntary termination of a genetically abnormal fetus in the mid-trimester when selected as an option for the pregnancy is no less anguishing than spontaneous pre-viable miscarriage or delivery, for it not only involves loss but requires conscious decision making at a time when one's mind is replete with emotions of remorse. Patients at this time need careful, caring and informative counseling to help with their decision making process. If at all possible, counseling with a geneticist is the ideal. As difficult as are the decisions associated with situations of fetal death or non-viability, more so are those diagnoses involving anomalous chromosomes or handicapping physical abnormalities in a fetus who will be born alive and survive. It is not my intention in this forum to be judgmental or express opinions about the ethics of any options a physician might offer a patient veiled with these onerous problems, but these patents, mothers and fathers together crave information and guidance. Again, all options must be discussed and offered in a venue of information, compassion and objectivity.
With advancing fetal age, the expanding volume of the uterus places increasing forces upon the cervix. In the normal pregnancy, the cervix maintains significant strength to resist these forces upon dilation and effacement usually through the second and early third trimester. Certain conditions predispose the cervix to premature dilation and effacement and this in turn can lead to premature labors and pregnancy losses. When this event of premature dilation and or effacement of the cervix occurs, it is presumed a consequence of weakened cervical tissue fibers and is therefore been called "The Incompetent Cervix." The incompetent cervix accounts for approximately 15 per cent of all second trimester losses. The most common etiologies or predisposing factors for an incompetent cervix are: 1. Maternal DES exposure 2. Prior conization biopsy of the cervix 3. Repeated dilation of the cervix 4. Traumatic injuries to the cervix 1. DES or diethylstilbestrol is a synthetic estrogen which was given to women in the 1950's and 1960's with the hope of preventing repeated miscarriages. It was discovered however in the early 1970's that the daughters of these women as they entered their teenage years were developing abnormalities of the cervix called adenosis and rarely, adenocarcinoma(cancer) of the vagina- an extremely rare form of cancer. Although most of the changes of adenosis are benign, women, as they enter their reproductive years have a higher incidence of infertility and miscarriage- particularly in the mid-trimester. The adenosis which affects the morphology of the cervix weakens its inherent strength resulting in an incompetent cervix. Most women however who are DES exposed do not have this problem but the history of DES exposure is very important so that pregnant "DES daughters" may be followed more closely. 2. Conization biopsy of the cervix is a procedure which is performed to diagnose and treat cancerous or pre-cancerous changes in the cervix. The procedure actually excises a large portion of the cervix which contains the abnormal(dysplastic) cells and in doing this, almost invariably removes a portion of the muscular and connective tissue fibers of the cervix which contributes to its weakening.
Newer techniques such as laser therapy and electrical loop excision therapy can theoretically reduce the amount of tissue distruction but should still be taken into consideration when evaluating a patients history. 3. Patients who have undergone multiple therapeutic abortions and dilation of the cervix are at increased risk for an incompetent cervix because the muscle and connective tissue fibers of the cervix can loose their elastic properties and remained stretched if dilation of the cervix with mechanical dilators is performed multiple times. The appropriate treatment for these patients is "expectant" by means of frequent cervical examinations in the mid trimester.
The diagnosis of the incompetent cervix is not an exact methodology. Examinations early in the second trimester are important in any women with a history of any of the above listed factors or any women with a history of an unexplained mid trimester loss., particularly if it occurred without much pain or bleeding-the so called "silent dilation of the cervix. Early diagnosis of premature dilation of the cervix can lead to therapy which can sustain the pregnancy through and beyond the period of viability. Ultrasound examinations of cervical length and thickness can also be helpful but its role is not as well defined. Should the cervix be found to be dilated or particularly thinned(effaced) a suture can be placed around the cervix and tied to give the cervix strength. This is called a cervical cerclage. The two most utilized techniques for cervical cerclage are the Shirodkar and the McDonald procedures. Both yield similar results and their different uses depend mostly on the training and experiences of the operating surgeons. The premise for the cerclage is to further close the cervix and reinforce the connective tissue with high tensile-strength suture so as to maintain the integrity of the pregnancy. The procedure is most commonly performed just after the first trimester and can be performed as an outpatient under regional(spinal or epidural) or general anesthesia. Although this provides a strength to the already weakened cervix, the therapy for incompetent cervix must also include bed rest-sometimes throughout the pregnancy, possible use of tocolysis(the process of stopping labor with medications) and hospitalization when needed. In the appropriately selected population, cervical cerclage can be very effective and yield an excellent prognosis for term or near term delivery
There are many causes that have been linked to recurrent pregnancy loss. One of the less frequently seen associations is known as the antiphospholipid antibody syndrome.
What are antiphospholipid antibodies?
Under normal circumstances, antibodies are proteins made by your immune system to fight substances recognized as foreign by your body. Some examples of foreign substances are bacteria and viruses. Sometimes the body's own cells are recognized as foreign. In the antiphospholipid antibody syndrome the body recognizes phospholipids (part of a cell's membrane) as foreign and produces antibodies against them. Antibodies to phospholipids (antiphospholipid antibodies) can be found in the blood of some people with lupus, but they are also seen in people without any known illness. Lupus anticoagulant (LAC) and anticardiolipin antibody (ACA) are the two known antiphospholipid antibodies that are associated with recurrent pregnancy loss.
What is the antiphospholipid antibody syndrome?
Different physicians may use slightly different definitions to diagnose the antiphospholipid antibody syndrome. In general you need to have a positive blood test for either the lupus anticoagulant or the anticardiolipin antibody, on two separate occasions, at least eight weeks apart. In addition to the blood tests you must also have one the following criteria: A history of thrombosis (clots within the blood vessels), thrombocytopenia (low platelet count) or recurrent pregnancy loss. Several other manifestations may be seen, but not always, in patients with the antiphospholipid antibody syndrome which include skin, heart and nervous system abnormalities.
What is the association between antiphospholipid antibodies and pregnancy loss?
Among women with recurrent pregnancy losses antiphospholipid antibodies have reported to be present in 11%-22%. Lupus anticoagulant (LAC) and/or medium to high anticardiolipin antibodies (ACA) have been associated with first, second, and third trimester pregnancy losses. The association is even higher when the antiphospholipid antibody tests are persistently positive. Although it is unknown exactly how the antiphospholipid antibody syndrome adversely affects pregnancy, one theory is that it may cause blood clots. These blood clots, which can be microscopic, may occur in the blood vessels of the placenta. The placenta provides nourishment to the baby and any interruption in this process can be harmful to the pregnancy. The antiphospholipid syndrome may increase the risk of miscarriage, poor fetal growth, pre-eclampsia (high blood pressure during pregnancy), and stillbirth. It has yet to be proven but many researchers think the antiphospholipid antibody syndrome may exist in a state of remission or exacerbation similar to other diseases such as lupus or rheumatoid arthritis. This means you could have periods of times when the antibodies are not active.
Who should be tested for antiphospholipid antibody syndrome ?
Women who have had a history of recurrent pregnancy losses should be tested for antiphospholipid antibodies in addition to other routine tests. A history of unexplained poor fetal growth and or the early onset of severe pre-eclampsia (toxemia, also known as high blood pressure in pregnancy) or an unexplained placental abruption are indications for testing. A history of thrombosis (clots in the blood vessels), stroke, heart attack, thrombocytopenia (low platelet count), presence of other autoimmune disorders such as lupus, an abnormal VDRL, or PTT blood tests would suggest the need for testing.
What is the treatment for the antiphospholipid syndrome in pregnancy?
The drug of choice for treatment is Heparin, which is an injection to prevent blood from clotting. It is used in combination with "baby" (low dose) aspirin. In certain cases Prednisone and baby aspirin are used to treat the antiphospholipid antibody syndrome. All medications have side effects and the choice of therapy should be made after the risks and benefits of the treatments have been discussed between the physician and the patient. These pregnancies should be monitored closely by ultrasound every month to check on fetal growth and by antenatal testing (non-stress tests and biophysical profiles) weekly, beginning at 32 weeks gestation. Although there are a few reports of successful pregnancies without treatment, the majority of researchers have reported a 70%-75% success rate with treatment.
Introduction
With recent advances in genetics, there are several inherited disorders which can now be diagnosed at a molecular level. For couples who are carriers or affected by any of these conditions and are at high risk for transmitting it to their offspring, it is currently possible to detect the disorder during pregnancy. This is done by one of two approaches: amniocentesis or chorionic villus sampling (which involves taking a small sample of the placenta at an early stage). However the couples have the dilemma of whether or not to terminate the pregnancy if the genetic abnormality is present. In some cases this may also not be a viable option for religious or moral reasons. An alternative would then be to diagnose the condition in embryos before the pregnancy is established. Only the unaffected embryos would then be transferred to the uterus. This technique is referred to as pre-implantation genetic diagnosis and would obviate the need for screening during a pregnancy and hence prevent the physical and psychological trauma associated with possible termination.
How can a diagnosis be made in the pre-implantation period?
Research towards developing techniques for early genetic diagnosis in humans were initiated in the UK in the late 1980s (Handyside et al, 89, Lancet.347. and Dokras et al,90, Hum Reprod,5.821.). In vitro fertilization (IVF) techniques are used to obtain ova (eggs) from the mother which are then fertilized in the laboratory with sperm obtained from the father. One or more cells are then removed from the developing embryo 2 days to 4 days after fertilization. This highly sophisticated technique called micromanipulation does not adversely affect further development of the embryo. The cells removed are then used for analysis, and the results can be obtained within 12-24 hours. The embryos without the genetic defects are then transferred into the uterine cavity to develop into a normal pregnancy.
What are the different conditions that can be screened?
Almost all genetically inherited conditions that are diagnosed in the prenatal period can also be detected in the preimplantation period. Diseases which have a high risk of transmission (25-50%) and are usually associated with significant morbidity and mortality can be screened for by this technique. The limiting factor however is that few cells (usually only 1-2) are available for diagnosis unlike following amniocentesis or chorionic villus sampling. Therefore the possibility of obtaining an accurate diagnosis has to be confirmed by laboratory experiments prior to the clinical application of this technique for a given disease.
Are there babies born after application of this technique?
The first report of the successful application of this technique came from the Hammersmith Hospital, London, UK which currently is the center with the highest number of births following preimplantation diagnosis. Over 30 pregnancies have now been reported globally including the USA. The conditions screened for include cystic fibrosis, Tay Sachs disease, hemophilia, Fragile X syndrome, and rarer conditions such as Barth's syndrome and Rett's syndrome.
Why does the technique involve IVF?
Currently IVF is the only available method for obtaining an embryo in the very early stages of development . Therefore, although couples with a high risk of transmitting a genetic defect to their offspring may have normal fertility, they would need to go through the IVF procedure to provide embryos for screening. Not surprisingly, the pregnancy rate in this group has been shown to be higher than that seen in patients with documented infertility.
Whom would this approach be applicable to?
This technique is currently available to couples whose offspring are at a high risk (25-50%) for a specific genetic condition due to one or both parents being carriers or affected by the disease. Also the genetic code associated with the condition must be known in order to allow diagnosis. Currently it is not feasible to routinely screen women at lower risks, such as women over age 35 for Downs Syndrome, since the means of establishing a pregnancy is with the help of IVF.
What Next?
Only a few centers in the world today are offering preimplantation diagnosis to couples at high risk or those who have an already affected child. Efforts continue to be focused on improving methods to obtain an accurate diagnosis from only one or two cells. Techniques are now available to screen for more than one condition simultaneously, however the accuracy of these modifications need to be tested further. Although there is certainly a demand for this approach as shown by studies, it will continue to be available only in select specialized institutions with excellent IVF and molecular biology laboratories.
Congenital heart disease is one of the most common congenital anomalies. Overall approximately 3% of newborns are found to have some major congenital anomaly, and about one in 6 of these have congenital heart disease. Looked at another way, about 30,000 infants die annually in the US between 5 months pregnancy and one year after birth. One in five die because of congenital anomalies, and one third of these are cardiovascular abnormalities.
The origin of cardiac abnormalities lies in the complex development of the heart. Starting out as a single, straight hollow tube, the heart must divide into two sides, and fold over on itself twice to begin to reach its final form. Some areas must differentiate into electrical conduction tissues, and others to muscle, while still others must develop into the strong tissues of the valves that keep blood moving in the proper direction. When one considers the incredible complexity of this process it becomes easier to understand that there are many ways in which it can develop abnormally. The most common fetal cardiac abnormalities are: Complete atrioventricular septal defect ("canal" defect, Hypoplastic left heart syndrome, and Double outlet right ventricle/metrology of Fallot. Other abnormalities are all much less common than these three (the third involves a spectrum of abnormalities that are all related etiologically). In newborns the most common defect is ventricular septal defect.
Newborns with congenital heart disease usually look pretty similar to unaffected newborns for the first few hours after birth. Before birth the heart is specially adapted for intrauterine life. The fetus does not breathe inside the womb, rather the placenta does the breathing work for the fetus. Normally there are connections between the right and left sided receiving chambers of the heart (the atria), and between the two main arteries that leave the heart, the aorta to the body and the pulmonary artery to the lungs.
Newborns with many types of severe heart problems do well until these normal connections begin their normal process of closing. At that point, fetuses with absence of one of the normal pumping chambers, the ventricles, for example, will begin to show the abnormal coloration or labored breathing that are often the first signs of cardiac abnormalities. These signs are similar to those seen in newborns with infections and some other problems, so it may take a couple of hours for the recognition that a heart problem is present. Especially in these days of early hospital discharges for apparently healthy moms and babies, problems may not arise until the child has been brought home. For new parents of a first child, even recognizing that there is a problem can take a while.
Certain groups of pregnant women have been identified as being at special risk of delivering a baby with a heart abnormality. Women who have had a prior child with heart disease have a 2-3% risk of having another (1 in 30-50). If mom herself was born with a heart abnormality the risk may be as high as 5% (1 in 20). Some medications, such as those used to control epilepsy, can damage the developing heart, but are still important for women to take for their own health. Recently, high doses of Vitamin A, 10,000 units a day or more, have been identified as causing a high risk of fetal heart abnormalities. Oral contraceptives and fertility medications, such as Clomid®, and Pergonal®, fortunately appear to be safe.
It is also fortunate that testing is available for pregnancies identified as being at high risk of fetal heart abnormalities. The test, called a fetal echocardiogram, uses the same ultrasound technology that is used for measuring the fetus and taking pictures of other parts of the fetus. In a fetal echocardiogram the entire heart is systematically examined for normal development. Any areas of suspected abnormality can be evaluated in detail, often by using special ultrasound techniques that measure the direction and speed of blood as it flows through the heart, called Doppler ultrasound. Fetal echocardiograms should be performed by physicians with special expertise in the examination of the fetal heart. These may be obstetricians, pediatric cardiologists, or radiologists, usually working in a team effort. Suspected abnormalities are generally referred to regional or supra-regional centers with extensive experience in evaluating the test.
What if a fetal heart abnormality is found? The first step is to perform a thorough examination of the rest of the fetal anatomy, to be sure that no other abnormalities are present that might complicate caring for the newborn. Next comes consultation with a pediatric cardiologist to discuss what might need to be done for the newborn. This usually includes discussion of delivery at a pediatric heart center that can operate on the baby if needed. It is especially important psychologically for the parents to be near the baby if at all possible. The possible operations that may need to be done are discussed, and the long term outlook for the baby can be outlined. If the pregnancy is early enough, and the long term outlook bleak, many families do choose to terminate the pregnancies, an unpleasant alternative to be sure in what are always wanted pregnancies, but an important choice to include in discussions with the parents. Delivery is usually vaginal, there is no evidence that cardiac babies do better if delivered by cesarean section.
Being prepared with knowledge of the presence of a heart abnormality, the pediatric team can plan for the delivery. We find it helpful for the parents to meet with the hospital neonatal intensive care specialists beforehand, and to get a tour of the nursery to familiarize themselves as much as possible with where their baby will be, and the people who will be taking care of their baby.
Introduction
The term placenta was introduced in 1559 and is derived from the Latin word for a "circular cake". The placenta or "afterbirth" is the organ of metabolic exchange between the fetus and mother. It has a portion derived from the developing embryo and a maternal portion formed by modification of the uterine lining. There is no direct mixing of fetal and maternal blood. The intervening tissue is sufficiently thin to permit the exchange of nutrients and oxygen into the fetal blood and the release of carbon dioxide and waste materials from it. The placenta in the third trimester of pregnancy is a disk-shaped organ measuring approximately 20 centimeters (cm) in diameter and 2 to 3 cm in thickness. It has a maternal surface, attached to the uterus, or womb, and a fetal surface. The umbilical cord extends from the fetus to the fetal surface of the placenta. There are many potential abnormalities of the placenta that can result in fetal death: 1. Placental abruption 2. Trauma 3. Circulatory disturbances 4. Abnormalities of plantation 5. Tumors of the placenta 6. Abnormalities of the umbilical cord
Placental Abruption
Placental abruption is defined as separation of the maternal surface of the placenta from the uterus before delivery of the fetus. It occurs in approximately 0.9% of pregnancies and accounts for 15% to 25% of all perinatal mortality (stillbirths and neonatal deaths). Unfortunately, placental abruption often occurs without advance notice. The most common symptom of abruption is painful vaginal bleeding, but the clinical presentation is variable. Some of the bleeding of placental abruption usually escapes through the cervix, resulting in recognizable external hemorrhage. Less commonly, the blood does not escape externally but is retained between the detached maternal surface of the placenta and the uterus, resulting in a concealed hemorrhage. Although abruptions may occur any time during a pregnancy, approximately 42% occur after 37 weeks (term). The primary cause of placental abruption is unknown, but there are several associated conditions including: maternal hypertension (both pregnancy-induced and chronic hypertension), cigarette smoking, cocaine use, advanced maternal age, increasing parity (number of births), abdominal trauma (especially motor vehicle accidents), and preterm premature rupture of the membranes. Placental abruption may be total or partial. Treatment for placental abruption varies depending upon the condition of the mother and fetus. If there is significant bleeding, blood transfusions and prompt delivery may be lifesaving for the mother and fetus. If the mother is stable and the fetus is immature (preterm) and not compromised, then expectant management with very close observation and continuous electronic fetal heart rate monitoring in hospital may be beneficial. However, facilities and personnel for immediate intervention must be available. The risk of recurrent abruption in a subsequent pregnancy is high, approximately 1 in 8 pregnancies. The frequency of placental abruption fatal to the fetus has declined to about 1 in 800 deliveries.
Trauma
Trauma and accidents are the leading cause of death in young reproductive age women. It is estimated that 1 in 12 pregnancies will be complicated by trauma. Motor vehicle accidents are the most common cause of blunt trauma to the pregnant woman. The use of seat-belts with shoulder straps is recommended at all times, including while pregnant. Other causes include falls and, unfortunately, assaults, which appear to be increasing in frequency. Traumatic placental abruption reportedly complicates 1% to 6% of "minor" injuries and up to 50% of major injuries. Placental abruption is discussed above and usually develops early following trauma. In the absence of placental abruption fetal injury and death are uncommon. If the placenta is lacerated, fetal blood may hemorrhage into the maternal circulation, a condition termed fetomaternal hemorrhage.
Circulatory Distubances
Infarction or infarct refers to an area of cell death and tissue necrosis resulting from insufficient blood supply. Microscopic thrombi (blood clots) may form within blood vessels, impeding blood flow, and are a common cause of infarction. This is usually what occurs during a heart attack ("myocardial infarction") secondary to occlusion of a coronary artery. Constriction or closure of blood vessels (vasoconstriction) can occur for a variety of reasons, most commonly as a result of hypertension. Additionally, certain substances, for example cocaine, are "vasoactive" and are known to cause closure of blood vessels and subsequent infarction. The placenta is a highly vascular organ. Any process that adversely affects blood vessels can damage placental blood vessels as well as the uterine blood vessels (spiral arteries) that "feed" the placenta. Placental infarcts are common features of a normal "aging" placenta. They are found in approximately 25% of uncomplicated term pregnancies are appear to be of no clinical significance. However, certain maternal diseases, such as severe hypertension and connective-tissue disorders (e.g., lupus, antiphospholipid antibody syndrome, scleroderma, and rheumatoid arthritis) may lead to extensive placental infarction. If the placenta is partially compromised (uteroplacental insufficiency) the fetus may not be able to grow appropriately (intrauterine growth retardation--IUGR). However, in severe cases, blood flow to and from the placenta may not be enough to keep the fetus alive.
Abnormalities of Placentation
When the placenta is located over or very near the internal opening (os) of the cervix, it is termed placenta previa. Placenta previa is classified as marginal, partial, or total, depending on the relationship of the placenta to the internal opening of the cervix (i.e., a total placenta previa completely covers the cervix). Placenta previa occurs when the zygote implants very low in the uterus, in close proximity to the internal cervical opening. These placentas usually "migrate" away from the cervix as the pregnancy progresses and the uterus increases in size to accommodate the growing fetus. Placenta previa complicates approximately 1 in 200 deliveries. The most common presentation is painless vaginal bleeding in the third trimester of pregnancy. The major complications of placenta previa are maternal hemorrhage and shock, and significant perinatal mortality (stillbirths and neonatal deaths). Although approximately half of patients are near term when bleeding first develops, preterm delivery remains a major cause of perinatal death. The primary cause of placenta previa is unknown, but there are several risk factors including: advanced maternal age, high parity (number of births), prior cesarean section, prior elective abortion, multiple fetuses, and cigarette smoking. Placenta previa may be associated with abnormal attachment of the placenta to the uterus (placenta accreta, increta and percreta), especially if the placenta previa is located over a previous cesarean section scar. As with placental abruption, the treatment of placenta previa varies depending upon the condition of the mother and fetus.
Tumors of the Placenta
Tumors may develop in the placenta as in other tissues. Chorioangiomas, the most common placental tumor, are benign hemangiomas of the fetal blood vessels. They have been reported in approximately 1% of placentas. Small tumors are usually asymptomatic and of no clinical significance. However, large tumors (greater than 5 cm in diameter) may be associated with polyhydramnios (too much amniotic fluid) and premature labor, or antepartum hemorrhage. Fetal death and malformations are uncommon complications. Metastases of malignant tumors to the placenta are exceedingly rare. Malignant melanoma is reportedly the most common malignancy metastatic to the placenta (others include leukemia and lymphomas). Gestational trophoblastic disease is a complicated topic referring to a spectrum of pregnancy-related placental trophoblast growth abnormalities. Briefly, gestational trophoblastic disease can be divided into hydatidiform mole (complete and partial molar pregnancy) and gestational trophoblastic tumor (invasive mole, choriocarcinoma, and placental-site tumor). Complete moles do not contain a fetus. The fetus of a partial mole is not viable. Hydatidiform moles (complete and partial) tend to present as incomplete or threatened abortions (miscarriage). Of note, rarely there may coexist 2 placentas with a hydatiform mole developing alongside a normal appearing placenta and its fetus. Gestational trophoblastic tumor (invasive mole, choriocarcinoma and placental-site tumor) almost always develop with or follow some form of pregnancy (normal, molar, and ectopic pregnancy, miscarriage, or elective abortion). Malignancy is rarely identified in the placenta of a normal appearing pregnancy, but may follow an otherwise normal pregnancy. With prompt treatment by experienced physicians specializing in these tumors, the prognosis and cure rates for patients are excellent.
Abnormalities of the Umbilical Cord
Abnormalities in cord length. Umbilical cord length varies considerably. The average length is approximately 55 cm. Abnormal extremes of cord length range from apparently no cord (achordia) to lengths of up to 300 cm. Vascular occlusion by thrombi (blood clots) and true knots are more common in excessively long cords. Long cords are also more likely to prolapse through the uterine cervix prior to delivery of the fetus. Cord prolapse is more common when the fetus is small (e.g., preterm deliveries) and in certain types of breech presentations (e.g., footling breech). Cord prolapse impairs blood flow to the fetus and is an obstetric emergency requiring immediate delivery by cesarean section. Fortunately, the incidence of cord prolapse is relatively low, complicating approximately 0.5% of all births. Footling breech presentations are typically delivered by elective cesarean section to prevent this and other potential complications of vaginal delivery. Rarely, abnormally short umbilical cords may rupture or cause placental separation (placental abruption). Abnormalities of cord insertion. The umbilical cord usually inserts near the center of the fetal surface of the placenta. The blood vessels in the umbilical cord are protected by a jelly-like substance (Wharton's jelly). In certain instances, the umbilical cord inserts at a distance from the placenta, and its blood vessels must travel relatively unprotected in the fetal membranes to reach the placenta. This condition is termed velamentous insertion of the umbilical cord and occurs in approximately 1% of pregnancies, but is more frequent with twins and triplets. Rarely, these unprotected vessels may rupture and result in fetal death from hemorrhage. Additionally, with velamentous insertion of the umbilical cord, some of the blood vessels traveling unprotected in the fetal membranes may cross the cervix, a condition termed vasa previa. With vasa previa, rupture of the fetal membranes ("breaking the bag of water"), either spontaneously or by the obstetrician/nurse-midwife (amniotomy), may be accompanied by rupture of a fetal blood vessel, which can result in fetal death from hemorrhage. Unfortunately, the amount of fetal blood loss enough to kill the fetus is relatively small. In contrast, hemorrhage from placental abruption is lost from the mother, and a much larger hemorrhage may be associated with a good outcome for the mother and fetus. Absence of one umbilical artery. The umbilical cord normally contains 3 blood vessels (1 vein and 2 arteries). Two vessel cords, with only 1 artery, are found in less than 1% of pregnancies (more common in twins, and fetuses of mothers with diabetes). Approximately 30% of all fetuses with 2 vessel cords have associated congenital anomalies. Additionally, fetuses with 2 vessel cords have a higher incidence of intrauterine growth retardation (IUGR), preterm delivery, and miscarriage (spontaneous abortion). Cord abnormalities ("accidents") capable of interfering with blood flow. Several abnormalities of the umbilical cord are capable of impairing blood flow between the placenta and fetus. True knots are thought to result from active fetal movements and are found in approximately 1% of pregnancies. Fetal death may result in approximately 6% of pregnancies complicated by true knots. The incidence of true knots may be increased with abnormally long umbilical cords and is especially high in monoamniotic twins. Loops of umbilical cord frequently become coiled around the fetus, most commonly the neck (nuchal cord). Fortunately, nuchal cords are an uncommon cause of fetal death. The umbilical cord normally becomes twisted as a result of fetal movements, a condition termed torsion of the cord. Rarely, twisting of the cord on itself is so severe that blood flow is compromised, resulting in fetal death. In monoamniotic twins, with no fetal membrane separating the fetuses, the 2 umbilical cords may become twisted around each other. Rarely, hematomas of the umbilical cord result from rupture of 1 of the umbilical blood vessels, usually the umbilical vein. Cysts of the umbilical cord may form but are rarely clinically significant. Of note, all of the so-called "cord accidents" are rare causes of fetal death and it is probably unwise to attribute fetal death to a cord accident until other causes have been ruled out.
The Placenta is the single most important factor in producing a healthy baby. The placenta, which is in fact part of the fetus, is critical for all aspects of pregnancy from implantation to delivery. As early as three days after fertilization, the trophoblasts, the major cell type of the placenta, begin to make human chorionic gonadotropin, a hormone which insures that the endometrium will be receptive to the implanting embryo. Over the next few days, these same trophoblasts attach to and invade into the uterine lining, beginning the process of pregnancy. Over the next few weeks the placenta begins to make hormones which control the basic physiology of the mother in such a way that the fetus is supplied with the necessary nutrients and oxygen needed for successful growth. The placenta also protects the fetus from immune attack by the mother, removes waste products from the fetus, induces the mother to bring more blood to the placenta, and near the time of delivery, produces hormones that matures the fetal organs in preparation for life outside of the uterus. In many ways the placenta is the SCUBA system for the fetus while at the same time being the Houston Control Center guiding the mother through pregnancy.
The placenta is dedicated to the survival of the fetus. Even when exposed to a poor maternal environment for example when the mother is malnourished, diseased, smokes or takes cocaine the placenta can often compensate by becoming more efficient. Unfortunately, there are limits to the placenta's ability to cope with external stresses. Eventually, if multiple or severe enough, these stresses can lead to placental damage, fetal damage and even intrauterine demise and pregnancy loss.
Just as the rings of a cut tree can tell the story of the tree's life, so too the placenta can disclose the history of the pregnancy. In cases of poor pregnancy outcome, microscopic examination of the placenta often reveals the stresses that caused the fetal damage observed in an affected newborn.
The major pathologic processes observable in the placenta that can adversely affect pregnancy outcome include intrauterine bacterial infections, decreased blood flow to the placenta from the mother and immunologic attack of the placenta by the mother's immune system. Intrauterine infections, most commonly the result of migration of vaginal bacteria through the cervix into the uterine cavity, can lead to severe fetal hypoxia as a result of villous edema (fluid build up within the placenta itself). Both chronic and acute decreases in blood flow to the placenta can cause severe fetal damage and even death. As well as supplying the fetus with nutrition, the placenta is also a barrier between the mother and fetus, protecting the fetus from immune rejection by the mother, a pathologic process that can lead to intrauterine growth retardation or even demise. In addition to these major pathologic categories, many other insults such as placental separation, cord accidents, trauma, viral and parasitic infections can adversely affect pregnancy outcome by affecting the function of the placenta.
A trained placental pathologist can examine a placenta and assist in the elucidation of the causes of poor pregnancy outcome. A complete placental examination is most useful shortly after the time of delivery when the affected family is most in need of understanding what happened to their baby. If a full placental examination is not possible at the time of delivery because no placental pathologist is available, then the placenta can be transferred to a center that is prepared to make such an examination. As long as tissue blocks are saved from the placenta, a microscopic examination of the placenta is always possible at a later time if the need arises.
Today, only a few specialized centers for placental examination exist in the US. As the cost of processing and examining placentas decreases, more of the 4 million placentas delivered every year will be able to be examined by appropriately trained physicians. This trend will lead to a better understanding of causes of poor pregnancy outcomes, which in turn will lead to better diagnostic and therapeutic approaches to complicated pregnancies. The ultimate goal of placental examination and research is to insure that wanted babies are healthy babies.
Definition of IUGR
The term intrauterine growth restriction (IUGR) is the most common generic term that is used to describe the fetus with a birth weight at or below the 10th percentile for gestational age and sex. This term is often erroneously used as synonymous of small for gestational age (SGA). The IUGR fetus is a fetus that does not reach his potential of growth; whereas the SGA fetus is a fetus who reaches his potential of growth. In other words, a fetus who has a potential of growth at the 50th percentile but because of maternal, fetal, or placental disorders occurring alone or in combination, becomes growth restricted (birthweight < 10th percentile) is a IUGR fetus and he is at risk for adverse perinatal outcome. A fetus with a potential of growth at the 7th percentile who reaches his potential of growth (7th percentile) is not a IUGR fetus but a SGA fetus. He is a normal small fetus and he is not at risk for adverse perinatal outcome.
The two components that are necessary to define a IUGR fetus are:
a) birthweight < 10th percentile;
b) pathologic process that inhibits expression of the normal intrinsic growth potential.
The two components that are necessary to define a SGA fetus are:
a) birthweight < 10th percentile;
b) absence of pathologic process.
Incidence
The incidence of SGA fetuses in the population is approximately 7%. Ten to fifteen percent of the SGA fetuses are IUGR fetuses.
Etiology
Both maternal and paternal race have a measurable effect on the fetal size, and, therefore an indirect effect on the incidence of SGA. These racial influences can have an impact on clinical practice. The application of a fetal growth curve derived from one population applied to a different population can result in over- or underestimation of the true incidence of SGA. Birthweight and fetal growth rates tend to be least among population of Asiatic extraction and greatest in populations of Nordic extractions. These racial differences can be quite dramatic, and at term the mean birthweight may vary as much as 1400 grams. The lowest mean birthweight has been noted in Africa (New Guinea- Lumi's tribe: mean birthweight = 2400 grams); whereas the largest mean birthweight has been noted in the Caribbean (Aguilla; mean birthweight = 3880 g).
IUGR may be considered the consequence of a disease process within one or more of the three compartments that sustain and regulate fetal growth - the maternal compartment, the placenta, or the fetus. In table I the most common causes of IUGR are reported.
Diagnosis of the risk of IUGR
Pregnancies at risk for IUGR may be diagnosed on the basis of previous history (low fetal birth weight in earlier pregnancies, etc.), associated disorders (autoimmune diseases, high blood pressure, etc.), and toxic habits (smoker, etc). Previous history of IUGR is the most important risk factor. In pregnancies with an increased risk, fetal growth should be closely monitored.
Diagnosis of presumed or suspected IUGR
This is perhaps the most important and the most difficult diagnosis to make, when we consider that most of the pregnancies are free of any associated conditions that would alert obstetricians to the possibility of IUGR. The discrepancy between gestational age and the size of the uterus is the most clearly indicative sign of IUGR. Therefore, basic screening for IUGR should be done using serial symphysis fundal height (SFH), reserving ultrasound biometrical data for those cases in which the SFH fell below the 5th percentile.
Diagnosis of probable IUGR
The diagnosis of IUGR is based on biometrical parameters recorded during ultrasound scanning. In order to reduce misreading to a minimum, gestational age should be precisely determined. The most used biometrical parameters are the biparietal diameter, head circumference, abdominal circumference, head/abdominal circumference ratio, length of femur and humerus, estimated fetal weight.
Fetal hemodynamics in growth restriction
IUGR is in most of the cases secondary to uteroplacental insufficiency. Much of the understanding of this phenomenon is derived from animal research. However, the advent of pulsed and color Doppler ultrasonography has allowed us to obtain non-invasive hemodynamic measurements from several vascular beds of the uterine, placental and fetal circulation in humans.
Doppler ultrasound
Doppler ultrasound give us information on the vascular resistance and, indirectly on the blood flow. Three indices are considered related to the vascular resistance: S/D ratio (systolic/diastolic ratio), resistance index (RI = systolic velocity - diastolic velocity/systolic velocity), and pulsatility index (systolic velocity - diastolic velocity/mean velocity).
Uterine circulation
The main uterine artery is the most commonly analyzed vessel. In normal pregnancy the S/D ratio or RI values significantly decrease with advancing gestation until 24 to 26 weeks. In the absence of this physiologic decrease, a higher incidence of hypertensive diseases and/or IUGR has been widely documented.
Umbilical artery
In the normal fetus, the pulsatility index decreases with advancing gestation. This reflects a decrease of the placental vascular resistance. In fetuses with IUGR there is an increase of the pulsatility index secondary to the decrease, absence or reversal of end- diastolic flow. The changes of these waveforms are thought to be indicative of increased placental resistance. The absent or reversed end-diastolic flows are strongly associated with an abnormal course of pregnancy and a higher incidence of perinatal complications, when compared to fetuses with IUGR but characterized by the presence of end-diastolic flow.
Umbilical vein
The umbilical vein has a continuous pattern following the first trimester. The presence of umbilical vein pulsations is associated to an increased risk of adverse perinatal outcome.
Ductus venosus
The presence of reversed flow in the ductus venosus is an ominous sign. Goncalves et al observed 5 fetuses with reverse flow velocity waveforms at the ductus venosus and all the fetuses died in utero. In 18 other fetuses with abnormal umbilical and middle cerebral artery waveforms, but without reverse flow in the ductus venosus, no deaths occurred.
Fetal cerebral circulation
The middle cerebral artery is the vessel of choice to assess the fetal cerebral circulation because it is easy to identify, has a high reproducibility, and it provides information on the brain sparing effect. Additionally, it can be studied easily with an angle of zero degrees between the ultrasound beam and the direction of blood flow and, therefore, information on the true velocity of the blood flow may be obtained.
Brain sparing effect
Animal and human experiments have shown that there is an increase in blood flow to the brain in the IUGR fetus. This increase in blood flow can be evidenced by Doppler ultrasound of the middle cerebral artery. This effect has been called "brain sparing effect" and is demonstrated by a lower value of the pulsatility index. In IUGR fetuses with a pulsatility index below the normal range there is a greater incidence of adverse perinatal outcome. The brain sparing effect may be transient, as reported during prolonged hypoxemia in animal experiments, and the overstressed human fetus can also lose the brain sparing effect. The disappearance of the brain sparing effect is a very critical event for the fetus, and appears to precede fetal death. Unfortunately, to demonstrate this concept, it is necessary to perform a longitudinal study on severely IUGR fetuses up to the point of fetal demise. This has been confirmed in a few fetuses in situations where obstetrical intervention was refused by the parents. If these information's are confirmed on a larger number of fetuses, the study of the middle cerebral artery may have tremendous implication for determining the proper timing of delivery.
Based on our personal experience, there are several phases of utero-placental insufficiency that may reflect changes in fetal hemodynamics.
Severe utero-placental insufficiency
The substrate for the development of uteroplacental insufficiency may be laid down as early as the time of the implantation. However, no effect is seen on growth or Doppler until 20-24 weeks gestation. These fetuses do not have signs of growth restriction or abnormal Doppler ultrasound prior to this period.
At 22-24 weeks gestation if the fetus is measurably small by ultrasound, several Doppler patterns may occur. 1) The umbilical artery may still have a normal pulsatility index (resistance index or S/D ratio); the middle cerebral artery may have either a normal or abnormal pulsatility index. 2) The umbilical artery has an abnormal pulsatility index; the middle cerebral artery has either a normal or abnormal value of pulsatility index. 3) The umbilical artery and the middle cerebral artery have both an abnormal value of pulsatility index.
The fetus needs to be monitored very closely. Bed rest and oxygen therapy may be useful; however, if both vessels have an abnormal value at this early gestational age, it is very likely that the process will deteriorate and the chance of a delivery at term is remote.
C) The pulsatility index of the umbilical artery may increase and the pulsatility index of the middle cerebral artery may decrease. The other fetal vessels may still appear normal and the only Doppler abnormalities are the umbilical artery and middle cerebral artery. The fetus starts to show signs of IUGR. The biophysical profile is normal.
At this time the lack of fetal growth, and/or the development of preeclampsia/eclampsia, or a persistent abnormal biophysical profile may interrupt the process with delivery of the fetus. These fetuses are at lower risk for the development of respiratory distress syndrome and intraventricular hemorrhage. We have reported that IUGR fetuses with brain sparing effect are less likely to develop IVH. The reason is not completely understood. However, production of steroids with stress may play an important role in this process.
If the fetus is not delivered, the process continues.
D) At this time tricuspid regurgitation may appear, ductus venosus reverse flow and umbilical vein pulsations may be present intermittently. The biophysical profile may still appear normal.
E) Ductus venosus reverse flow and umbilical vein pulsations are present continuously. The fetus starts to lose the brain sparing effect. The biophysical profile becomes abnormal.
F) Fetal demise.
The time interval between E and F is variable (from 6-12 hours to 2 weeks). Oligohydramnios may be present at any stage of the above process.
This theory applies to a specific, common IUGR and not to the fetuses who have other causes such as smoking, abruption, and toxic drug exposure who may have a different pathology.
Mild utero-placental insufficiency
Uteroplacental insufficiency starts either at, or after the implantation. However, no effect is seen on Doppler and growth until 26-32 weeks gestation. The umbilical artery and the middle cerebral artery waveforms may be abnormal. However, the process is not severe enough to stop fetal growth completely or to deteriorate as above. These cases may be followed with outpatient monitoring and they often deliver at term.
Conclusion
Fetuses with IUGR show evident modifications of Doppler parameters in the uteroplacental and fetal circulation. At present, the condition of fetuses with IUGR can accurately be assessed by sequential studies of Doppler waveforms from different vascular areas. There are, however, still many uncertainties concerning the relationships between the Doppler changes and the metabolic situation of the fetus and therefore, on the optimal timing of delivery to prevent an intrauterine injury.
After fertilization the embryo differentiates into fetal and placental tissue. The fetal tissue develops into the baby and the placental tissue provides nourishment for the baby from the mother. During the first trimester, the placenta or trophoblast, is many times larger than the fetus and has the ability to grow independently. The placenta may continue to grow even without a viable fetus present. In rarer cases a pregnancy consists of abnormal placental tissue, called a molar pregnancy, which can have the potential for uncontrolled growth, like a tumor or cancer. These tumors are also called gestational trophoblastic disease. Molar pregnancy, or hydatidiform mole, is a pregnancy which has defective growth patterns. The placental tissue grows abnormally appearing as multiple cysts that have been classically described as a "bunch of grapes". There are two subtypes of moles: complete and partial. Complete moles have no fetal tissue present while partial moles have some fetal tissue and some normal placental tissue.
The chromosomal make up of molar pregnancies is quite interesting. Complete moles arise from fertilization of an "empty egg" i.e. an egg which has lost its genetic material. All the genetic material arise from the father by fertilization of either two sperm at once or one sperm which duplicates its genes within the egg. A partial mole also has a duplicate paternal genetic material though the maternal chromosomal complement is intact and therefore the genetic material is in triplicate.
Molar pregnancy is a clinical problem not only because it produces an abnormal pregnancy which in most cases needs to be terminated but also because of its ability to have residual disease and, in severe cases, result in metastasis. The malignant form of the disease is called an invasive mole or choriocarcinoma.
EPIDEMIOLOGY
The incidence of molar pregnancy varies greatly by region, with a higher rate in Asian countries. In Taiwan the incidence is 1/125 live births while the incidence in the United States is 1/1500. The main risk factor is advanced maternal age. Women over age 40 have a 5-10 fold greater chance of molar pregnancy. Other possible risk factors are related to poor nutrition, particularly a low intake of carotene (Vitamin A precursor). However the association is poor.
SYMPTOMS & SIGNS
Almost all patients with a complete molar pregnancy have vaginal bleeding in the first trimester. For the most part the symptoms mimic those of a miscarriage. 50% of patients with a complete mole have uterine enlargement which is advanced for their gestational age. As is true in normal pregnancy, nausea and vomiting are common complaints. The disease toxemia, marked by high blood pressure, swelling and protein in the urine, which is for the most part limited to the third trimester can be seen before 20 weeks in patients with a complete mole. A few patients can have findings of hyperthyroidism such as a fast heart beat, tremulousness, and feeling warm.
Patients with partial moles in general have fewer symptoms. They rarely have uterine enlargement, hyperthyroidism or toxemia of pregnancy.
DIAGNOSIS
A complete molar pregnancy has characteristic findings on ultrasound. The placental tissue is swollen into cyst-like structures and there is the absence of a fetus. A partial mole is much harder to delineate from an early miscarriage in which the pregnancy is no longer viable. Another tool to help diagnose a molar pregnancy is the beta HCG levels. This is a protein produced by the placenta which is used in pregnancy tests. It can be measured in both the urine and blood. The blood test has the advantage of giving a quantitative level which corresponds to the gestational age of the pregnancy. In a complete mole the level of beta HCG can be abnormally high, >100,000 mIu/ml. A partial mole may have beta HCG levels in a high to normal range. More specific tests to delineate a molar pregnancy from an early pregnancy are being developed which measure different subunits of the HCG protein.
MANAGEMENT
Once the diagnosis of a molar pregnancy or a non viable pregnancy suspicious for a partial mole is made, evacuation of the uterus is recommended with termination of the pregnancy. The products of conception are sent to pathology for a final diagnosis. A pre-operative work up should be performed to rule out any spread of the disease such as a chest x-ray and liver function tests.
FOLLOW-UP
Because 20% of patients with a complete mole and 5-7% with a partial mole may have residual disease, close follow up is necessary. Beta HCG levels are monitored weekly until two normal values are obtained and then monthly for 6 months. It is important for the patient to use contraception for 6 months so that rising HCG levels while normal for pregnancy are not confused with residual disease. The birth control pill does not increase the risk of post-molar disease. After normal HCG values are obtained for 6 months pregnancy is considered safe.
Persistent molar disease is assumed if the HCG levels plateau or rise, are still elevated 6 months after the termination of the pregnancy, or are >20,000 mIu/ml four weeks after the termination. If choriocarcinoma, a malignant form of the disease, is found on the pathology specimen, or if metastasis are found on physical exam or chest X-ray further treatment is also necessary.
TREATMENT
Persistent disease is characterized as local or metastatic (spread to other organs). Metastatic disease is divided into two subgroups, called good and poor-prognosis, based on how long the disease is present, the pre treatment beta HCG level, location of the spread and if the patient failed prior chemotherapy. For local spread and good-prognosis metastatic disease the cornerstone of therapy is single agent chemotherapy such as methotrexate. This drug kills rapidly dividing cells and is used for treatment of early ectopic pregnancies as well. The cure rate for this low risk group approaches 100%.
The treatment of poor-prognosis metastatic disease is multiple chemotherapeutic agents. If brain metastasis are found then local radiation therapy is needed. The cure rates for the poor prognosis group is more than 70%.
FUTURE FERTILITY
Fear of becoming pregnant after treatment for molar pregnancy is common. Most women can be assured that they will have a normal future pregnancy. Though, patients with a prior molar pregnancy have a 1-2% risk of subsequent molar pregnancy. Early detection by ultrasound of a normal embryo and fetal heart beat is important. Also beta HCG levels should be followed after delivery. There is no increase in fetal anomalies in patients who were treated with chemotherapy for persistent molar disease.
Introduction:
Ovulation typically occurs two weeks into the menstrual cycle. The oocyte is released from the ovary and enters the end of the fallopian tube furthest from the uterus known as the fimbriated end. Fertilization takes place in the fallopian tube close to the ovary. As the embryo develops within the first week, it traverses the fallopian tube where it will eventually implant into the wall of the uterus. This process occurs in greater than ninety-eight percent of pregnancies. An ectopic pregnancy, or tubal pregnancy, occurs when implantation of the embryo occurs anywhere outside of the uterus. The majority of ectopic pregnancies are located along the length of the fallopian tube (>97%). A remaining percentage will occur in the portion of the uterus where the fallopian tube enters (known as the cornua), in the ovary or cervix, or even within the abdominal cavity outside the uterus. Another type of ectopic pregnancy which may occur is known as a heterotopic ectopic pregnancy and this refers to an ectopic which coexists with an intrauterine pregnancy.
How common is an ectopic pregnancy and what is the significance?
The past two decades in the United States has seen a marked increase in the number of ectopic pregnancies. In 1992 almost 2% of all pregnancies were ectopic, and ectopic pregnancy related deaths accounted for 10% of all pregnancy related deaths. The heterotopic ectopic pregnancy is rare and occurs at a rate of 1 in 7000 pregnancies. Ectopic pregnancy remains the second leading cause of maternal mortality in the US, and is the leading cause of maternal mortality in the first trimester.
Why do people get ectopic pregnancies?
There are many underlying problems which predispose women to having an ectopic pregnancy. In general there is a problem with the tube which fails to permit the passage of the fertilized ovum to enter the uterus. Some specific risk factors include:
1. History of infection of the tube. This may include pelvic inflammatory disease as well as other sexually transmitted diseases. The inflammation associated with the infection causes damage to the internal walls of the fallopian tube, narrowing the lumen. 2. Adhesions around the tube. Adhesions are band-like pieces of tissue which can form after surgery within the abdomen, infections, or endometriosis. These bands can cause a kinking of the fallopian tube and make passage of the embryo difficult. 3. Previous ectopic pregnancy. After having one ectopic pregnancy there is between a 7% and 15% risk of having another one. 4. Developmental abnormalities of the tube. While rare, it is possible to have abnormalities of the fallopian tube. Women who were exposed to diethylstilbestrol while in utero have an increased risk of anomalies of the genital tract. 5. Cigarette smoking at the time of conception has been shown to increase the risk of ectopic pregnancy. 6. Assisted reproduction. There have been several studies showing that several forms of assisted reproduction have been associated with increased risk of ectopic pregnancies. However, further studies seem to indicate that this risk is associated with concurrent tubal disease. 7. Hormonal imbalance. Excessive levels of estrogens or progesterones may interfere with the normal contractility of the fallopian tube. 8. Previous tubal sterilization. In women who become pregnant after a tubal ligation procedure there is a 16% to 50% rate of ectopic pregnancy.
How do women with ectopic pregnancy present?
Typically women who have ectopic pregnancies present with complaints of lower abdominal pain. In addition, they may notice absence of menses, irregular bleeding or spotting. Most importantly these symptoms are present in the setting of a positive pregnancy test. The most common misdiagnoses for ectopic pregnancy include gastrointestinal disorders, normal pregnancy with an ovarian cyst, and pelvic inflammatory disease.
The greatest risk related to an ectopic pregnancy is rupture. As the pregnancy grows outside of the uterus the embryo begins to enlarge beyond the size of the tube. In combination with the increased blood flow to a growing embryo, the risk of rupturing through the tube also means that women can lose a significant amount of blood in a very short period of time. Women who have a ruptured ectopic pregnancy classically present with sudden onset of severe lower abdominal pain, possible fainting episode, lightheadedness or dizziness, and a history of irregular bleeding.
How is it diagnosed?
Initially when a woman presents to their doctor with the complaints described above, a urine pregnancy test is performed. At the same time a blood sample is drawn and sent for the beta human chorionic gonadotropin level (B-hCG). The B-hCG is the blood test sent to determine whether a woman is pregnant or not. While a urine pregnancy test can tell whether a woman is pregnant or not, the blood test will give a numeric value which correlates with how far along in the pregnancy a woman is. In normal pregnancies the B-hCG level doubles about every two days. However, in an ectopic pregnancy the rise is less than normal. In addition, the B-hCG level will correlate with certain ultrasound findings.
After the initial urine pregnancy test is positive and the blood B-hCG is sent to the lab, an ultrasound is performed. Based on the last menstrual period an approximate gestational age is determined. A transvaginal ultrasound can see evidence of an intrauterine pregnancy as early as 5 weeks. The majority of ectopic pregnancies cannot be seen on ultrasound, therefore we use the presence of an intrauterine pregnancy on ultrasound to rule out an ectopic pregnancy. In addition, if the B-hCG level returns >1500 we should be able to see evidence of an intrauterine pregnancy on transvaginal ultrasound. If the blood B-hCG level does not correlate with the ultrasound findings, our suspicion for an ectopic is raised.
If the B-hCG level is too low to see an intrauterine pregnancy we are faced with a dilemma. At this point we assess the severity of the patients current symptoms. If the patient is stable (meaning normal blood pressure and heart rate, able to sit up without getting lightheaded, and having only a mild amount of pain,) then we may send the patient home to follow-up with another blood B-hCG level. If this second level is double the initial level, then we suspect a normal pregnancy and repeat the ultrasound. If the level is less than double then our suspicion for an ectopic pregnancy is high.
If the B-hCG rise is abnormal (less than double) then either an ectopic pregnancy or an abnormal intrauterine pregnancy exists. A dilatation and curettage performed now can document whether there was evidence of abnormal embryonic tissue within the uterus. If present then there was an abnormal intrauterine pregnancy. However, if there is no evidence of embryonic tissue then an ectopic pregnancy is suspect.
Laparoscopy (the visualization of the pelvic organs using a telescope-like instrument inserted through the belly button) or laparotomy (making an incision and looking directly at the internal organs) are the procedures of choice for the definitive diagnosis of an ectopic pregnancy. In any patients that are felt to be unstable one of these procedures should be undertaken immediately.
Other procedures and tests have been used for the diagnosis of ectopic pregnancy by various physicians. A serum progesterone level has been shown to be low in abnormal pregnancies, however, the level cannot differentiate between an ectopic and an abnormal pregnancy. Culdocentesis is a procedure where fluid is removed from the abdominal cavity by inserting a needle through the vaginal wall next to the cervix. The fluid removed can help diagnose a ruptured ectopic.
What is the treatment?
Once an ectopic pregnancy has been diagnosed there are two major treatment options based on the severity of the case in question as well as expectant management .
The majority of cases, including those ruptured, are managed surgically. Laparoscopy or laparotomy is performed and the ectopic pregnancy is removed This is done by either opening the tube with a small incision and allowing the embryo to be removed, or in the event that there is significant bleeding or the embryo cannot be fully removed a portion of the tube is removed.
In a small proportion of the cases it is possible to treat ectopic pregnancies medically with a drug called Methotrexate. This drug interferes with DNA synthesis (the building blocks of chromosomes which tell cells what to do.)The criteria for medical management with Methotrexate is that the patient is stable, the tubal pregnancy is unruptured, the size is smaller than <3.5cm, and the peak B-hCG is <15,000.
Expectant management is undertaken in those women who present early, with decreasing B-hCG levels, and are stable. These women must follow-up closely to assure that the levels continue to decline and that they do not develop evidence of rupture. There have been cases of patients whose levels have returned to almost normal and then ruptured, indicating the importance of close monitoring.
What is the prognosis for future pregnancy?
Overall the subsequent conception rate leading to a live birth is about 35%. This number is significantly higher in those women who have a history of an unruptured ectopic pregnancy. So early diagnosis is extremely important. Women who have had an ectopic pregnancy in the past should make their physician aware and be followed closely early on to assure proper implantation of the embryo.
Introduction
Premature rupture of membranes (PROM) constitute one of the most important dilemmas in current obstetric practice. The term is applied to leakage of amniotic fluid in the absence of labor irrespective of gestational age. PROM before 37 weeks gestation is referred to as preterm premature rupture of membranes ( PPROM ). Overall, about 10% of all gestations are complicated by PROM. At term, the incidence of PROM varies from 6 to 19%. Nearly all women with PPROM will eventually deliver before term, and the majority of these women will deliver within one week of rupture regardless of their gestational age at the time of membrane rupture.
Mechanisms Of Premature Rupture Of Fetal Membranes
The chorioamniotic membranes possess elastic-like properties. However, there is evidence to suggest that when the membranes are stressed, either by internal pressure due to labor or by infection, they are weakened and have an increased susceptibility to premature rupture.[66] Several studies have shown that both the cytoarchitecture of the amniotic membrane and the quality and quantity of membrane collagen are altered in the patient with PROM. Specifically, it appears that type 3 collagen may be reduced in patients with PROM.[67] [68] Additionally, enhanced collagenolytic activity has been found in prematurely ruptured amniotic membranes.
There is now compelling evidence that infection is a major etiologic factor in a significant proportion of preterm labor and preterm premature rupture of fetal membranes. The most commonly associated organisms found were those causing bacterial vaginosis, Trichomonas vaginalis, mycoplasmae, chlamydia trachomitis, Neisseria gonnorhea, group B Streptococci. In addition, bacteroides fragilis, peptostreptococci, and fusobacterium, bacteria commonly isolated from the amniotic fluid in the presence of preterm labor, and other common vaginal bacteria including lactobacilli and staphylococcus epidermidis may release inflammatory mediators which may cause uterine contractions. This leads to cervical change, separation of the chorion from the amnion, and premature rupture of the membranes (PROM).
Maternal and fetal " stress" may also lead to the release of stress mediators via the
hypothalamic-pituitary-adrenal axis leading to enhanced production of placental corticotrophin releasing hormone ( CRH ). The latter acts as a paracrine effector, enhancing the release of enzymes and compounds which may lead to pre term, premature rupture of fetal membranes.
Other risk factors for PROM include cigarette smoking, [69] [70] [71] vaginal bleeding,
incompetent cervix and poor nutritional status. Other factors, called not remediable factors, include PROM in a previous pregnancy (recurrence rate of 21% ); Ehlers-Danlos syndrome, placenta previa, placental abruption, marginal insertion of the umbilical cord, battledore placenta, multiple gestation, polyhydramnios, and incompetent cervix.
COMPLICATIONS OF PROM
The consequences of PROM for the neonate fall into three major overlapping categories. The first is the significant neonatal morbidity and mortality associated with prematurity. Second are the complications during labor and delivery that increase the risk for neonatal resuscitation, and thirdly infection. The morbidity and mortality associated with PROM increases with decreasing gestational age. Maternal complications include infection and increased risk of cesarean section.
Once membranes rupture, the duration of the latency period varies inversely with the
gestational age. When PROM occurs between 28 and 34 weeks, 50% are in labor within 24 hours and 80 - 90"7o within 1 week.[72] [73] Maternal infection is termed chorioarnnionitis and fetal infection may occur as septicemia, pneumonia, urinary tract infection, or local infections such as omphalitis (infection of the umbilical cord) or conjunctivitis. The incidence of chorioamnionitis, in association with PROM varies with the population studied. In prolonged rupture of membranes, the incidence is 3 - 15 % and it appears to be more common in PPROM with a frequency of 15 to 25%.[74] [75] Major neonatal infections occur in about 5% of all cases of preterm PROM, and in 15 - 20% of those with chorioamnionitis.
The relative contributions of prematurity and perinatal infections to perinatal mortality are responsible for most of the controversy surrounding the optimal management of PPROM. In most cases, perinatal mortality consequent upon PPROM arises from complications of prematurity such as respiratory distress syndrome ( RDS ), intraventricular hemorrhage ( IVH ), and necrotizing enterocolitis ( NBC ). Thus, in a 26 week gestation, the relative contribution of prematurity to the risks of perinatal morbidity and mortality far outweigh any risks from infection, and thus all efforts at prolonging pregnancy would seem reasonable. However, in a fetus at 34 weeks, at which point perinatal mortality is not substantially different from that for the fetus at term, the relative contribution of infection becomes more important.
Umbilical cord prolapse occurs more frequently in PROM with a reported incidence of
1.5%.[76] It has now become clear that cord compression, even without prolapse, is
more common in PROM because of the accompanying oligohydramnios.[77] [78] Studies of antepartum testing in patients with PPROM suggest a high incidence of antepartum fetal distress requiring intervention for fetal heart rate ( FHR ) patterns consistent with umbilical cord compression occurring even prior to the onset of labor.[79] Vintzileos et. al.[80] reported a good correlation between the severity of oligohydramnios and the frequency of severe variable decelerations, low apgar scores , and perinatal mortality.
The final major complication that may result from PPROM is the fetal deformation syndrome. PROM occurring very early in pregnancy can result in growth retardation, compression anomalies of the fetal face and limbs, and most importantly, pulmonary hypoplasia Sustained adequate amniotic fluid and normal fetal breathing movements are necessary for normal lung growth. Itoh and Itoh[81] reported that fetuses with renal agenesis ( insult before 4 - 6 weeks ) have defects in all three stages of lung development whereas fetuses with early oligohydramnios ( insult before 20 weeks ) exhibit nearly normal bronchial branching and cartilage development but have histologically immature alveoli.
Fetal pulmonary hypoplasia has a 90% mortality rate. The reported incidence in PPROM varies between 3%[82] [83] and 28%[84]. Prenatal diagnosis of pulmonary hypoplasia is difficult and there have been unsuccessful attempts to correlate monographic features such as fetal thoracic dimension, fetal lung length, and absent fetal breathing movements with diagnosis. [85] [86]
Making The Diagnosis Of Prom
The diagnosis of rupture of membranes is based on the logical sequence of history, physical examination and investigation. In many instances, it is clear from a history of sudden gush of fluid from the vagina and its continuing intermittent trickle. However, most fluid might have escaped and fluid may not be present in the vagina making it difficult to confirm or refute the diagnosis. Furthermore, fluid may be contaminated with urine, cervical mucus, bath water, vaginal discharge, blood or meconium. Because of these difficulties, even when fluid is available, differentiation between amniotic fluid and urine, or vaginal secretions is essential. Indeed, Kragt and Keirse[87] found that 20% of women with preterm gestations who came to a labor and delivery unit with a primary complaint of 'aqueous discharge ' did not have ruptured membranes. No one test has been found to be completely accurate, and diagnosis still requires an integration of the clinical history, physical examination and laboratory testing. Three tests are currently used for diagnosis of ROM: ferning, nitrazine test, and observation of a pool of fluid (pooling) in the vagina. Arborization or " fern-like " pattern occurs in a variety of body fluids when put on a glass slide and allowed to dry, because of the presence of proteins and electrolytes.
Positive "ferning" is considered a sign of ruptured membranes. However, the nitrazene
test is probably the most widely used for helping establish the diagnosis of ruptured
membranes. Nitrazine is an indicator paper with a narrow set point of pH 6.4 - 6.8 where it undergoes the characteristic color change to blue in the presence of amniotic fluid. Overall, the combination of history, physical examination, nitrazinc testing, and microscopy for fern like pattern of amniotic fluid should lead to the correct diagnosis of up to 90% of cases of premature rupture of membranes. The question as to whether or not to perform vaginal examination in patients with PROM is a controversial area of practice. The most widely held opinion is that a visual speculum examination alone is sufficient to provide most of the necessary information required for management.
Management of Preterm Prom
The major risks to the baby following PPROM are related to the complications of
prematurity. The neonatologist and obstetrician should work as a team to ensure that optimal care is provided for the mother and fetus. Several studies have shown that small changes in gestational age have significant impact on survival especially for neonates delivered between 24 and 26 weeks. Morbidity is also dependent on weight and decreases with increasing birthweight.
Since the goal of management in PPROM is prolongation of pregnancy, the most commonly accepted management scheme for the patient less than 36 weeks is expectant management in the hospital. This consists of careful observation for signs of infection, labor or fetal distress in an effort to gain time for fetal growth and maturation. Although most patients commit themselves to delivery by going into labor, some do reach term and the timing of delivery must be decided. When the patient reaches 36 or 37 weeks, delivery may be accomplished but documented lung maturity may permit a somewhat earlier delivery. This expectant approach is complicated by controversies surrounding the efficacy of tocolytic agents to stop uterine contractions, prophylactic antibiotics, corticosteroids to accelerate fetal lung maturation, and amniocentesis for diagnosis of occult infection and fetal lung maturity. In any event, where adequate facilities for intensive perinatal and neonatal care is lacking, it is prudent to refer the patient to a center where such facilities are available.
Documentation of Fetal Well-being in PROM
PROM is associated with an increased frequency of maternal infection, neonatal infection, and fetal distress during preterm and term labor. The main challenge therefore, is how to recognize and detect intrauterine infection at its incipient stages. In the United States, analysis of amniotic fluid obtained by amniocentesis is currently the most widely practiced method to determine the presence or absence of bacteria in the amniotic cavity and to determine fetal pulmonary maturity. The most common tests for the detection of bacteria are Gram stain and cultures for aerobic and anaerobic bacteria including Mycoplasma species. In order to improve the efficacy of Gram staining, other markers of infection have been examined by different groups such as amniotic fluid white blood cell count, leukocyte esterase, and glucose. Although there is currently inadequate evidence on the value of amniocentesis in PROM, it would appear that the routine use of transabdominal amniocentesis to detect silent intraamniotic infection, is justified. The amniotic fluid is used to document pulmonary maturity studies. The demonstration of a lecithin : sphingomyelin ( L/S ) ratio greater than 2 from the amniocentesis sample or the presence of a phosphatidyl glycerol band in the vaginal pool specimen is usually taken as indication of pulmonary maturity. Ultrasonography has become an essential part of the evaluation of patients with
Pre term Premature Rupture of Fetal Membranes(PPROM)
The evaluation includes assessment of dates and size, exclusion of fetal anomalies, and determination of fetal behavior.
Antibiotic Therapy in Expectant Management of PPROM
The use of prophylactic antibiotics in PPROM could reduce maternal and perinatal risks of infection and secondly, the interval from PROM to delivery might be prolonged ( since occult infection is a probable cause of PPROM and preterm labor ). In a metaanalysis of antimicrobial therapy in PPROM , Mercer and Arheat[88] showed that antimicrobial treatment offered significant benefit in pregnancy prolongation and fewer women delivered by 24 hours with anti microbial therapy. There was also a decrease in chorioamnionitis as well as infectious maternal and infant morbidity including sepsis and pneumonia. However, many questions remain to be answered including whether or not these findings are applicable to all populations, what is the best antibiotic including route and duration of therapy, and whether or not a selective approach is feasible reserving antibiotic therapy for a specific group of patients at higher risk. Until these issues are addressed, the use of antibiotic prophylaxis in PPROM should be individualized and blanket use should not yet be regarded as " standard of care " as it may increase iatrogenic morbidity from superinfection due to resistant bacterial species.
Corticosteroids after PPROM
The benefit of antenatal corticosteroid therapy has been demonstrated in several randomized controlled trials. The overall reduction in the odds of neonatal RDS is about 50%.[89] This beneficial effect on RDS is thought to have a domino effect on other forms of neonatal morbidity including a 10% and 80% reduction in the odds of periventricular hemorrhage[90] and necrotizing enterocolitis[91] respectively.
In the light of available evidence, corticosteroid therapy should be initiated as soon as possible in all cases of PPROM from 24 to 34 weeks unless immediate delivery is indicated for chorioamnionitis, antepartum hemorrhage, cord prolapse or fetal distress. Treatment should consist of dexamethasone by intramuscular injection in two doses at 12 hour intervals. If the patient remains undelivered after I week, an attempt should be made to assess lung maturity and to repeat the corticosteroid regime if necessary.[92]
Tocolysis in PPROM
Several prospective randomized controlled trials of tocolytic agents (agents that reduce uterine contractions) in patients with PPROM have been conducted[93] [94] [95]. Overall, there was no difference in pregnancy prolongation beyond 24 hours or any difference in the any index of perinatal mortality or morbidity measured. Two randomized trials of prophylactic oral tocolytics also failed to show pregnancy prolongation.[96] [97] These data offer no support for suggestions that prophylactic oral tocolysis before the onset of uterine contractions is worthwhile. A possible but unproven advantage of tocolysis lie in the postponement of labor in order to facilitate in - utero transfer in PPROM.
Previable PROM
In cases of PROM very early in pregnancy, survival after delivery at or less than 23 weeks is limited, and neonatal morbidity and mortality after delivery at 24 to 26 weeks are high. If labor or clinical infection is present at initial evaluation of these patients, delivery is indicated. For the remainder of patients, there are two options, expectant management or termination. It is extremely important that the patient be involved in the decision process. On going counseling and psychological support are essential in the management of this morbid pregnancy complication.
Management of Prom at term
Labor induction or expectant management? The question as to whether to induce
labor immediately or not when PROM occurs at term is a vexed issue. The practice of immediate induction of labor can lead to higher cesarean section rates which were thought to be due to the fact that the cervix was unripe in many cases. However, a recent careful large randomized controlled trial that included 5041 women with PROM at term[98] showed that induction of labor with intravenous oxytocin, induction of labor with vaginal prostaglandin E2 gel, and expectant management are all reasonable options for women and their babies if membranes rupture before the start of labor at term, since they result in similar rates of neonatal infection and cesarean delivery. However, induction of labor with intravenous oxytocin resulted in a lower risk of maternal infection and women viewed induction of labor more positively than expectant management.
Should prophylactic antibiotics be used? In the recent Centers for Disease Control and Prevention recommendations for preventing early onset neonatal group B streptococcal ( GBS disease, prolonged rupture of membrane for more than 18 hours was classified as a risk factor for GBS infection and antibiotic chemoprophylaxis with penicillin or ampicillin was recommended in this setting. For women who are allergic to penicillin, clindamycin or erythromycin would be suitable alternatives.
Summary
Premature rupture of the fetal membranes is an obstetric enigma and several aspects of management of PPROM and PROM at term remain controversial. Although clinical judgment, physician experience, and careful individualization of management will often come into play, certain principles are widely accepted as being essential. The issues to be addressed by the obstetrician caring for the patient presenting with PROM are : Are the membranes indeed ruptured ? What is the gestational age ? Should the cervix be examined ? Should labor be suppressed ? Should labor be induced ? Should the mother be transported? Is there any reason not to administer glueocorticoids ? How and when should delivery be accomplished? These questions are best answered based on the best available evidence. Future studies are warranted in PROM to identify the optimal methods prolongation of the[99] latency interval while avoiding compression deformities and pulmonary hypoplasia in cases where membrane rupture occur very early in pregnancy as well as the optimal mode of surveillance in these pregnancies.
Substance abuse during pregnancy poses a threat to the health and well-being of both the mother and her unborn child. It is difficult to know exactly how many women abuse alcohol and drugs during their pregnancies, but the problem is clearly of concerning size. About 15% of women who present for prenatal care have been shown to have a positive urine test for one or more of the following: alcohol, marijuana, cocaine, and opiates (such as heroin).
This is worrisome not only because almost every substance of abuse freely crosses the placenta into the fetus but also because of the risky behaviors which can be associated with substance abuse, including unsafe sex, exchanging sex for drugs and money, and engaging in physically unsafe behavior.
Although many of the substances described below may cause fetal death, this article takes a broader look at the effects of both licit and illicit substances on a woman and her fetus. This article summarizes what is known about the effects of certain substances during pregnancy in the hope that education will help women to understand the risks of using substances during pregnancy and will help them to choose to abstain while they are pregnant.
Tobacco
Tobacco smoke is a highly complex substance containing many possibly harmful ingredients including nicotine, tar, carbon monoxide, and cyanide. All of these appear to contribute to the health problems affecting mothers who smoke, including respiratory illnesses, peptic ulcer disease, esophageal reflux, and in the long term, cancer.
Nicotine is particularly problematic during pregnancy because it tends to make blood vessels constrict which causes there to be less blood flow to the placenta which translates into less oxygen and nutrients for the fetus. In addition to decreasing blood flow, smoking can lead to a complication called placental abruption, a condition in which the placenta detaches from the wall of the uterus before the fetus is ready to be born. One in 500 cases of severe abruption leads to fetal death.
In general, smoking is associated with an increased frequency of miscarriage with the risk of miscarriage is increased 1.2 fold for every 10 cigarettes smoked. A report by the Surgeon General in 1983 estimated that 4600 infants died each year in the United States as a result of smoking during pregnancy.
Babies of smokers also tend to be born prematurely and to have lower birth weights with birthweight reduction being directly related to the number of cigarettes smoked each day. Increased rates of neonatal death and of the sudden infant death syndrome (SIDS) have also been observed. The long-term effects of smoking are still under investigation, but smoking during pregnancy has been associated with impaired growth after birth, impaired intellectual development, and behavioral disorders including hyperactivity and attention deficit disorders.
Alcohol
Alcohol use during pregnancy is a significant problem: it has been estimated that as many as 1 in 300 infants are born with some stigmata of fetal alcohol exposure. The most well described stigmata are part of the Fetal Alcohol Syndrome (FAS) which includes 1) prenatal and postnatal growth retardation, 2) central nervous system involvement, and 3) characteristic facial features. The central nervous system effects include tremulousness, poor suckling, abnormal muscle tone, hyperactivity, attention deficit, and mental retardation. The typical facial features include microcephaly (a small head), a thin upper lip, a short upturned nose, a flattened nasal bridge (upper portion of the nose), and general underdevelopment of the midface area.
Drinking patterns vary among women, and it appears that heavier drinking is associated with more congenital problems. However, it is important to know that no safe level of alcohol intake during pregnancy has ever been defined. Both binge drinking and daily drinking increase the risk both of fetal abnormalities, such as in the FAS, and of fetal death. Alcohol use during pregnancy is associated with an increased incidence of second trimester miscarriage in moderate to heavy drinkers. Abruption of the placenta and breech presentation also appear to be more common in fetuses with the fetal alcohol syndrome.
Other fetal defects which may be associated with alcohol exposure include congenital heart defects, brain abnormalities, spinal bifida, limb defects, urinary tract defects, and genital defects.
Marijuana
Marijuana is the most commonly used illicit substance in the United States, and it is the most common recreational drug used during pregnancy. It is important to know that the psychoactive ingredient in marijuana, 1,9-tetrahydrocannabinol (THC), is a substance which accumulates in fat. THC is eventually broken down by the liver before being excreted, but it may stay in fat tissue for days. Thus, the effects of using marijuana may persist for some time. Marijuana has multiple effects on the mother including producing tachycardia (a fast heart rate), exercise intolerance, bronchitis (inflammation of the airways in the lungs), sinusitis (inflammation of the sinuses), and pharyngitis (inflammation of the back of the mouth and throat). The effects of marijuana on the fetus are the subject of some debate. There are reports in the literature of decreased body length, intrauterine growth retardation, neurobehavioral effects, and an increased incidence of prematurity. These findings, however, have not been consistent in all studies so there are no firm conclusions about the effects of marijuana on a fetus.
Cocaine
Cocaine acts as a potent stimulator of the brain which produces the euphoria experienced by the user, and it has been estimated that 10 percent of the obstetric population uses cocaine. Cocaine's other effects, however, can be quite dangerous. The mother may experience a number of serious side effects including a fast heart rate, dangerously high blood pressure, a heart attack, an irregular heart beat, muscle twitching, seizures, a stroke, increased body temperature, and even sudden death. The effects of these conditions on the fetus can be dramatic and may be fatal. Placental abruption is seen in up to 8% of cocaine abusers. Miscarriages during the first trimester are estimated to occur at a rate approaching 40%. Babies of cocaine abusers tend to have low birth weights, intrauterine growth retardation, and are more likely to be premature.
Cocaine, like nicotine, tends to constrict blood vessels, sometimes with dire consequences. Constriction of blood vessels is thought to be responsible for certain fetal abnormalities associated with cocaine abuse including failure to form part of the intestines and failure to form the limbs properly. Congenital heart defects and urinary tract abnormalities have also been observed. The effects on the fetus' central nervous system varies from major disruptive brain anomalies to the disordered behaviors seen in newborns. Newborns tend to have depressed interactive behavior and have difficulty organizing their responses to the outside world. Research is currently underway to study the long-term effects of cocaine use during pregnancy.
Opiates
Heroin and methadone are the most frequently encountered drugs in this class used during pregnancy. Although neither causes congenital abnormalities, they pose a significant threat not only because use of heroin involves needles and thus may increase the risk for HIV infection but also because withdrawal can be fatal to the fetus. Problems with the mother may encounter from using heroin include overdose, skin and subcutaneous tissue infections, inflammation of the veins used for injection, endocarditis (infection of the tissues of the heart), and urinary tract infection. Also, there is an increased incidence of inflammation and infection of the placenta and the uterus. Opiate use is also associated with an increased risk of premature labor and delivery, low birth weight, fetal distress, and neonatal infections.
Withdrawal in the mother can cause agitation, lacrimation (tearing), rhinorrhea (runny nose), yawning, perspiration, abdominal and uterine cramps, diarrhea, and myalgias (muscle aches). Withdrawal in mother may be fatal to the fetus because it results in hyperactivity, hypoxia (lack of oxygen to the fetus), and meconium (passage of the fetus' first bowel movement while still in the uterus which is a sign that the fetus is in distress). All babies born to mothers using heroin will be addicted to the drug and 80% of those born to mothers on methadone will be addicted to opiates. The addicted babies will undergo the Neonatal Withdrawal Syndrome. The symptoms begin in the first 12-24 hours after birth and include high-pitched crying, frantic fist sucking, frantic searching for food, and tremulousness. The baby can have seizures, can display a disrupted sleep-wake cycle, and can have rigid muscles. The long-term effects of opiate use have yet to be defined. In terms of using heroin versus methadone, methadone is thought to be better because the levels of the drug are more constant and there is much less likelihood that the mother will withdraw.
Amphetamines
Amphetamines are central nervous system stimulants with effects on the brain similar to cocaine. Tolerance develops with use leading the user to need more to achieve the same euphoric feelings.
Amphetamines may cause the user to be hyperactive, to be paranoid, to hallucinate, to suffer insomnia, and to be malnourished secondary to a decreased appetite. These drugs can be used intravenously, and this may increase the risk for HIV infection. Very little is known about what amphetamines do to the fetus. Although no defined set of congenital anomalies exists, there is some indication that amphetamine use my be associated with placental abruption, prematurity, and low birth weight.
Hallucinogens
The most commonly used hallucinogens are lysergic acid diethlamide (LSD, "acid") and phencyclidine (PCP, "angel dust"). The effects on the mother are significant because users tend to put themselves in dangerous situations which can lead to harm of the mother and her fetus. Users can become violent which may lead to direct trauma. The direct effects of these substances on the fetus are not well defined. There are some reports in the literature suggesting that use of hallucinogens is associated with decreased birth weight and decreased head circumference, but these findings may be attributable to environmental factors. Neonates, nonetheless, can withdraw from hallucinogens with such symptoms as tremors, jitteriness, and irritability. The long-term effects are still being investigated but may involve developmental delays.
Conclusions
Using drugs and alcohol during pregnancy can cause a variety of problems for both the mother and her fetus ranging from malnutrition in the mother to major congenital abnormalities involving vital structures such as the heart or brain. There are a few points to remember. There is no safe level of use of any of the substances discussed above. Even in a substance of abuse does not have an obvious syndrome of abnormalities associated, it may be affecting the fetus in ways that will not become apparent until the baby has reached school age or adulthood. Also, it is often the environment in which substances are abused and the fact that when one substance is abused it is more likely that many substances will be abused that poses the greatest threat to the mother and the fetus. And finally, the time to deal with substance abuse is before pregnancy begins because many of the vital organs are formed during the first 60 days of pregnancy, before some women are even aware that they are pregnant.
Introduction
Hypertensive disorders are the most common medical complications of pregnancy, and the major cause of maternal and infant disease and death worldwide. They comprise two different entities: One (pregnancy-induced hypertension, PIH) appears for the first time during pregnancy and is reversed by delivery. The other (chronic hypertension), is a preexisting condition unrelated to but coinciding with pregnancy, which may be unmasked for the first time during pregnancy and which does not resolve with delivery.
Regardless of pregnant or non-pregnant state, hypertension is in many cases the result of small vessels' spasm (vasoconstriction). Therefore, the major risks to the fetus result from decreased placental perfusion leading to decreased supply of oxygen and nutrients necessary for fetal growth and well-being. Maternal risks include hypoperfusion of major organs such as kidney, liver, and brain. Hypertension may also lead to brain edema and hemorrhage, and to seizures.
Management of hypertensive disorders in pregnancy requires very careful maternal observation and measurement of fetal-placental function and fetal maturity, in order to balance maternal risks of continuing pregnancy against risk to the infant of premature extrauterine existence. Even mild hypertension may rapidly lead to catastrophic complications such as placental abruption or seizures, that have no parallel in non-pregnant individual with mild hypertension. By timely recognition of the disease and treatment, these complications may be prevented. However, while therapeutic agents are useful, it is also essential to understand their pharmacokinetics and recognize possible side effects to both mother and fetus.
Classification
The terminology used to classify hypertensive disorders of pregnancy has been inconsistent and confusing. More than 60 names in English and 40 in German have been applied to these conditions. In the past, hypertensive disorders of pregnancy were commonly called toxemia of the pregnancy, which reflected the opinion that these disorders resulted from circulating toxins. This theory is now known not to be true, and the term toxemia has been abandoned by the medical community. Therefore, the Committee on Terminology of the American College of Obstetricians and Gynecologists[100] prepared a classification system for hypertension in pregnancy which was approved by the National Institutes of Health (NIH) in 1990, and which is now in use all over the world.
Chronic hypertension
The ACOG Committee defines hypertension as blood pressure higher than 140/90. Chronic hypertension is defined as hypertension present before pregnancy or diagnosed before the 20th week of gestation. Hypertension that persists beyond 42nd day postpartum is also classified as chronic hypertension.
PIH: preeclampsia and eclampsia
The definition/diagnosis of preeclampsia includes: elevated blood pressure, the abnormal presence of proteins in the urine (proteinuria), and leakage of blood plasma into the tissues (edema). The blood pressure in preeclampsia must either (a) exceed by 30mmHg systolic and 15 mmHg diastolic the blood pressure before 20 gestational weeks or (b) be more than 140/90 after 20 weeks. As it is sometimes difficult to define elevated blood pressure (e.g. when systolic pressure is elevated, but diastolic normal), Page and Christianson[101] advocated the use of mean arterial pressure (AMP) as a criterion for elevated blood pressure in pregnancy: MAP= {Syst BP+ (2 x diastol BP)}/3.
Proteinuria is defined as excretion of 0.1g/l of proteins in a randomly sampled urine specimen or 0.3g/l in a 24 hour specimen. Edema is diagnosed by tissue swelling and/or increase in body weight due to water retention.
preeclampsia may be classified as mild or severe. One or more of the following may indicate severe preeclampsia:
(a) the blood pressure is > 160 systolic or >110 diastolic, registered on at least two occasions at least 6 hours apart in a patient at bed rest
(b) proteinuria is > 5g/24h
(c) Urine production is < 400 ml/24h (oliguria)
(d) Cerebral/visual disturbances
(e) Epigastric pain
(f) Pulmonary edema, cyanosis
(g) Impaired liver function
(h) thrombocytopenia
Criteria for mild preeclampsia include the following, documented on two occasions, 4 hr apart:
(a) blood pressure of 140/90 or MAP>105
(b) proteinuria > 0.3g/l in 24hr urine sample.
Eclampsia is preeclampsia accompanied by seizures: It has been known since Hippocrates' time as a convulsive disease occurring in pregnant women, but was not distinguished from epilepsy until the 19th century. However, the path from preeclampsia to eclampsia is highly variable: In some cases the preeclampsia is very mild, and seizures can occur even in a patient with only elevated blood pressure, or without proteinuria.
Transient hypertension is an elevated blood pressure after 20 weeks of pregnancy or in the first 24 hours postpartum, that is not associated with other signs of preeclampsia or chronic hypertension and which disappears 10 days after delivery.
Preeclampsia Superimposed upon Chronic Hypertension
This diagnosis is made in a pregnant patient with known hypertension when the baseline blood pressure increases by 30mmHg systolic and 15 mm Hg diastolic, or 20mmHg MAP, together with edema and proteinuria.
Pathophysiology of Preeclampsia-Eclampsia
The major pathophysiologic feature of preeclampsia-eclampsia is vasospasm. This concept, first introduced 1918 by Volhard, is based upon direct observation of small vessels in the retina, nail beds and bulbar conjunctiva, and histologic examination of various organs during preeclampsia. Vasospasm causes increased resistance to blood flow, leading to arterial hypertension and damage to the endothelium of blood vessels. The areas of damaged endothelium become sites of platelet and fibrinogen deposition and thrombus formation, which, together with hypoxia caused by vasospasm, weaken the vessel wall and lead to hemorrhage, necrosis and organ dysfunction.
One of the explanations for the generalized vasospasm in preeclampsia is increased vascular responsivity to normal concentrations of endogenous pressors (angiotensin II, norepinephrine, vasopressin)[102]. Similarly, women with chronic hypertension, who are refractory to angiotensin II between 21-25 gestational weeks, start to loose this refractoriness after 27 weeks. [103] The blunted response to angiotensin II in normal pregnancy is probably caused by endothelial synthesis of prostaglandins. [104] Prostacyclin, one of the prostaglandins, is a very potent vasodilator produced by the endothelium. Vessels of preeclamptic women and umbilical veins of their fetuses produce far less prostacyclin as compared with normal pregnancy.[105] Nitric oxide is another vasodilator produced by endothelium (EDRF, endothelium-releasing factor) which acts synergistically with prostacyclin.[106] Nitric oxide production is also decreased because of endothelial cell injury. Therefore it seems clear that endothelial injury and decreased production of vasodilators play a major role in pathogenesis of pregnancy induced hypertension.
Maternal and fetal consequences of preeclampsia-eclampsia
Deterioration of maternal organs secondary to vasospasm and hypoperfusion is a direct consequence of pregnancy induced hypertension. Similarly, deterioration of fetal status is caused by vasoconstriction and placental hypoperfusion.
Cardiovascular system
Blood pressure elevation in severe pregnancy induced hypertension constitutes an acute threat to the mother. Pressures as high as 200/120 are sometimes encountered. Cerebral hemorrhage and cardiac decompensation are potential complications of such blood pressure increases, and heart failure is one of the most common causes of maternal death due to preeclampsia; it is rarely encountered in young women who are otherwise healthy. Circulatory collapse (sudden decrease in systolic blood pressure to less than 70mmHg) may occur few hours after delivery. Another serious complication is pulmonary edema as a part of generalized edema. However, pulmonary edema is far more frequently a consequence of treatment and not of PIH itself; typical causes of iatrogenic fluid overload are aggressive replacement of fluids after cesarean section, and prolonged administration of oxytocin.
Cerebral involvement
Vascular resistance in cerebral vessels is unaltered in normal pregnancy, but is increased in 50% of women with PIH. This leads in some patients to cerebral hemorrhage, one of the common causes of death in women with PIH. Some patients with severe preeclampsia may have cerebral edema, which occurs by the same mechanisms as generalized or pulmonary edema. Headache, altered consciousness, and blurred vision are common symptoms of cerebral edema. They also typically precede eclamptic seizures.
Liver function
Liver involvement is seen in about 10% of women with severe preeclampsia: A variety of liver functions may be deranged. [107] Most commonly transaminases are mildly elevated, as are bilirubin levels. Liver functions usually return to normal once preeclampsia is treated by delivery of the fetus.
Renal function
Glomerular filtration rate increases in normal pregnancy and therefore the serum concentration of creatinine, urea, and uric acid decrease. In preeclampsia, vasospasm and glomerular endothelial swelling lead to a reduction of glomerular filtration rate of 25% below that of normal pregnancy. Serum creatinine is however rarely elevated in preeclampsia, but uric acid is commonly increased. In some studies, uric acid levels of more than 5mg/dl have been associated with poor fetal outcome.[108]
Hematological changes
Most prominent hematological changes involve plasma volume and hematocrit, clotting factors, and platelets. In severe preeclampsia there is a reduction in plasma volume which may be indicated by rise in hematocrit. In 20% of patients with severe preeclampsia there is evidence of increased consumption of coagulation factors.[109] The best indicators of the activation of the clotting system are decreased concentrations of plasma antithrombin III (a substance which inhibits coagulation by preventing reaction between thrombin and fibrinogen) and a decrease in the ratio of clotting factor VIII activity to factor VIII antigen. Low platelet count (< 150,000/mm ) is also a common finding in preeclamptic patients. Repeated platelet-count testing is an important aid in the management of established hypertensive disease in pregnancy.
The HELLP Syndrome
There is described a syndrome of hemolysis, elevated liver enzymes, and low platelets (HELLP) in severe preeclampsia.[110] Criteria for the diagnosis of this syndrome include: 1) hemolysis, defined by abnormal peripheral blood smear and increased bilirubin (>1.2mg/dl); 2) elevated liver enzymes, defined as increased alanine liver transferase (ALT>70U/L) and increased lactate dehydrogenase (LDH>600U/L); and as platelet count less than 100 000/ml. Not all women have all of these findings. It is essential to understand that this syndrome may develop even in women with mild preeclampsia , i.e. in women with no severe hypertension.[111] Patients may present with the syndrome either before the delivery or shortly thereafter. Usually patients present before term complaining of malaise, epigastric pain or pain under the right diaphragm, nausea and vomiting, and some symptoms similar to those of viral infection, and are often misdiagnosed as having some other medical condition. Pregnancies complicated by HELLP syndrome are associated with poor maternal and fetal outcome. Most HELPP patients require blood product transfusions and are at increased risk of developing acute renal failure, pulmonary edema, pleural effusions, and hepatic rupture. Moreover these patients are at increase risk for abruptio placentae and disseminated intravascular coagulopathy. During the course of the disease it is essential to establish fetal wellbeing by continuous fetal heart monitoring and ultrasound examinations. In the postpartum period, the majority of patients with HELLP syndrome manifest symptoms within 48 hours. Eighty percent of these patient were diagnosed with preeclampsia prior to delivery, while 20% have no such evidence before delivery or intrapartum. Patients with this syndrome should be treated at specialized obstetrical care centers. The first priority is to assess and stabilize the maternal condition, particularly to control bleeding and coagulation abnormalities. The next step is to evaluate fetal well-being using fetal heart monitoring and ultrasound examination. Then, a decision must be made whether immediate delivery is indicated. Amniocentesis may be recommended in patients at less than 34 weeks of gestation, but must be balanced against risks of bleeding complications. The presence of this syndrome is NOT an indication for cesarean delivery, which may be actually detrimental to both mother and the fetus. Patients with delayed resolution of HELLP syndrome after delivery are typically treated with fresh frozen plasma transfusions.
Placenta
In pregnancies complicated by preeclampsia there is an inadequate maternal response to placentation i.e. a fraction of spiral uterine arterioles fail to dilate in the same way as in normal pregnancy, thus decreasing the blood supply to fetus.[112] Electron microscopic studies have shown characteristic damage to endothelial cells that is somewhat similar to that of vessels in transplanted but rejected kidney. This observation has led to suggestion that immunological mechanisms i.e., rejection of the fetus by maternal immune system, may be operative in preeclampsia.[113]
Management of Preeclampsia
Delivery is the only cure for preeclampsia. The ultimate goal of treatment is always maternal safety first, then the delivery of a live, mature newborn. Beyond hospitalization for preeclampsia and the monitoring of blood pressure, biochemical tests, and fetal well-being, the major goal is prevention of eclampsia. The majority of eclamptic episodes occur in labor or early postpartum period. The agent of choice for seizure prevention is magnesium sulfate, which typically prevents seizures without sedating the mother. Magnesium sulfate is given intravenously. Normal magnesium concentration in serum is 1.8-2.0mEq/l; therapeutic concentrations for anticonvulsive purposes are 4-7mEq/l. At magnesium levels above 7mEq/L signs of toxicity appear (loss of patellar reflex). Excessive accumulation of magnesium can be fatal: Respiratory depression/arrest occur at levels of 10-15mEq/l, and cardiac arrest ensues when magnesium concentration reaches 30mEq/l. The major advantage of magnesium-sulfate is that it is very safe for the fetus and neonate.[114]
Although at present there is no proven method to prevent preeclampsia, several studies have indicated a beneficial effect of low-dose (60-80mg) aspirin prophylaxis to prevent growth retardation.[115] Aspirin reduces generation of platelet derived vasoconstrictors and thus alleviates the basic pathologic changes in pregnancy induced hypertension. However, the long term effects of aspirin induced inhibition of prostaglandin synthesis on fetal homeostasis are not known, and this type of therapy is reserved for women at high risk for development of preeclampsia.
Antihypertensive agents are not routinely given to women with preeclampsia, as there is no evidence that it improves fetal well-being or risk of seizures in the mother. Therapy is reserved for women with severe hypertension (blood pressures elevated to more than 160/110) to decrease risks of intracranial bleeding. Ideally, blood pressure should be lowered to mildly elevated levels to keep good placental perfusion. Alpha-methyldopa (Aldomet) is the preferred agent.
Labor is usually uneventful in preeclamptic women. Pain control by epidural anesthesia may be provided. The feared complications of this type of anesthesia are sympathetic blockade, pooling of blood and hypotension with compromise of placental perfusion and fetal stress.
Prognoses (mother and child)
The perinatal mortality rate is higher for infants of preeclamptic women.[116] Causes of infant death are placental insufficiency and placental abruption, leading to intrauterine death or prematurity.[117] The perinatal mortality rate is highest in preeclampsia superimposed on already preexisting hypertensive disease. Growth restriction is also very common in infants of preeclamptic mothers and increases in severity with increasing maternal blood pressure.[118] However, by careful observation of intrauterine well-being, perinatal infant mortality rate has decreased in recent years.
Preeclampsia usually resolves promptly and completely after delivery. Proteinuria resolves within one week, and hypertension within two weeks. The risk of recurrent preeclampsia in subsequent pregnancies is 10-25% if the disease was diagnosed in the third trimester and as high as 60-70% if the disease was diagnosed in the second trimester.
Women with multi-fetal pregnancies (twins, triplets and more) face the issue of pregnancy loss just as women with singletons do; however, they also face issues involving losses in which certain aspects are unique to their multiple gestations. In the simplest case, women with twins suffer fetal losses through the “vanishing twin syndrome.” The advent of widespread ultrasound use has shown us that many twin pregnancies suffer the loss of one twin quite early in pregnancy, and were ultrasound not available, neither the patient nor caregiver would have recognized the pregnancy as anything but a singleton pregnancy. Sebire et al evaluated pregnancies at 10–14 weeks with transvaginal ultrasound and determined that about 5% of all twin pregnancies have a demise of one (3.5%) or both (1.5%) twins at that time. Obviously, unrecognized losses do not causing families to “suffer” loss. In cases in which the losses are recognized, feelings of loss often seem muted compared to cases of loss of a singleton. The reason for the milder reaction may be due to a feeling that the “pregnancy” hasn’t miscarried and there is still a viable fetus, due to ambivalent feelings about having “twins” or simply due to the fact that these losses are very early and in many cases a fetus (or even fetal heart beat) was never seen so the sense of “bonding” was lessened.
Beyond the case of the vanishing twin, women with multiple gestations may be faced with three other broad categories of fetal loss with special implications: the elective reduction of a high-order (arguably triplets or more) pregnancy to a low-order one to improve outcome for the fetuses, the potential loss of a normal fetus when the selective termination of an abnormal twin is considered, the issues of fetal and neonatal loss surrounding preterm interventions when one twin is severely compromised in utero and the other is healthy.
It is probably generally known that, in general, twins deliver earlier than singletons, triplets earlier than twins, and the more fetuses in the womb, the earlier the average delivery. Likewise, while many preterm and extremely preterm infants survive, the earlier one delivers, the higher the risk of serious and possibly life-long complications. In recent years, the increased use of assisted-reproduction technologies has resulted in a rise in the number of triplets and higher-order multiple gestations. While it is clear that this has been a godsend to many couples with long histories of infertility, it has also placed many in the uncomfortable circumstance of carrying triplets and quadruplets with a high potential to have one, two or more children with major, life-long handicaps including lung disease, mental retardation, seizure disorders, blindness and cerebral palsy. Consequently as early as 1986, physicians were reporting on attempts to perform reductions of high-order pregnancies to low-order ones. This procedure has been refined and become more widely available. Studies have been fairly convincing that quadruplet pregnancies which are reduced do better than those which are not. While he data for triplets is not as clear, early evidence suggests there is some improvement in outcomes. It does not appear that triplets reduced to twins do quite as well as natural twins though. Thus couples now are routinely informed of this procedure with two obvious issues. First, they have been trying very hard to get pregnant and gone to the extremes of high-tech interventions only to be faced with a decision to terminate one of their much-desired fetuses in order to improve the chances for the others. Many women who choose to undergo reduction experience feelings of loss. Berkowitz et al found 65% of women had acute feelings of emotional pain and stress, 70% mourned for their lost fetuses and 37% had an anniversary grief reaction. Although persistent depressive symptoms were mild, nearly 18% experienced lingering guilt or sadness and anger. Despite these feelings, 93% of the women said they would make the same choice to undergo reduction again. A second consideration is that the procedure it self does carry a risk of causing a miscarriage of the whole pregnancy. Fortunately, this complication is uncommon in experienced hands. In a recent series of 400 patients undergoing reductions, 92% delivered one or more infants after 24 weeks’ gestation. The risk of miscarriage was 7.3% in triplets, 8.4% in quadruplets, 6.1% in quintuplets and 17.6% in those with 6 or more fetuses. Nonetheless, when a miscarriage occurs, the reactions of grief and anger may be significant given that the patient’s decision to undergo reduction has led to the loss of a much desired and worked for pregnancy.
A similarly complicated decision faces parents with multiple gestations in which one fetus has an abnormality and the other(s) is(are) normal. While women carrying singleton pregnancies may face the decision to terminate an abnormal pregnancy, women with twins must consider the possibility that their decisions could affect the normal fetus. It has been shown that the selective termination of the abnormal fetus is associated with a 3–8% risk of miscarriage. The emotional strain on a couple brought about by the discovery of an abnormality in their fetus is complicated by the findings that selective termination of the non-presenting twin (the one furthest from the cervix) actually lowers the risk of preterm delivery compared to twins. Should the couple terminate to improve the chances for the normal one? What if they miscarry and lose both? What it they choose not to terminate and then the abnormal twin induces a complication which results in a preterm delivery with damage to or loss of the healthy one? No matter what decision they make, they may look back on it with regret if they suffer a loss of both children—on top of the feeling of loss itself.
Finally parents of twins may face circumstances in which complications results in the compromise of one twin and decisions must be made on how to manage the pregnancy. As with all of our previously listed circumstances, patients are called upon to make decisions which may result in the death or compromise of a normal fetus, making the emotions relating to the loss more difficult compared to the case when extraneous factors bring about the loss. There are two subsets of this situation, the cases of identical twins with a shared placenta, and the case of non-identical twins or identical twins with separate placentas. It is sometimes hard to distinguish between the two groups during pregnancy, particularly if a patient’s first visit is relatively late in gestation. In the first case, a situation arises in which one twin becomes severely compromised, such as when an abnormal placenta leads to poor feeding and oxygenation. The compromised fetus can be “starved” to the point of damage and, ultimately, death. Cesarean delivery may be the only option offered to improve the outcome for that fetus; however, delivery of both twins would be performed. Depending on gestational age, this could expose the healthy twin to the complications of prematurity. Parents may be faced with a decision to risk the life of the healthy twin in an attempt to save the sick one or to sacrifice the sick twin so as not to expose the healthy twin to unnecessary risks. In the subset of cases with identical twins having shared placentas, it can be more complicated. Investigators have reported numerous cases of identical twin pregnancies (with shared placentas) in which the demise of one twin caused damage to the other. While the early hypothesis was that something was released from the dead fetus which damaged the other one, more recently it has been hypothesized that the loss of blood pressure in the dead twin results in the live twin pumping blood across to the other one with a transient loss in blood pressure causing the damage. Unfortunately, studies have not clearly established the level of concern we should have. Estimates on the risk of major morbidity or mortality to the surviving fetus range from very low to 46%. In one report, while there were no cases of damage to the surviving fetus, a high incidence of fetal distress was noted among women retaining a living fetus in utero for at a week or more. A final consideration is that the markers for damage don’t appear until weeks after the damage has occurred. Unless an impending demise is expected and occurs while a patient is being monitored, there is no way to know whether the healthy fetus suffered a hypotensive crisis, which should produce changes in the fetal heart rate, or not. Thus, parents are sometimes asked to be involved in making decisions with limited data available to guide them.
As when consider the issues surrounding loss in the multiple pregnancy, one other factor separates this from the singleton. When couples suffer a fetal demise in a singleton pregnancy, they either miscarry or undergo a procedure to end the pregnancy. Few mothers desire to carry the dead fetus for more than a few days, and most desire to end the pregnancy quickly. In the case of the multiple gestation with one demise, the mother is often called upon to continue carrying the dead fetus for weeks to months. This may have implications for her grieving process as well as for her feelings toward the surviving twin. Caregivers must recognize that even the birth of a healthy baby will be a time of sorrow as well as joy. We must be careful not to adopt the attitude of “don’t complain, be grateful—at least you got one healthy baby.” We must take the time to acknowledge and affirm the appropriateness of the couple’s emotions of loss while letting them see that they have much to be thankful for.
Thus, the issues surrounding the losses incurred in multiple gestations are frequently more complicated than losses in the singleton, but the emotions are the same. The primary difference is that in many cases, parents are forced to make decisions which have a direct impact on and sometimes bring about damage or death to one or more of the fetuses. This may alter the normal feelings of pain, stress and anger which occur when fetal losses occur completely outside the control of the parents.
Infectious agents has been long recognized as a cause for spontaneous abortion and perinatal mortality (the perinatal period is from the 22nd week of pregnancy to the 28th day after birth). Scientific understanding of this phenomenon has helped in developing effective preventive measures and treatment for many of these infection. It is important for pregnant women to know the basic mechanism of infections that can potentially affect pregnancy outcome, and how to prevent them.
In general there are three major mechanisms that an infectious agent can affect pregnancy outcome: ascending infections, transplacental infection and infections acquired through the birth canal.
Ascending infections occur when microorganisms residing in the external genitalia of the pregnant women gain access to the amniotic sac. This event can debilitate the sac and eventually rupture it. The infectious agent then will spread over the amniotic fluid. At this point the fetus can become infected by aspirating the microorganisms to the lungs, by swallowing them or by penetration to the ear canal. Also the inflammatory reaction on the amniotic sac triggered by the infection could initiate labor.
In cases of transplacental infection the mother must have the infection along with presence of circulating microorganisms in blood. Then they penetrate the placenta and affecting its well functioning and could also invade the fetus. Some microorganisms cannot ascend to the amniotic sac nor cross the placenta barrier. They colonize the female external genital tract. However during the delivery the fetus will contaminate by exposure to maternal blood and secretions at the birth canal.
Other less common routes of neonatal infection include breast milk, infections acquired in neonatal intensive care units, nurseries etc. In terms of the timing, any microorganism that seriously affect the fetus or the mother in the first 20 weeks of pregnancy can cause fetal death and subsequent spontaneous abortion. If the infection occurs between 20 and 37 weeks it can cause preterm labor and delivery. Preterm delivery is associated with low-birth-weigh infants and with increase complication as well as neonatal mortality. Finally, infants that acquire infections during passage through the birth canal can develop neonatal infections and in some cases it spread to produce sepsis and death during the first days of life.
Following is a brief review of common infection that can complicate pregnancy outcome. Preventive measures and treatment will also be discuss when appropriate.
Syphilis:
Syphilis is a sexually transmitted disease caused by a microorganism called Treponema pallidum. The incidence of syphilis had been declining since the 1950s after the introduction of penicillin therapy. However, there was an increase in the incidence of in the United States that peaked in 1990 and has slowly decreased since then. Many investigators have reported a strong association of maternal syphilis with drug abuse, lack of prenatal care and race.
The syphilis infectious agent readily crosses the placenta and infects the fetus causing congenital syphilis. Usually there are multiple fetal internal organs affected like lungs, liver, spleen and pancreas. The frequency of congenital syphilis varies depending on the duration and stage of the maternal infection. Fetus born to mothers with recent infection (primary or secondary) are more likely to be infected that from mothers with latent disease. The complications of untreated syphilis are well described in reports from the pre-antibiotic era. Approximately two third of the cases will be complicated by perinatal death, preterm labor and intrauterine growth retardation. Approximately 40% to 50% of the neonates will have symptomatic congenital syphilis with a variety of symptoms and damages. More recently, an observational study from a large medical center attending inner city population showed a rate of 18.4 cases of congenital syphilis per 10000 births. There were 34% of stillborn and preterm labor was significantly more common than in non affected pregnancies. The resultant perinatal mortality rate in that series was 464 per 1000.
Fortunately syphilis is relatively easy to diagnose and to treat if there is adequate prenatal care. Usually the diagnosis is made by demonstrating specific antibodies in serologic testing (obtained from blood sampling), The most common tests is called VDRL. Because of the devastating effects of congenital syphilis and the effectiveness of the treatment, every pregnant woman should have a VDRL test.
Syphilis is effectively treated with penicillin. Pregnant women with syphilis and allergic to penicillin should undergo inpatient desensitization to be able to get treatment with penicillin.
Toxoplasmosis
Toxoplasmosis is an infection caused by a protozoan known as Toxoplasma gondii. It is widely distributed in nature and the domestic cat is a very common host. Approximately one third of the adult women in the USA have toxoplasma antibodies which indicates prior infection. Toxoplasma is acquire by eating undercooked meat of animal containing infective tissue cysts or by inhaling or ingesting the microorganism excreted in the feces of domestic cats. It is also transmitted from mother to fetus. It has been shown that transmission to the fetus occur almost only when women acquire the infection during pregnancy. Conversely, women that has been infected before being pregnant have virtually no risks of transmitting the disease to their offspring. One exception is the immunocompromised patients including mothers infected with HIV.
Acute toxoplasma infection goes undetected in approximately 90% of cases. The signs and symptoms are so minor and unspecific that patients usually don’t seek medical attention. When symptomatic, acute toxoplasmosis presents with fever, malaise and adenopathy, mostly in head and neck.
Transmission of toxoplasma to the fetus can cause abortion or infected fetuses with congenital toxoplasmosis. Approximately 50% to 60% of fetuses whose mothers acquire the infection during the pregnancy will be affected. Three quarter of them will be asymptomatic but will show sequelae later in life. Congenital toxoplasmosis can cause Chorioretinitis, hydrocephalus and microcephalus. Congenital infection is more common after maternal infection during the third trimester but the sequelae less severe.
Serology (presence of antibodies against toxoplasma on the serum) is the best method for diagnosis of maternal toxoplasmosis. Unfortunately the inaccuracy of available tests and the low prevalence of acute toxoplasmosis in pregnancy makes routine screening not recommended in the USA. In other countries where maternal toxoplasmosis is a more common disease, routine screening during prenatal visits is mandatory. The American College of Obstetrics and Gynecology recommends that if serologic screening is considered in women of reproductive age, the best time to perform it will be prior to pregnancy. If there is presence of specific antibodies it will indicate prior infection and maternal immunity that will avoid congenital disease. However this approach is not helpful in cases of absence of antibodies prior to conception. Other authors in the USA have advocated for a routine serological screening suggesting that congenital infection is much more common problem and is being under detected because of the lack of routine prenatal testing.
In cases where the diagnosis of acute toxoplasma infection is made early in pregnancy, therapeutic abortion has been recommended. Another alternative is treatment with antibiotics. Spiramycin has been widely used in Europe for this purpose. It reduces the frequency of maternal transmission in about 60%. This antibiotic is not currently approved by the FDA for this use in the USA. However, it is available to physicians through the FDA on a case-by-case basis. Combination of other drugs might be more effective but also more teratogenic in the first trimester.
Rubella
Also known as German measles is a disease caused by a virus. In not pregnant women and general population it is a disease of little consequences. It is contagious and could present with fever, rash and neck adenopathy, especially post auricular lymph node enlargement. A large number of cases will present without symptoms. Epidemics of rubella have virtually disappeared in developed countries because of routine vaccination during childhood.
In the USA, however, it is estimated that 6% to 25% of women are still susceptible. It has been well documented that rubella acquired during pregnancy has devastating effects to the fetus. One published series of mother who acquired rubella during pregnancy showed that 4% had spontaneous abortion and another 2% had stillbirths. Of the fetus that survived, all of them whose mother were infected before the 11th week had congenital defects but only 36 percent when the infection occurred after the 13th week.
The clinical manifestation of congenital rubella varies depending on the timing of maternal infection and the stage of fetal development. It could include eye lesions resulting in blindness, heart diseases, deafness, lung abnormalities, chromosomal abnormalities etc.
The main preventive measure is vaccination. However, it is not currently recommended shortly before or during pregnancy because the vaccine is made of live viruses. Therefore it is very important to establish presence of antibodies (which indicates prior infection) in all women of reproductive age before pregnancy. In cases where antibodies are present it will be extremely rare for the mother to infect a fetus if re-exposed. If antibodies could not be demonstrated, vaccination is mandatory. The person should not get pregnant for the next three months.
Measles
Measles is a viral disease very contagious and common during childhood. It has become a rare disease in developed countries because of routine vaccination during childhood. It usually manifests as fever, malaise, rash, pharyngitis and conjunctivitis. It could be more complicated in adults and about 3% will develop pneumonia. Pregnant women does not appeared to have a more complicated course. There are not conclusive studies about the effects of the virus on the fetus probably because of the rarity of the disease on pregnancy . There is consensus, however in that measles can cause an increase rate of abortion and premature. In a recent report of 58 pregnancies complicated by measles, 50% of them ended within 14 days of the onset of measles rash. That included five spontaneous abortion and 11 preterm deliveries. The virus does not appear to be Teratogenic, meaning that fetuses that survived will not have an increased risk of malformations.
Measles that is apparent in the first 10 days of life is considered congenital. The mortality rate in those cases is around 30%. The mortality rate in premature infants with congenital measles is approximately 50%.
Parvovirus
Human parvoviruses are a group of viruses from which the most common is the B19. It causes a disease known as fifth disease , erythema infectiosum or roseola infantum. It is more common in children, very contagious and generally mild. It could be asymptomatic or present with facial rash (slapped cheek appearance), fever and malaise. In adults rash is not present usually and more commonly will present with fever, arthralgias and adenopathy. In the United States, 50% to 75% of women in reproductive age are immune with antibodies in serum.
In cases of primary infection during pregnancy parvovirus B19 can be transmitted to the fetus through the placenta. Fetal infection can cause spontaneous abortion, intrauterine fetal death, fetal anemia and hydrops fetalis. It is not clear, however how frequent this complications will occur. There are a number of series published in the literature showing cases of fetal loss associated with B19 infection but in most of them, the rate of pregnancy loss among women infected during pregnancy was not significantly higher than the normal population.
The current recommendation is that women exposed to parvovirus during pregnancy should be screened for presence of antibodies. If IgG is present, meaning prior infection, she can be reassured. If IgG is absent and IgM (reflects acute infection) is also absent, she is susceptible, therefore should reduce the risks of exposure. This is especially important in day care workers and school teachers. If IgG is absent and IgM is present, the mother should be followed closely with serial ultrasounds to detect earlier any fetal abnormality, including hydrops.
Varicella
Varicella-zoster virus causes chickenpox. The disease is common in childhood and most adult women are already immune because of previous infection. There are reports that suggest that chickenpox could be especially severe in pregnancy. Pneumonitis, a serious complication, could present more frequently in pregnant women with chickenpox than in non-pregnant affected adults, thus increasing the chances of fetal complications.
It is well documented that maternal chickenpox during the first 20 weeks of pregnancy will cause congenital varicella syndrome in about 2% of the cases. This syndrome is characterized by fetal malformations, typically bony defects and scarring in limbs, chorioretinitis, hydronephrosis etc.
There has been cases of spontaneous abortion and fetal death after 20 weeks secondary to in-utero varicella infection but it is rare. In a series of 1373 pregnant women with chickenpox, only 1 case of spontaneous abortion at 16 weeks and one case of fetal death at 23 weeks could be proved to be related to in-uterus varicella infection.
Cytomegalovirus
Cytomegalovirus (CMV) is a virus that infects about 80% of the population. After the primary infection the virus becomes latent and periodically is reactivated, meaning that there is not effective lifetime immunity after the first infection. Cytomegalovirus infection is a serious health problem only in immuno-supressed people and in fetuses and newborns.
Most infections are asymptomatic and in only about 15% of the cases the person will present mononucleosis type symptoms.
CMV can be transmitted to the fetus via the placenta and also through the birth canal, since CMV could infect the uterine cervix. There are no reports that suggest that CMV infection in-uterus can cause spontaneous abortion or fetal death. CMV, however can cause congenital cytomegalovirus infection which produces devastating effects in newborns and their family. The syndrome includes intracranial calcifications, chorioretinitis low birthweight resulting in blindness, deafness and mental retardation. It could also cause neonatal death.
It is estimated that 0.5% to 2% of all neonates are infected. From those 5% to 10% could have neurologic sequelae. Severe disease thus will occur in 1 every 10000 to 20000 newborns. It has been shown that only fetuses from mothers with primary infection are at risk for severe sequelae, in approximately 25% of those cases. It also more common if the infection occur during the first trimester than in subsequent trimesters. Newborns exposed in utero to recurrent infection has a minor risk of having sequelae and probably have no risk of developing mental retardation.
Unfortunately there is no treatment to maternal infection nor there is a way to prevent fetuses to become infected once the mother acquires the infection. While there is ongoing investigation to develop an effective vaccine, the only effective way to reduce this public health problem is by prevention. Most experts will recommend that women in reproductive ages should have their CMV-antibody status determined. This will show if a person has been already infected in which case the risk of having a baby with significant sequelae will be very low in the event of a new infection during a pregnancy. Women who are CMV-seronegative and therefore susceptible to primary infection should be counseled. Once they become pregnant they should avoid contact with urine and saliva from infants and practice careful hygiene. Minimize sharing of glasses and other utensils and avoid sexual contact with a partner with evident mononucleosis like infection, since CMV can also be transmitted sexually.
If a primary infection is documented during pregnancy and/or if fetal abnormalities consistent with CMV congenital infection are found, therapeutic termination of the pregnancy should be considered.
Listeriosis
Listeriosis is caused by a bacteria called Listeria monocytogenes. Listeria is usually a food-borne pathogen, often found in contaminated, poor or non-pasteurized dairy products. It can also be isolated from soil, water, sewage and human feces.
Listeriosis is a rare but catastrophic complication of pregnancy. The infection could presents without symptoms or as a febrile illness that could be confused with influenza or other infectious diseases. Listeria infection in the mother is spread hematogenously (through the blood) to the uterine cavity and the fetus. Although there is no data showing the percentage of fetuses that will be affected, not all fetuses will be infected during maternal Listeriosis.
The diagnosis is made by isolation of the bacteria in maternal blood, amniotic fluid, placenta or from the fetus in case of fetal infection. Maternal Listeriosis will cause a high incidence of second and third trimester pregnancy losses. The mortality of a neonate born with congenital Listeriosis is around 50%.
There is now scientific evidence that treating the mother with antibiotic combinations intravenously may prevent perinatal mortality.
Salmonellosis
Salmonella is a bacteria commonly found contaminating poultry and egg products. It is a major cause of food poisoning, characterized by diarrhea, abdominal pain, cramping, fever etc. Usually it is a self-limited infection, requiring no antibiotic treatment. There are two major groups of salmonella species: typhy and non-typhoid. Salmonella typhy could spread through the blood and cause a more serious disease known as Typhoid. In pregnant women typhoid could cause pregnancy loss in around 80% of the cases if not treated with appropriate antibiotics. The diagnosis is made by isolation of the bacteria in blood or stools or by serologic testing. The incidence of pregnancy losses caused by non-typhoid salmonella is probably much less. However there is no data in the literature to fully illustrate the effect of this specie in pregnancy.
Shigellosis
Shigella is another relatively common cause of food poisoning, characterized by bloody stools, abdominal cramping and general toxicity. Like the majority of the salmonellosis, is a self-limited infection and does not require antimicrobial treatment. The main risk that shigellosis cause in pregnant women is by producing dehydration and electrolyte imbalances secondary to intense secretory diarrhea.
Lyme Disease
Lyme disease is caused by a spirochete that is transmitted by the bite of ticks. Initially the disease is localized, causing a characteristic skin rash and a influenza-type illness and lymph node enlargement. If not treated, the infection may affect other organs like the heart, joints and central nervous system.
The diagnosis is usually made on clinical findings. Serologic testing (presence of specific antibodies in serum) is also useful. Lyme disease is usually treated with antibiotics with better results if treated earlier.
The consequences of Lyme disease in pregnancy are not totally known. There are a few case reports of women acquiring Lyme disease during pregnancy resulting in dead fetuses. In these reported cases the spirochetes were isolated from different fetal organs, suggesting that Lyme disease may had a role in those pregnancy loss. More recently, however, a larger series of pregnant women in an area endemic for Lyme disease showed that maternal infection was not associated with fetal death, preterm deliveries or malformation. Until more conclusive date is available, preventive intervention, specifically against tick bites, is the best way to avoid Lyme disease.
Hepatitis:
Hepatitis, meaning inflammation of the liver, can occur as result of many different insults to the liver. Here we will focus on hepatitis caused by viruses infection, which is in general the most common form of hepatitis. Viral hepatitis is also the most common liver disease in pregnant women. Currently there are five different viruses that can cause hepatitis: A, B, C, D and E. In this discussion we will include the most common ones: Hepatitis A and B
Hepatitis A is usually benign in well nourished people. The main aspect during the disease is to rest and being able to maintain a good nutrition. There is no data suggesting that Hepatitis A increases the risk of spontaneous abortion more than any other febrile diseases. Nor it increases the risks of fetal malformation. There may be a slightly higher risk of preterm labor during an acute maternal infection.
The major impact on the mother and fetus could be caused by Hepatitis B. There is no clear evidence that the Hepatitis B virus could be transmitted through the placenta to the fetus. The major mechanism of fetal infection, however, appear to be ingestion by the newborn of infected maternal blood and fluids during the delivery. Approximately 80 to 90 percent of newborns of mothers who develop acute hepatitis B in the third trimester will acquire the virus. A small percentage of these will develop fulminant hepatitis and die during the first few months. Another small group may not get infected. The rest, about 80%, will become chronic carries and will be at a higher risk of developing cirrhosis and liver cancer. The incidence of spontaneous abortion in first trimester patients with acute hepatitis B is increased. When it occurs during the third trimester there is also an increased incidence of preterm labor. Teratogenic effect has never been demonstrated.
Gonorrhea
Gonorrhea, a disease caused by a bacteria known as Neisseria gonnorheae, is a relatively common sexually transmitted disease. Most of the times the infection is limited to the genitals, especially the cervix. In women gonorrhea could be asymptomatic, hence the importance of routine screening especially in pregnant women.
If the infection is not diagnosed and treated, it increases the risks of spontaneous abortion most likely secondary to cervix inflammation during the first trimester. It also increases the risks of preterm labor and infections of the uterine cavity.
Human Immunodeficiency Virus(HIV)
Transmission of human immunodeficiency virus (HIV) from mother to infant is now well established. Possible routes of transmission include the placenta, by contact of contaminated fluid and blood during the delivery, and postnatally in association with breast feeding. It is not clear however the frequency of each of these mechanism. Approximately 10% to 40% of infants born to sero-positive women will become infected. The average in most series is about 30%. The majority of infants with congenitally acquire HIV will die within the first two years of life.
Initially it was thought that HIV infection did not interfere with the pregnancy outcome. Recently, however, a report of a series of HIV infected mother showed an increase rate of spontaneous abortion. The rate was higher in mothers that already developed the acquired immunodeficiency syndrome (AIDS) than in asymptomatic mothers.
The rate of HIV transmission during pregnancy can be successfully diminished with anti-retroviral therapy. Treatment with Zidovudine starting between 18 to 34 week and continued until delivery can decrease the percentage of infected newborns to below 10%. Some authors also recommend delivery by cesarean section to avoid contact of the fetus with contaminated blood and fluid during passage through the birth canal. Breast-feeding should also be avoided because of virus transmission through breast milk.
Herpes
Herpes Simplex Virus (HSV) has become one of the most common sexually transmitted disease. The first episode known as the primary infection is usually more sever . Is characterized by multiple fluid-filled lesion in the genitalia associated with extreme pain and discomfort. Is also commonly associated with flu-like symptoms. After the first episode, the virus stays latent and the person remain without symptoms. The recurrences are typically milder and shorter.
Unfortunately, the benefit of currently known anti-viral medications is to shorten the active episode but the virus cannot be totally eliminated. Transmission of HSV from mother to fetus could have catastrophic consequences. The virus is rarely transmitted through the placenta. The fetus almost always acquires it by passage through the birth canal; or the virus my ascend through ruptured membranes and contaminate the fetus. If the herpetic neonatal infection is localized, the outcome is generally good. However in disseminated neonatal infection the mortality is around 50% to 60%. Interestingly the risks of neonatal infection are approximately 50% in cases in which the mother has a primary infection; versus approximately 5% during recurrent infections.
The evidence of the effect of herpes infection in the pregnancy outcome is controversial. A number of reports have suggested that first-episode infection is associated with some increased risk of spontaneous abortion. However these result are not being reproduced in a several other investigations. There is more agreement in that it increases the risk of premature delivery in the range of 30% to 50%. There is no data to suggest bad pregnancy outcome as a result of recurrent infection. If herpes infection is diagnosed during labor, the current recommendation is to deliver by cesarean section. This is to avoid further contact of the newborn with contaminated maternal tissue. It has been recently shown that treating mothers known to have had herpes in the past with Acyclovir (an antiviral ) from the 36th week until delivery will effectively reduce the recurrences, neonatal infections and avoid cesarean sections.
Chlamydia:
Lower genital tract infection with Chlamydia trachomatis is currently the most commonly diagnosed sexually transmitted disease. It has been estimated that 20 to 40% of sexually active women in the United States has been infected with chlamydia. The infection can be asymptomatic. It could also caused muco-purulent vaginal discharge and pain. When untreated, it could ascend to upper genital organs and cause Pelvic Inflammatory disease (PID). PID is rare in pregnancy but when it occurs, it can cause pregnancy loss in approximately 50% of the cases. Chlamydia and Gonorrhea are the two most common causes of PID.
The effects of chlamydia infection on the newborn are well characterized. Usually if the mother’s genital tract is colonized, he newborn will acquire the infection during the delivery. Conjunctivitis will develop in up to 50% of infected newborns. This complication could potentially lead to blindness if not treated. Ten to 20% will develop pneumonia. What is more debatable is the role of maternal chlamydial infection in the pregnancy outcome. Some reports suggested that chlamydial infection is strongly associated with spontaneous abortion, preterm labor and uterine infection. However there are also investigations that were unable to prove any relationship. More recently it has been shown that only women with evidence of recent infection were at a higher risk of developing premature rupture of membranes and preterm labor.
Under current obstetrical practices all pregnant women are routinely checked for chlamydia infection early in the pregnancy. If the culture results are positive treatment with antibiotics is prescribed.
Mycoplasma
Mycoplasma species that colonize the female genital tract include M. hominis and Ureaplasma urealyticum. These microorganism are probably sexually transmitted. They have been cultured from the genital tract in 15% to 75% of sexually active women, being more prevalent in women with more sexual partners.
Mycoplasma colonization has been suggested, not without controversy, as a cause of recurrent spontaneous abortion, stillbirth and preterm delivery. Several studies have found mycoplasma in fetal material in significantly larger numbers of spontaneous abortion compared to induced abortion. Similarly several investigators have reported a higher incidence of genital colonization with mycoplasma in women experiencing repetitive spontaneous abortion compare to normal women. These results may suggest an association between mycoplasma genital colonization and spontaneous pregnancy loss. These studies, however are not conclusive enough to establish that mycoplasma has indeed infected the fetus causing its death; it is also possible that the fetus dies from other causes and then becomes more susceptible to be infected by ascending microorganisms. Mycoplasma has also been implicated as a cause of preterm birth. However a recent multi-center report showed that mycoplasma colonization was not correlated with preterm labor, preterm delivery or low birth-weight infants. Similarly, studies investigating the role of routine mycoplasma cultures and even empirical treatment with antibiotics before pregnancy in women with recurrent pregnancy loss have not consistently found to be beneficial. The presence of genital mycoplasma does not appear to cause serious newborn illnesses, even after contact during the birth process.
In summary, current scientific data does not support the hypothesis that mycoplasma colonization of the genital tract increases risk of pregnancy loss; nor it recommends routine cultures for mycoplasma or treatment with antibiotics.
Group B Streptococcal Infection:
Group B Streptococcus (GBS) is a bacteria that commonly colonizes the female genital tract. Between 10 to 30% of pregnant women are colonized with GBS in the vaginal or rectal area. Unfortunately this organism has been recognized as cause of illnesses and death in newborn infants and in parturient women.
In the pregnant women GBS can cause urinary tract infection, infection of the uterine cavity, especially after a cesarean section, as well as infection of the surgical wound. In newborns GBS is responsible for infection of different organs (meningitis, pneumonia, cellulitis etc.) that can spread to cause sepsis and death. The risk of sepsis in the United States is about 1.8 per 1000 live birth. The mortality rate is between 5% to 20%.
Early reports have suggested that GBS genital colonization was associated to an increase risk of stillbirth, preterm rupture of membranes, and premature deliveries. However data to support this association has been inconsistent. What is more accepted is the association between GBS bacteriuria (presence of the bacteria in urine) and preterm delivery. Bacteriuria is an indicator of heavy genital colonization. In other words, women that are heavy colonized with GBS are at a higher risk of preterm delivery. Women lightly colonized are probably at the same risk than women not colonized. The main route of neonatal contamination thus is the passage through the birth canal. Also important is through ruptured membranes that allow ascending of the bacteria to the uterine cavity.
Besides being heavily colonized, there are other risk factors that influence in the rate of newborn GBS infection. These risk factors include rupture of membranes for more than 18 hours before delivery, preterm birth and maternal chorioamnionitis (infection of the uterus and pregnancy related tissues).
Fortunately, GBS are very susceptible to antibiotic therapy. The main issue is to whom and when to give it in order to prevent neonatal infection.
Several national agencies have developed guidelines to administer antibiotic to pregnant women close to or in labor. These are basically based on the presence of risk factors. It is well establish that timely administration of antibiotics to colonized women will effectively prevent neonatal complication as well as postpartum infections.
Renal agenesis and hypoplastic lung syndrome are congenital malformations of the neonates involving the kidneys and the lungs respectively i.e. the newborns are born with these disorders. The etiology of these malformations is probably multifactorial i.e. there are both inherited and environmental factors in the causation of the malformations. Often time both conditions co-exist as part of multiple congenital malformations.
Renal Agenesis
Renal agenesis is the complete absence of the kidney(s). The kidneys
are the organs that filter the blood of waste products, eliminating them as
urine.
There are two kidneys in the human under normal circumstances. Absence
of the kidney could be unilateral or bilateral. If it is unilateral, it means
only one kidney is absent. However, if it is bilateral, it means both kidneys
are absent. Unilateral absence of the kidneys is compatible with life whereas
bilateral absence of the kidneys is incompatible with life.
Development of the Kidneys
The kidneys are parts of the urinary system. Other members of the
system include the ureters, bladder and the urethra. The urinary system
develops in close association with the genital organs.
The kidneys are developed in three main stages called the pronephros,
mesonephros and the metanephros (nephros means kidneys). The pronephros are non
functional and soon degenerate being replaced by the mesonephros which function
for a short time before they are in turn replaced by the metanephros, the
definitive kidneys. The permanent kidneys i.e. the metanephros begin to
develop in the fifth week of intrauterine life. Urine formation begins about
the end of the first trimester i.e. the 12th week and continues for the rest of
the pregnancy. The urine produced by the fetus is secreted into the amniotic
cavity and forms part of the amniotic fluid. In the fetus, the placenta is the
main organ of excretion, therefore, the kidneys don’t need to become functional
for excretory purposes during intrauterine life. However, the kidneys must be
ready to assume their excretory functions at birth.
Earlier in pregnancy, the kidneys are located in the pelvis but by the
ninth week of pregnancy the kidneys have attained their adult’s positions in
the abdomen. This variation in positions is due to the differential increase in
the growth of the abdomen. For this reason, it is often observed that the
kidneys have various sources of blood supply during development which gradually
degenerate as the kidneys ascend to the abdominal cavity. Not surprising, the
adult kidneys sometimes have aberrant blood supply due to its migratory
developmental nature.
From the foregoing discussion, it becomes apparent that complete
absence of the kidneys (bilateral renal agenesis) results when the metanephric
buds fail to develop while unilateral renal agenesis will result from
ipsilateral (one sided) metanephric bud absence.
Clinical Features
During prenatal life renal agenesis could be diagnosed with ultrasound
examination both by the observation of oligohydramnios i.e. reduced amniotic
fluid volume and absence of the kidney(s). In most centers in USA targeted
ultrasound for detailed anatomical survey of the fetus is carried out around
the 18th -20th week of gestation. At this time, based on the reduced fluid
volume clinical suspicion is high, thus scheduled detailed anatomical survey
will reveal the absence of the kidney(s). It is pertinent to note however, that
ultrasound examination may not always reveal the absence of kidneys due to
oligohydramnios. Moreover, adrenal tissues may be confused with renal tissue.
In this situation, serial evaluation over a period of 4-6 hours to confirm
absence of urine production as demonstrated by failure to visualize the fetal
bladder may be very useful in establishing with certainty the diagnosis.
Suffice to say that absence of one kidney is compatible with life with
the other kidney enlarging to compensate for the absent one. It is for this
reason that as adults we could donate one kidney and still carry on effectively
with the remaining kidney. In the unlikely event of an absent kidney not
diagnosed before birth, it may be diagnosed in adulthood as an incidental
finding during imaging studies of the abdomen for some other reasons.
With regards to bilateral renal agenesis, the fetus is usually
stillbirth in more than 40% of cases while the majority of infants born alive
usually die within 4 hours of life. The characteristic features of the infants
described as Potter’s facies include: redundant and dehydrated skin, wide set
eyes, prominent fold arising at the inner canthus of each eye, parrot beak
nose, receding chin, large low set ears with deficient auricular cartilages,
absent urine output and non palpable kidneys. Death shortly after birth is
attributed to either pulmonary hypoplasia or renal failure. Other congenital
anomalies associated with bilateral renal agenesis include absence of the
urinary bladder, bilateral pulmonary hypoplasia, genital organs abnormalities
such as absence of the vas deferens and the seminal vesicles in the males and
the uterus and upper vagina in the females, anal atresia, absence of the rectum
and the sigmoid colon, esophageal and duodenal atresia, single umbilical artery
and major abnormalities of the lower limbs.
Management of Renal Agenesis
As earlier on mentioned, unilateral renal agenesis is compatible with
life with the only available kidney enlarging to compensate for the absent
pair. On the other hand, complete absence of the kidneys is not compatible with
life. The fetus usually die in utero or shortly after birth. The best
management approach therefore is taking preventive measures as much as is
possible to prevent congenital malformations from occurring. For instance a
pregnant woman with uncontrolled diabetes mellitus is prone to having a baby
with congenital malformations including renal agenesis. Therefore adequate
control of diabetes in pregnancy will reduce the likelihood of developing this
malformation.
Hypoplastic Lung Syndrome
This is simply underdevelopment of the lungs. It commonly results from
abnormal development of the diaphragm, a muscular structure which separates the
thoracic (chest) from the abdominal cavity.
It also may occur as part of multiple congenital anomalies affecting a fetus
including: renal agenesis, urinary tract outflow obstruction, extra-amniotic
fetal development, thoracic dystrophies. Other associations include
intrauterine central nervous system damage sufficient to decrease fetal
breathing movement, trisomy 21, erythroblastosis fetalis otherwise called fetal
isoimmunization and certain drugs e.g.ACE inhibitors. As earlier mentioned,
abnormal development of the diaphragm is the more common cause and this is
amenable to surgical correction soon after birth. I will therefore describe in
more detail development of the diaphragm and how its malformation may result in
hypoplastic lung syndrome.
Development of the Diaphragm
The diaphragm develops from four structures including the septum
transversum, pleuroperitoneal membranes, dorsal mesentery of the esophagus and
the body wall. The septum transversum is that part of the embryonic mesoderm
which separates the ventrally located pericardial cavity from the dorsally
located gut. It forms the definitive central tendon of the diaphragm. The
central tendon is a trifoliate aponeurotic structure which fuses with the
pericardium of the heart. The pleuroperitoneal membranes separate the pleural
and the peritoneal cavities. The pleural cavity contains the lungs while the
peritoneal cavity contains the abdominal organs. By the sixth week of
intrauterine life the pleuroperitoneal membranes usually fuse with the dorsal
mesentery of the esophagus and the septum transversum thus effectively
demarcating the pleural and the peritoneal cavities (i.e. the chest and the
abdomen). In fetal life, the pleuroperitoneal membranes represent a large
portion of the diaphragm, however, they represent a small part of the
definitive diaphragm. The dorsal mesentery of the esophagus is a double layer
of peritoneum which forms the median portion of the diaphragm. Two slips of
muscles called the right and left crura arise from the lumbar vertebrae to grow
into the dorsal mesentery around the ninth to twelfth week of intrauterine
life.
The body wall is the most peripheral part of the diaphragm. The
developing fetal lung and pleural cavities usually invade the body wall. At
this time the body wall divides into two layers with the inner layer forming
the definitive peripheral rim of the diaphragm. During development of the
diaphragm, the septum transversum the first indication of the developing
diaphragm lies in the cervical (neck) region opposite the third to the fifth
cervical somites. During the fifth week of development, the muscle cells from
these somites migrate into the developing diaphragm, taking their nerves
(phrenic nerves) with them from the cervical region. As the diaphragm migrates
to its final location in the thorax the phrenic nerve accompanies it, thus
traversing a long course of almost 30 centimeters.
Congenital Diaphragmatic Hernia.
This is a relatively common congenital malformation of the diaphragm
occurring in 1:2000 newborn infants. It results from a defect in the
posterolateral region of the diaphragm. Congenital posterolateral defect of the
diaphragm is due to non fusion of the pleuroperitoneal membranes with the
septum transversum and the dorsal mesentery of the esophagus. It is usually
unilateral, occurring commonly on the left side. The reason for the left sided
preponderance is due to the early closure of the right pleuroperitoneal
membrane secondary to the presence of the bulky embryonic liver on the right
side. Normally, the pleuroperitoneal membranes fuse with the other
diaphragmatic components by the seventh week of intrauterine life. If a
pleuroperitoneal membrane is unfused by the time the intestine return from the
umbilical cord to the abdomen around the tenth week of intrauterine life, the
intestine usually pass into the thorax. The spleen and stomach may also herniate
into the thorax. At birth, the thoracic intestines usually dilate with
swallowed air, compromising the functions of the heart and lungs. The
mediastinum and its contents including the heart is usually displaced to the
right while the lungs are hypoplastic i.e. underdeveloped. Normally during
pregnancy the lungs are filled with fluids which helps to maintain the lung
volumes. However, with compression from intraabdominal organs the lungs are not
able to accumulate enough fluid to maintain the requisite volumes hence their
underdevelopment.
Diagnosis of Diaphragmatic Hernia
At birth the newborn infant will demonstrate evidence of respiratory
distress syndrome with dyspnea, tachypnea, cyanosis, tachycardia etc. The lungs
may be dull to percussion due to non expansion after birth and air entry to the
lungs will be remarkably reduced on auscultation. Imaging studies of the chest
and abdomen will reveal the presence of abdominal organs in the thoracic
cavity.
Clinical Management
The immediate goal is to return the abdominal organs to their
definitive positions in the abdomen and closure of the diaphragmatic defects.
Once the hernia is reduced, the affected lungs usually expand with aeration and
ultimately achieve their normal size.
Conclusion
The etiology of congenital anomalies is usually multifactorial i.e.
both genetic and environmental factors play a role. Some of the causative
factors are amenable to control by the way of preventive measures. Some good
examples are the recommended intake of folic acid in pregnancy to reduce the
likelihood of malformations of the brain and tight glucose control to
ameliorate possible renal malformation. Others include avoidance of certain
medications such as ACE inhibitors during pregnancy and avoidance of over the
counter medications of unproven safety. Until such a time that we are able to
determine with certainty the etiology of congenital anomalies, the best that
can be done is mainly preventive. In any case, it is said that prevention is
better than cure and certainly cheaper in the present managed health care
environment.
Introduction
It was Ballantyne in 1902[119] that first made reference to postterm pregnancy in modern obstetrics. However, in 1954 Clifford[120] described more succinctly a syndrome found in infants born after the expected date of delivery which in many respects resembled intrauterine growth retardation; thus there was often thick meconium staining of the amniotic fluid and signs of fetal distress in labor in these postmature infants. Auberg[121] and Lanman[122] also showed that there was an increased risk of intrapartum death associated with prolonged pregnancy and studies from Scandinavia confirmed that prolonged pregnancy was associated with an increased risk of perinatal death.[123] An observational study from Dublin examined the risks of postmaturity in 6301 pregnancies delivered at 42weeks. [124] In the postmature pregnancies, intrapartum stillbirth was four times and neonatal death three times as common as in the women delivered at term, and early neonatal seizures were ten times as common. Crowley [125] also compared the outcomes of labor in 247 women delivered after 42 weeks with 247 matched controls delivered between 37 and 42 weeks: meconium stained amniotic fluid occurred twice as often in the postmature women and the need for fetal blood sampling was four times as common .
Prolonged pregnancy has gained prominence in the last decade as a probable high-risk condition after widespread use of antenatal testing. This notoriety has developed more as a consequence of the inability to find the appropriate sensitive antenatal test rather than from the acceptance of its truly life threatening condition for some fetuses. This point is clearly observed when one reviews recent publications stating that perinatal mortality is the same among prolonged and term gestations. [126] [127]
Epidemiology
The World Health Organization (WHO)[128] and International Federation of Gynecology and Obstetrics (FIGO)[129] have defined prolonged pregnancy as 42 completed weeks or more. It is a pregnancy lasting more than 2weeks beyond the confirmed expected date of delivery (EDD). The expressions postterm pregnancy, prolonged pregnancy, postdates pregnancy and after-term pregnancy are used synonymously. They are therefore used interchangeably in this review.
The accurate determination of the expected day of confinement (EDC) is a key issue in the antenatal and neonatal periods for both clinical obstetrics and research. It has profound personal, social and medical implications for the expectant mother. There are problems in estimating the incidence of prolonged pregnancy, not just because of differing definitions but also because of incomplete recording of pregnancies, differences between hospital and population surveys, differing policies for induction of labor, and varying proportions of women with uncertain dates.[130] Between 4% and 14% (average 10%) of women are prepared to reach 42 weeks gestation, and 2% to 7% (average 4%) to reach 43 weeks gestation depending on the population studied[131]. There have been recent suggestions that the duration of normal pregnancy may be related to maternal characters, such as height[132] parity [133] and race. [134] In studies where conception has been estimated from basal body temperature charts[135], and ultrasound measurements [136], it has been shown that the error in menstrual dating is heavily skewed to the right - i.e., there is a tendency to overestimate gestation.
In spite of all these evidences, the last menstrual period (LMP) continues to be the basis for estimating the duration of pregnancy, on a worldwide scale. Often this is unknown, in which case gestational age may be estimated by ultrasonographic measurements of fetal parameters such as the crown - rump length [137] until about 12 weeks and the biparietal diameter (BPD)[138] from about 14 to 22 weeks' gestation. There is no uniform dating policy when both a valid LMP and ultrasonographic dates are available. In practice, many obstetrics and ultrasound departments follow a 7-, 10-, or 14-day rule [139] whereby preference is given to menstrual dates if they are within 7,10, or 14 days, respectively, from the ultrasonographic estimate. However the random error in dating by ultrasound measurement of the biparietal diameter (BPD) in the second trimester has been estimated at 3.2 days[140] and unlike menstrual dates this error is normally distributed. [141] It is now clear that even if menstrual dates are considered certain; there is no advantage taking them into consideration for calculating the expected date of delivery if a dating ultrasonography result is available. Dating by ultrasonographic biometry in the first half of pregnancy results in a more accurate prediction of the delivery date than using menstrual date alone or in combination with ultrasonography.[142]
Diagnosis
It is obvious from the available literature that the correct diagnosis of postdate pregnancy is very difficult. The World Health Organization definition[143] of term pregnancy as the interval from 259 to 294 days of 77 menstrual age was based on statistical data derived from menstrual dates. It has been shown that even if the LMP is recalled with accuracy, it will not be a reliable indicator of the actual date of conception. This is because the onset of ovulation within the menstrual cycle is erratic and may also vary from one cycle to the next.[144] Dating policies have important clinical implications.
Because of unreliability of the menstrual dating[145] and the fact that most obstetric units induce labor for postmaturity and postterm based on the menstrual history , this method of historical diagnosis will result in a high proportion of women having induction of labor unnecessarily for postmaturity. However ultrasonography in the first half of pregnancy will reduce the percentage of pregnancies classified as postterm by WHO definition (42 weeks) from 11.5 to 3.5 (i.e., by 70%).
Mothers, midwives and physicians are often uncertain as to which date should be used, and this may lead to considerable parental confusion, A uniform dating policy would reduce much of the uncertainty in pregnancy dating [146]. The available evidences are strongly in support that dating by ultrasonography alone is the most accurate method for predicting expected date of confinement. Confinement occurred on the day predicted in 3.6% if EDC was based on the LMP and in 4.3% if it was based on the scan. Delivery took place within 7 days of the EDC in 49.5% cases when LMP alone was used and in 55.2% if ultrasonography alone was used. If this margin of error was widened to 10 days the corresponding figures were 64.1% and 70.3%.[147]
Fetal Surveillance
We now have available to us many forms of testing to follow the well being of the postterm fetus while still in utero. There is still considerable uncertainty, however, as to how well these tests measure fetal compromise and how effective treatment is when we use these tests in our management. Whatever form of testing is chosen, it is important to remember that the condition of the fetus can change quickly and thus, monitoring should be at frequent intervals, and that none of the tests are immune from false positives, false negatives.[148] Perinatal mortality rates (excluding lethal congenital anomalies) have been reported to be as low as 1.1-1.2 per 1000 with close surveillance.[149] Post-term perinatal deaths continue to occur, however, and some of these deaths have occurred within 24 to 48 hours of normal fetal assessment. Furthermore, despite current techniques of fetal surveillance, there continues to be reports of higher risks of fetal and neonatal morbidity and operative delivery with postterm compared to term pregnancy.[150] The summary of the available tests is given below.
Fetal movements counting
Fetal movement counting has been a popular method of fetal surveillance as it allows the mother to participate actively in the evaluation of her baby's health.[151] Although one small controlled trial suggested that this form of monitoring might be effective in decreasing the perinatal mortality rate, another larger trial undertaken in many centers in Europe and USA showed no beneficial effect.[152] Neither of these trials focused on Postterm pregnancy. In the Canadian Multi center Postterm Pregnancy Trial, women allocated to the expectant group were asked to count daily until they count six movements, or for two hours (whichever took less time). If after two hours the woman had felt less than six movements; she was to contact her Obstetricians for further evaluation. Only 2.2% (38/1707) of women reported decreased fetal movements. The two women in the trial with stillbirths (excluding lethal anomalies) did not report decreased fetal movement counts.[153]
Amniotic fluid volume
The volume of amniotic fluid has been estimated to decrease by 150-170ml per week after 42 weeks of pregnancy.[154] More recent investigations using real-time ultrasound confirm decreasing amniotic fluid as pregnancies continue past 41 weeks. [155] [156] The reason for this decrease is not completely understood but may be due to decrease fetal urine production.[157] Amniotic fluid volume as assessed by ultrasound has been evaluated in blind and unblinded studies in post term pregnancies and there is now good evidence that postterm pregnancy with no or low volumes of amniotic fluid are at higher risk of adverse perinatal outcome than pregnancies with a normal amount of amniotic fluid.[158] Low volumes of amniotic fluid, assessed by ultrasound, in postterm pregnancy have been defined in various ways. When the largest pocket of amniotic fluid is less than 3cm in depth, when the sum of the depth of the largest pocket of amniotic fluid in each of four quadrants of the uterus is less than 5cm (amniotic fluid index) [159] or when the product of the length x depth of the largest pocket is less than 60cm. This test is currently considered one of the most sensitive for postterm fetal surveillance and has been used as part of expectant management in five of the randomized controlled trials of induction of labor compared to expectant management in postterm pregnancy. [160] [161] [162]
Amnioscopy/Amniocentesis for assessing the presence of meconium
It is known that postterm pregnancies are more frequently complicated by meconium staining of the amniotic fluid than term pregnancy and that meconium staining of the amniotic fluid is associated with higher risks of adverse perinatal outcome.[163] It is not unreasonable to suggest therefore, that amnioscopy or amniocentesis might be a good screening test for fetal compromise in postterm pregnancies. In fact two randomized controlled trials comparing induction of labor with expectant management have used amnioscopy as part of the surveillance for expectant management.[164] One trial which assessed the effectiveness of weekly amniocentesis (and induction of labor if meconium were present) in postterm pregnancies, did not find this better than a program of weekly contraction tests.[165]
Contraction stress tests:
Some authors have reported on the use of contraction stress tests as a method of fetal surveillance in postterm pregnancy. Both nipple stimulation and intravenous oxytocin have been used as mechanisms for inducing contractions. The test results appear in some populations to correlate with outcome and some Obstetricians prefer this test method of fetal surveillance. The disadvantages are that it takes time to administer and, in the case of oxytocin challenge test, requires an intravenous infusion.
Non-stress test:
The non-stress test has been a popular method of fetal surveillance for postterm pregnancies[166]. Abnormal test results (non-reactivity and decelerations) have been associated with higher risks of adverse perinatal outcome.[167] Although the test is easy to administer, and was used in seven of eleven randomized controlled trials of induction of labor in postterm pregnancy, there is evidence to suggest that it is not an effective method of fetal surveillance. The overview of randomized trials of non-stress testing in the Oxford Database of Perinatal Trials indicates that this testing may result in a higher, rather than a lower, risk of perinatal death because of false reassurance.[168]
Biophysical profile:
The biophysical profile is one of the most popular methods of fetal surveillance for postterm pregnancies. The profile is performed using real-time ultrasound and consists of four distinct measures: fetal breathing, fetal movement, fetal tone and amniotic fluid volume with or without the non-stress test. Many of those who use this as the primary method of fetal surveillance in postterm pregnancy consider the amniotic fluid volume to be the most important measure of the biophysical profile for assessing fetal well-being and, if this one aspect is abnormal, consideration should be given to expediting delivery.
Doppler ultrasound
Doppler ultrasound of the fetal vessels is the most recent addition to the armamentarium of fetal surveillance for postterm pregnancy. Some studies suggest that it may help to identify those pregnancies at higher risk of adverse outcome,[169] whereas others have not found this form of testing to be particularly helpful.[170]
Hormonal tests
Hormonal tests, such as serum or urinary estriols or serum human placental lactogen, have been used to monitor postterm pregnancies. These methods of surveillance are no longer very popular. This is perhaps more because of the cost of these tests and the time required obtaining a result, than false diagnosis.
Management
The management of postterm pregnancy that is otherwise uncomplicated is controversial. Central to this controversy is whether the fetus is at increasing risk of deterioration as the pregnancy advances. The management options available for consideration for postterm pregnancy are 'active management' when pregnancy is terminated by induction of labor after 41 weeks of gestation. Cervical ripening agents such as prostaglandins [171] are used to prepare the cervix and, if necessary, oxytocin and amniotomy are also used. The other popular option is the 'expectant management' in which the pregnancy is allowed to progress to 42 weeks and beyond. Labor is induced only if the cervix is well effaced or dilated, or both, or if fetal compromise occurs. The fetal condition is evaluated by various techniques.
Postterm pregnancy has historically been considered a risk factor for adverse perinatal outcome. Before the introduction of fetal surveillance techniques, prolonged pregnancy has been associated with a two fold to ten fold increase in the incidence of fetal distress in labor.[172] Induction of labor emerged as a means of reducing perinatal risks in the prolonged pregnancy.
The development and application of modern techniques of fetal assessment have been associated with a reduction in perinatal risk in prolonged pregnancies. In 13 studies between 1978 and 1987 in which antenatal fetal surveillance was used for follow-up of postterm pregnancies, the risk of perinatal mortality was similar to that of pregnancies delivered at term.[173] Such report demonstrated that expectant management of postterm pregnancy was an acceptable alternative to induction of labor. However, several recent studies have suggested that in spite of modern monitoring techniques, the postterm fetus remains at risk for certain perinatal morbidity such as meconium aspiration, fetal distress in labor and macrosomia with its attendant complications.[174] These findings have rekindled the controversy surrounding the optimal management of prolonged pregnancy. In response, several prospective randomized trials using contemporary management schemes have compared induction and expectant management in prolonged pregnancy.[175] [176] These trials have yielded conflicting results that have been attributed to differences in-patients selection (ripe Vs unripe cervix at entry), methods of labor induction (PGE2 with or without oxytocin, amniotomy or stripping of the membranes), and techniques of antenatal fetal surveillance.
There have been doubts expressed about the value of induction of labor in prolonged pregnancy, mainly that it may result in more operative intervention without necessarily preventing fetal hypoxia and perinatal death from asphyxia. Furthermore, there is a perception among obstetricians that women do not want induction of labor, which may stem from the outcry in the lay press in the 1970s against induction. Thus in many maternity units induction rates have been falling. This controversy has been partly resolved by the results of sixteen randomized trials, a meta-analysis of which provides clear answers to many of the questions concerning induction of labor.
In conclusion, the available data suggests that induction of labor should be recommended to women with certain dates at 41-plus weeks gestation, for it will reduce the likelihood of perinatal mortality and of cesarean section for fetal distress.
Should Induction Of Labor Be Routine? Is It Cost Effective?
From the foregoing, the following conclusions can be deduced. Firstly, contrary to what many obstetricians believe induction of labor for prolonged pregnancy does not increase the likelihood of cesarean section, rather, it decreases it. Secondly, the risk of fetal distress from uteroplacental insufficiency due to prolonged pregnancy can be reduced by induction of labor, even to the point of preventing perinatal death from asphyxia. The available evidence suggests that although cesarean sections
may be few with induction of labor at 40 weeks, this is offset by an increase in instrumental vaginal delivery. There is little justification for policy of routine induction of labor at such a relatively early gestation even though perinatal mortality is lowest at 40 weeks gestation.
Should one recommend induction of labor at 41-plus weeks gestation to all women with certain dates? Despite the evidence from 11 randomized trials some obstetricians may not be convinced. The perinatal mortality with induction of labor at 41-plus weeks is 0.3 per 1000 (one death in 2905 cases) and in the control group is 2.5 per 1000 (seven deaths in 2822 cases). Thus, in order to prevent one perinatal death, one would have to induce as many as 460 women at 41-plus week's gestation. The reduction in cesarean section rates in a particular maternity unit is 20%, 460 inductions would result in 13 fewer cesarean sections, hardly a huge saving! Thus a big effort by way of induction of labor has to be undertaken in order to secure comparatively a modest gain.
The result of The Canadian Multicenter Postterm Pregnancy Trial and of the meta-analysis, combined with the significant difference in cost between the two strategies (active vs. expectant management) unambiguously support the induction strategy as "win-win" alternative in the management of postterm pregnancies. That is, an induction management policy produces better outcome at a lower cost .[177] These findings also support recent recommendations that induction of labor should be offered to women with pregnancies of 41 or more weeks.[178] More research is needed to determine the most effective methods of induction (e.g. medication, nipple stimulation, stripping or sweeping of the membranes or mechanical methods).
Women's Views About Management Options
The controversy surrounding the management of prolonged pregnancy has reached a critical point in recent times. As described. the available data points to the fact that a huge effort by way of induction of labor only secures a modest gain. What research is there on women's views however is reassuring. Thus Cardozo[179] asked women after delivery to clarify their satisfaction with their treatment allocation into three categories. Dissatisfaction was not associated with treatment allocation, but was strongly associated with operative delivery, regardless of treatment allocation. The study by Roberts et al.[180] showed that the majority of women preferred induction.
One stone casts one shadow
Which cradles the secrets of eternity.
Interred, remains but the bones of your children
For their flesh and their spirit,
Like the seeds of ancient wildflowers,
Have dissolved into the earth to become one with all humanity.
Nothing will live longer.[181]
We are a society of communicators. Through our speech and literature we portray ourselves like paint on a canvass. We should not underestimate the influence of our words for they are empowering. In a moment they can help; in less time they can hurt. They can bring peace and they can create turmoil. A few simple words in an appropriate situation can have inordinate influence. I recently received a note from a father who just lost his prematurely born twin daughter to a condition called twin- to- twin transfusion Syndrome. One twin died in utero and the remaining twin was born at twenty-five weeks, gravely ill and on life support systems in the newborn intensive care unit. After a brave but futile struggle, she too died. Her father contacted me from England asking if I could suggest some words to read at the memorial service for his children. I sent these few lines to these bereaved parents:
Let us not succumb to winter's portent,
the solstice of our darkest hour...
In their reply I learned they will be placing these words upon the headstone of their twin's grave and will be reading another poem of mine at their memorial service. Needless to say, I was quite humbled by this use of my poetry. I intend my words to be available to comfort and it may take several if not hundreds of contacts with my work before they serve such purpose, but when they do, I know that by benefiting just one family, their purpose has been served. I write each poem to reach one family at a time. By not expecting a multitude of recipients and acknowledgments, each individual acknowledgment becomes that much more special.
I have read your poetry and it has
brought to me such comfort and also
inspired me to write my feelings down in
that form. It is a tremendous release.
I thank you once again for bringing me
peace through your work.
Although modernity has exiled poetry and taken it from the center of society outwards to the periphery[182], I feel re-uniting poetry with the now, near-ubiquitous Internet will restore the paradigm of the humanities with that of modern technology. Following is communication from an "Internet" correspondent which best illustrates the power of the "new technology" in helping lessen the age-old feelings of sorrow:
Dear Dr. Berman,
As I lay in bed this evening waiting for sleep to come, I realized that
I couldn't rest until I wrote to you. Recently I visited your Hygeia web
site because of a tragedy in my life. I have had three miscarriages in
the past year and I was looking for some hope or comfort through the
experiences of others. As I read through your poems, one in particular,
Cameron, seemed so poignant that I copied and saved it. I was moved by
it because it reminded me of my best friend's nephew, Alex.
Alex was five years old. He fought a long and difficult battle with
leukemia, and then finally a more virulent and pervasive cancer, since
his second birthday. He bravely cooperated with his doctors at the
Hospital. They had tried chemotherapy, a bone marrow transplant, and
cord blood transfusion. He had periods of remission and of hope. His
parents, devout Catholics, prayed for a miracle and Alex and his dad
even made a pilgrimage to Lourdes, France.
On July 31st, Alex's doctors told his parents that he would not live
past the weekend. My friend called my husband and me to tell us the sad
news. They wanted to organize a tribute to Alex, but were unsure what to
do. I discussed it with my husband, a video producer. He immediately
suggested a video which would incorporate photographs, music, and video
clips of Benjamin's life. We met with the family on July 1 to assemble
the mementos. I remembered your poem and put it in my purse as I was
leaving for our meeting.
That evening we chose some music that we all thought was appropriate.
But how to end the video? I remembered your poem and suggested it as
an end. Everyone loved the poem, and tears flowed as we all read it and
realized how appropriate it was. The next day as my husband started to
organize the video, he began with the end first, copying your poem in a
beautiful script font on a black background. The last two words ...
through Eternity... fade into a picture of the Milky Way. The music for
the poem is "Friendship Theme" from Beaches. We changed one word of
the
poem, and I am sure you won't mind. We changed the word Nature's to
God's, because of the family's deeply religious beliefs.
I just learned that my friend's sweet and brave nephew died today,
August 6. I didn't think to write and ask you for approval to use the poem
because
we were working so quickly, but your name and copyright are included on
the cover of the video box, along with the text. The family will be
making copies of the video for close relatives.
I would be very honored to send you a copy of the video, if you like.
I'm sure that as you watch it, you will be as touched by this little
angel and his loving family as all of us have been. And you will also
see how appropriate your beautiful poem is. R.R., Los Gatos California
The need to reach out to others is both inherent and acquired. There is a "beauty and a tenderness that man can give to man"[183]. Through family nurturing and a casting of family values, we as children grow to appreciate that without a thoughtfulness of others, our motives will be selfish and unfulfilling. "No man is an island, entire of itself; everyman… is a part of the main[184]". We have a need and obligation to care for others. Physicians I believe are in a foremost position to carry out the deeds which through their practice they profess. Whether in academic, research or clinical practice, laboratory medicine or diagnostic imaging, the physician's role is to bring comfort and to heal-others. From such healing comes self-reward, self-fulfillment and honor. If we are surrounded by despair and inequities and have the opportunity to help with their dissolution, it is our obligation to do so. Such is my mission through my work and my poetry. If one person, one family, can be helped or can gather hope through the words I write, it can bring reward equal to the healing with my hands as a physician. I believe hope is a singular gift we must never destroy in ourselves. It is an endless song in an endless concert; a nocturne bright in the darkest of nights. Poetry is its instrument whose music can enable hope.
We as human beings can be distinguished from our ancestors by our capacity to think, to speak, to choose, to procreate and to understand the value of our actions. To bare children concerns our desire not only to procreate but to establish a family and instill our values into our offspring. We are not parents without our children unless our children, conceived through our love and nurtured through our bodies and our spirits are lost to death. There is such remorse when our children die and when our pregnancies fail that a part of our own humanity is lost, never to be found. Tears cannot justly portray our grief as we begin a search for reason and comfort. Words we write, words we read, and words we hear can serve as an invaluable source of solace. Words are songs from our hearts and can be "songs of hope, songs for hope"[185]
The Virgin Winter
Let us not succumb to this portent,
The solstice of our darkest hour.
For it is but a finite point
Upon an infinite journey
Which began with all creation and
Upon whose path walk
The souls of our children;
Pure as the silence of the virgin winter,
Alive with winds of indomitable hope.
Written in memory of a dear mother and child
The End
Woodbridge Connecticut
March, 1999
Source: Personal data from http://www.hygeia.org, September, 1998.
This table represents thirty-two months of registrations to the hygeia.orgÒ database and is representative of nearly every type of pregnancy and perinatal loss which can be experienced.
Reason for Loss Number % % excluding "unknowns"
unknown |
829 |
33.74% |
|
miscarriage/missed abortion/blighted ovum |
131 |
5.33% |
8.05% |
alveolar capillary dysplasia |
104 |
4.23% |
6.39% |
incompetent cervix |
91 |
3.70% |
5.59% |
placental abruption |
85 |
3.46% |
5.22% |
cord accident |
77 |
3.13% |
4.73% |
chromosome- trisomy 18 |
75 |
3.05% |
4.61% |
ectopic pregnancy |
61 |
2.48% |
3.75% |
pre-term labor and delivery-prematurity |
60 |
2.44% |
3.69% |
congenital heart disease |
49 |
1.99% |
3.01% |
molar pregnancy |
43 |
1.75% |
2.64% |
prom-premature rupture of membranes |
42 |
1.71% |
2.58% |
chorioamnionitis/infection/sepsis |
35 |
1.42% |
2.15% |
chromosome- trisomy 13 |
35 |
1.42% |
2.15% |
severe toxemia/preeclampsia/pregnancy induced hypertension |
30 |
1.22% |
1.84% |
chromosome- trisomy 21-down's syndrome |
29 |
1.18% |
1.78% |
neural tube defect-including spina bifida, hydrocephaly |
29 |
1.18% |
1.78% |
potter's syndrome |
27 |
1.10% |
1.66% |
multiple gestation |
26 |
1.06% |
1.60% |
twin-to-twin transfusion syndrome |
24 |
0.98% |
1.47% |
chromosome- triploidy |
23 |
0.94% |
1.41% |
asphyxia |
20 |
0.81% |
1.23% |
multiple congenital anomalies |
20 |
0.81% |
1.23% |
neural tube defect-anencephaly |
20 |
0.81% |
1.23% |
extreme prematurity |
19 |
0.77% |
1.17% |
chromosome- turner's syndrome |
18 |
0.73% |
1.11% |
recurrent miscarriage/pregnancy loss |
18 |
0.73% |
1.11% |
stillbirth at term |
16 |
0.65% |
0.98% |
chromosome- trisomy other |
15 |
0.61% |
0.92% |
SIDS-sudden infant death syndrome |
15 |
0.61% |
0.92% |
intrauterine growth retardation-iugr |
13 |
0.53% |
0.80% |
hypoplastic left heart syndrome |
12 |
0.49% |
0.74% |
diaphramatic hernia |
10 |
0.41% |
0.61% |
luteal phase defect |
10 |
0.41% |
0.61% |
meningitis |
10 |
0.41% |
0.61% |
cord accident |
9 |
0.37% |
0.55% |
cord accident |
9 |
0.37% |
0.55% |
extreme prematurity |
9 |
0.37% |
0.55% |
fetal demise |
9 |
0.37% |
0.55% |
antiphospholipid syndrome |
16 |
0.65% |
0.98% |
multicystic (polycystic kidneys) |
16 |
0.65% |
0.98% |
neural tube defect- holoprosencephaly |
8 |
0.33% |
0.49% |
renal agenesis |
8 |
0.33% |
0.49% |
vaters syndrome |
8 |
0.33% |
0.49% |
cord accident- true knot |
7 |
0.28% |
0.43% |
intraventricular hemorrhage |
7 |
0.28% |
0.43% |
partial molar pregnancy |
7 |
0.28% |
0.43% |
cord accident- velamentous insertion of cord |
6 |
0.24% |
0.37% |
group b strep sepsis |
6 |
0.24% |
0.37% |
hyperemesis gravdiarum -severe |
6 |
0.24% |
0.37% |
meconium aspiration syndrome |
6 |
0.24% |
0.37% |
omphalocele |
6 |
0.24% |
0.37% |
vanishing twin syndrome |
6 |
0.24% |
0.37% |
congenital heart disease- transposition of great vessels |
5 |
0.20% |
0.31% |
cord accident- vasa previa |
5 |
0.20% |
0.31% |
non-immune fetal hydrops |
5 |
0.20% |
0.31% |
misc. antibody disorder |
4 |
0.16% |
0.25% |
meconium aspiration syndrome |
4 |
0.16% |
0.25% |
parvo virus/fifth's disease |
4 |
0.16% |
0.25% |
pseudomonas infection |
4 |
0.16% |
0.25% |
uterine anomalies |
4 |
0.16% |
0.25% |
viral infection- Listeria |
4 |
0.16% |
0.25% |
asphyxia |
3 |
0.12% |
0.18% |
chromosome- Klinefelter's syndrome |
3 |
0.12% |
0.18% |
chromosome- translocation |
3 |
0.12% |
0.18% |
chromosome- trisomy 14, 15 |
3 |
0.12% |
0.18% |
chromosome- trisomy 15 |
3 |
0.12% |
0.18% |
diabetes |
3 |
0.12% |
0.18% |
fetal distress |
3 |
0.12% |
0.18% |
fibroid tumor of the uterus |
3 |
0.12% |
0.18% |
group b strep sepsis |
3 |
0.12% |
0.18% |
hydrops fetalis (non-immune) |
3 |
0.12% |
0.18% |
lupus syndrome |
3 |
0.12% |
0.18% |
monoamniotic twins |
3 |
0.12% |
0.18% |
subchorionic hemorrhage |
3 |
0.12% |
0.18% |
agenesis of the adrenal gland stillborn at 36 weeks |
2 |
0.08% |
0.12% |
asphyxia |
2 |
0.08% |
0.12% |
chromosome- ring 13 chromosome |
2 |
0.08% |
0.12% |
chromosome- tetraploid |
2 |
0.08% |
0.12% |
chromosome- trisomy 22 |
2 |
0.08% |
0.12% |
chromosome- trisomy 8 |
2 |
0.08% |
0.12% |
dilated cardiomyopathy |
2 |
0.08% |
0.12% |
fetal hydrops |
2 |
0.08% |
0.12% |
Goldenhar syndrome |
2 |
0.08% |
0.12% |
hellp syndrome |
2 |
0.08% |
0.12% |
maternal chicken pox |
2 |
0.08% |
0.12% |
neonatal sepsis |
2 |
0.08% |
0.12% |
possible chromosome problem |
2 |
0.08% |
0.12% |
probable progesterone deficiency |
2 |
0.08% |
0.12% |
renal failure |
2 |
0.08% |
0.12% |
rah factor |
2 |
0.08% |
0.12% |
short rib polydactyly syndrome (srps) |
2 |
0.08% |
0.12% |
staph infection |
2 |
0.08% |
0.12% |
varicella- chickenpox |
2 |
0.08% |
0.12% |
viral infection- cmv |
2 |
0.08% |
0.12% |
acute fatty liver of pregnancy |
1 |
0.04% |
0.06% |
acute myocardial infarction |
1 |
0.04% |
0.06% |
age related pregnancy loss |
1 |
0.04% |
0.06% |
alveolar capillary dysplasia |
1 |
0.04% |
0.06% |
amniotic band syndrome |
1 |
0.04% |
0.06% |
amniotic fluid embolism |
1 |
0.04% |
0.06% |
asphyxia |
1 |
0.04% |
0.06% |
blood clot in cord |
1 |
0.04% |
0.06% |
brain tumor |
1 |
0.04% |
0.06% |
breast & lung cancer |
1 |
0.04% |
0.06% |
breast cancer |
1 |
0.04% |
0.06% |
breech delivery |
1 |
0.04% |
0.06% |
brown recluse spider bite |
1 |
0.04% |
0.06% |
burn victim |
1 |
0.04% |
0.06% |
car accident |
1 |
0.04% |
0.06% |
chemical reaction to necessary medication |
1 |
0.04% |
0.06% |
chromosome translocation |
1 |
0.04% |
0.06% |
chromosome- deletion |
1 |
0.04% |
0.06% |
chromosome- duplication |
1 |
0.04% |
0.06% |
chromosome- marker |
1 |
0.04% |
0.06% |
chromosome- other |
1 |
0.04% |
0.06% |
chromosome- ring 21 chromosome |
1 |
0.04% |
0.06% |
chromosome- translocation 4,8 |
1 |
0.04% |
0.06% |
chromosome- trisomy 16 |
1 |
0.04% |
0.06% |
congenital adrenal hyperplasia |
1 |
0.04% |
0.06% |
Digeorge disease w/congenital heart disease |
1 |
0.04% |
0.06% |
eclampsia |
1 |
0.04% |
0.06% |
eclampsia |
1 |
0.04% |
0.06% |
endometriosis |
1 |
0.04% |
0.06% |
endometriosis |
1 |
0.04% |
0.06% |
factor v leiden |
1 |
0.04% |
0.06% |
fatal dwarfism-specific diagnosis to be determined |
1 |
0.04% |
0.06% |
fetal maternal hemorrhage at 39 weeks |
1 |
0.04% |
0.06% |
fetal sacrococcygeal teratoma |
1 |
0.04% |
0.06% |
folic acid deficiency |
1 |
0.04% |
0.06% |
funeate insertion |
2 |
0.08% |
0.12% |
graves disease |
1 |
0.08% |
0.12% |
hemophatisitic limphohisto citosis |
1 |
0.04% |
0.06% |
hyperemesis gravidarum |
1 |
0.04% |
0.06% |
hypoplastic lung syndrome |
1 |
0.04% |
0.06% |
Joubert syndrome |
1 |
0.04% |
0.06% |
LCHAD |
1 |
0.04% |
0.06% |
lupus anticoagulant positive - (loss at 39 weeks) |
1 |
0.04% |
0.06% |
massive brain hemorrhage |
1 |
0.04% |
0.06% |
meconium aspiration |
1 |
0.04% |
0.06% |
microcephaly |
1 |
0.04% |
0.06% |
Nager syndrome |
1 |
0.04% |
0.06% |
NEC-necrotizing enterocolitis |
1 |
0.04% |
0.06% |
Niemann-Pick disease |
1 |
0.04% |
0.06% |
ovarian cyst- torsion with loss of pregnancy |
1 |
0.04% |
0.06% |
physical abuse-miscarriage |
1 |
0.04% |
0.06% |
pneumothorax |
1 |
0.04% |
0.06% |
possible bad ovarian eggs |
1 |
0.04% |
0.06% |
possible infection |
1 |
0.04% |
0.06% |
posterior urethral valve obstruction |
1 |
0.04% |
0.06% |
prader-willi syndrome |
1 |
0.04% |
0.06% |
preeclampsia |
1 |
0.04% |
0.06% |
probable placental problem |
1 |
0.04% |
0.06% |
probable unknown genetic |
1 |
0.04% |
0.06% |
regretted termination |
1 |
0.04% |
0.06% |
salpingitis isthmica nodosa |
1 |
0.04% |
0.06% |
shoulder dystcocia |
1 |
0.04% |
0.06% |
Tay Sachs |
1 |
0.04% |
0.06% |
tethered spine |
1 |
0.04% |
0.06% |
thanataphoric dysplasia |
1 |
0.04% |
0.06% |
tracheal stenosis |
1 |
0.04% |
0.06% |
trauma |
1 |
0.04% |
0.06% |
tumor of the bladder |
1 |
0.04% |
0.06% |
urea cycle defect - genetic disorder |
1 |
0.04% |
0.06% |
uterine rupture |
1 |
0.04% |
0.06% |
volvulus |
1 |
0.04% |
0.06% |
Total |
2457 |
100% |
100% |
Infant mortality rates, fetal mortality rates, and perinatal mortality rates, according to race: United States, Selected Years through 1996
[Data are based on the National Vital Statistics System]
Neonatal, Perinatal and Infant Mortality rates
Race and Year |
Infant |
Under 28 days |
Under 7 days |
Post-neonatal |
Fetal |
Late Fetal |
Perinatal |
All Races-1996 |
7.3 |
4.8 |
3.8 |
2.5 |
6.9 |
3.6 |
7.4 |
White Child-1980 |
11.0 |
7.5 |
6.2 |
3.5 |
8.1 |
5.7 |
11.9 |
White Mother-1980 |
10.9 |
7.4 |
6.1 |
3.5 |
8.1 |
5.7 |
11.8 |
White Mother-1996 |
6.1 |
4.1 |
3.3 |
2.2 |
5.9 |
3.3 |
6.5 |
Black Child-1980 |
21.4 |
22.8 |
20.3 |
9.9 |
23.2 |
- - - |
34.5 |
Black Mother-1980 |
22.2 |
14.6 |
12.3 |
7.6 |
14.7 |
9.1 |
21.3 |
Black Mother-1996 |
14.7
|
9.8 |
8.2 |
5.3 |
12.7 |
5.7 |
13.8 |
Infant Mortality Rate: (under 1 year of age), Neonatal (under 28 days), Early neonatal (under 7 days), and Post neonatal (28-365 days).
Fetal Mortality Rate: fetal deaths of 20 weeks or more
gestation per 1,000 live births plus fetal deaths.
Late Fetal Mortality Rate: Number of fetal deaths of 28 weeks or more gestation
per 1,000 live births plus late fetal deaths.
Perinatal Mortality Rate: Number of late fetal deaths plus infant deaths within
7 days of birth per 1,000 live births plus late fetal deaths.
Infant deaths are tabulated by race of decedent; live births
and fetal deaths are tabulated by race of child
Infant mortality rates in this table are based on infant deaths from the
mortality file (numerator) and live births from the natality file
(denominator). Inconsistencies in reporting race for the same infant between
the birth and death certificate can result in underestimated infant mortality
rates for races other than white or black. Infant mortality rates for minority
population groups are available from the national linked files of live births
and infant deaths. Data and Text Sources: Centers for Disease Control and
Prevention, National Center for Health Statistics: Vital statistics of the
United States, vol. II, mortality, part A, for data years 1950-96. Public
Health Service. Washington. U.S. Government Printing Office; Peters KD,
Kochanek KD, Murphy SL. Report of final mortality statistics, 1996. Monthly
vital statistics report; vol. 45. Hyattsville, Maryland: 1998; and data
computed by the Division of Health and Utilization Analysis from data compiled
by the Division of Vital Statistics.
Infants with low birthweight, born preterm, or in multiple births have
a higher risk of dying in the first year of life. Babies born to teens and
women in their forties and to mothers who did not complete high school, were
unmarried, did not receive timely prenatal care, or smoked during pregnancy
also have higher infant mortality rates.
A new report from the National Center for Health Statistics, Centers for Disease Control and Prevention, presents infant mortality statistics from the latest linked birth/infant death data set to identify factors that impact infant mortality or survival. The report is a special analysis of birth and death information provided through the Nation's vital statistics system.
Birthweight is one of the most important predictors of an infant's subsequent health and survival. In 1995, 7.3 percent of infants were low birthweight, defined as less than 2,500 grams (5 lbs., 8 oz), however, 63 percent of all infant deaths were among low birthweight babies. Survival of low birthweight infants has improved, however. Over the past decade, mortality rates declined most rapidly for infants weighing 750-1,499 grams--the largest of the very low birthweight infants. Mortality for these babies dropped by more than 50 percent between 1985 and 1995.
The infant mortality rate for male infants was 8.3 in 1995, 22 percent higher than the rate of 6.8 for females. Babies born in multiple births have an infant mortality rate 5 times that of single births. Infant mortality rates are highest for teens and women in their 40's and lowest for women in their 20's and early 30's. The infant mortality rate was twice as high for unmarried women as for married women. In general infant mortality declined with increasing education of the mother. Mothers who had not completed high school had infant mortality rates more than twice that of women with college education.
Analysis of the vital statistics data also showed that mortality rates varied considerably by race of mother. In 1995 the overall infant mortality rate from the linked file was 7.6 deaths per 1,000 live births. Mortality rates were lowest for infants born to Asian and Pacific Islander mothers (5.3), followed by white (6.3), American Indian (9.0), and black (14.6) mothers. The Hispanic infant mortality rate (6.3) was the same as for non-Hispanic white infants, and ranged from 5.3 for infants of Cuban mothers to 8.9 for Puerto Rican infants.
For American Indian infants, death rates were highest in the post-neonatal period with death rates from sudden infant death syndrome and accidents about 3 times the rate for white infants. For black infants, disorders related to short gestation and low birthweight was the leading cause of death with black infants more than 4 times as likely to die from this cause as white infants.
"Infant Mortality Statistics from the Linked Birth/Infant Death Data Set--1995 Period Data," by Marian F. MacDorman and Jonnae O. Atkinson is based on information from the death certificate linked to the corresponding birth certificate for each infant under 1 year of age who died in 1995. The purpose of the linkage is to use the additional information from the birth certificate to conduct more detailed analyses of infant mortality patterns to provide better information for prevention, research, and medical care. Birth and death certificates are linked by the State vital statistics offices where the original records are filed and reported to NCHS through the National Vital Statistics System.
National Center for Health Statistics
New Study Identifies Infants at Greatest Health Risk
February 26, 1998
Copies of the report are available from NCHS.
Contact: NCHS Press Office (301) 436-7551
The estimated incidences for the leading categories of birth defects are provided in the table below. Birth defects are grouped into three major categories: 1) structural/metabolic; 2) congenital infections; and 3) other conditions. Birth defects of the heart and circulatory system affect more infants than any other type of birth defect. Of all infants born each year, approximately 1 in 115 has heart and/or circulatory defects.
1. Structural/Metabolic |
Estimated Incidence |
Heart and circulation |
1 in 115 births |
Muscles and skeleton |
1 in 130 births |
Club foot |
1 in 735 births |
Cleft lip/palate |
1 in 930 births |
Genital and urinary tract |
1 in 135 births |
Nervous system and eye |
1 in 235 births |
Anencephaly |
1 in 8,000 births |
Spina bifida |
1 in 2,000 births |
Chromosomal syndromes |
1 in 600 births |
Down syndrome (Trisomy 21) |
1 in 900 births |
Respiratory tract |
1 in 900 births |
Metabolic disorders |
1 in 3,500 births |
PKU |
1 in 12,000 births |
|
|
2. Congenital Infections |
|
Congenital syphilis |
1 in 2,000 births |
Congenital HIV infection |
1 in 2,700 births |
Congenital rubella syndrome |
1 in 100,000 births |
|
|
3. Other |
|
Rh disease |
1 in 1,400 births |
Fetal alcohol syndrome |
1 in 1,000 births |
Note: all numbers are based on the best available estimates, which underestimate the incidence of many birth defects.
Sources: March of Dimes, Metropolitan Atlanta Congenital Defects Program, and California Birth Defects Monitoring Program.
For more than 20 years, birth defects have been the leading cause of infant mortality. In 1995, birth defects accounted for 6,554 infant deaths, reflecting a rate of 168.1 per 100,000 live births. Prematurity / low birthweight (LBW) was the second leading cause of infant mortality (100.9), followed by sudden infant death syndrome (SIDS - 87.7), respiratory distress syndrome (RDS - 37.3), and maternal pregnancy complications (33.6). Together, these five causes accounted for more than half of all infant deaths in 1995.
Cause of Death |
Rate per 100,000 Live Births |
Birth Defects |
168.1 |
Preterm/Low Birthweight |
100.9 |
SIDS |
87.1 |
RDS |
37.3 |
Maternal Pregnancy Complications |
33.6 |
Placental Cord Compression |
24.7 |
Infections |
20.2 |
Accidents |
20.2 |
Pneumonia/Influenza |
12.6 |
Hypoxia/Birth Asphyxia |
12.2 |
Source: National Center for Health Statistics: Adapted from March of Dimes Perinatal Data Center, 1998.
acute fatty liver of pregnancy- condition of unknown etiology occurring most commonly in the third trimester or in the early postpartum period where a patient shows signs and symptoms of liver failure including nausea, vomiting, increased bleeding time, hematemesis (vomiting blood) and jaundice, as well as abnormal laboratory values signifying liver disease and dysfunction. Treatment is supportive and consists of intravenous fluids, glucose, fresh frozen plasma and prompt delivery. Mortality has been significantly reduced over the years secondary to early recognition, but there is still a fairly high rate of death. Survivors demonstrate no liver deficits, and there is no increased risk in subsequent pregnancies.
agenesis of adrenal gland (stillborn at 36 weeks)- this is the congenital lack of the adrenal glands caused by absence of their progenitor cells during embryogenesis. This is an extremely rare, but fatal, condition and is associated with many other congenital anomalies.
alveolar capillary dysplasia- a congenital condition where the capillaries (end-unit of the vascular tree)in the lungs of an infant do not make contact with the alveolar (end-unit of respiratory tree) epithelium, thus the blood-gas barrier is not formed normally. This is a rare cause of pulmonary hypertension.
amniotic band syndrome- in utero swallowing, adhering or constricting of amniotic bands when there is early rupture of the amniotic membrane causing congenital anomalies including omphalocele, syndactyly (joined fingers or toes), and distorted cranio-facial features such as widely separated eyes and displaced nose. The ADAM complex ( amniotic deformities, adhesions, mutilation) is a result of this syndrome, but much less severe sequelae may be seen such as constriction grooves on the limbs. The earlier in gestation the event occurs, the worse the syndrome.
amniotic fluid embolism- a rare, but most often lethal, event where a small amount of amniotic fluid enters the vascular system during labor and delivery or placental abruption. The presence of this fluid in the vascular system sets off a cascade of events causing a bleeding problem, vascular collapse and bronchospasm. Treatment is aimed at supporting the respiratory system and correcting the shock and coagulopathy. Mechanical ventilation, rapid administration of fluids, and transfusion of blood components should be prompt.
antiphospholipid syndrome- an autoimmune disease that in the non-pregnant state is subclinical but often causes problems during pregnancy from circulating antibodies that bind to phospholipids. Recurrent abortion, early fetal loss, severe intrauterine growth retardation, preterm birth and thromboses are all associated with this disorder. However, it is not usually diagnosed until after one of the above events. Treatment for subsequent pregnancies includes heparin and aspirin.
asphyxia- a situation when oxygen supply to fetus is diminished causing hypoxia and acidosis. Causes include placental pathology, acute maternal hypotension, chorioamnionitis, dystocia (difficult labor and delivery), and prolapse, rupture or entanglement of the umbilical cord. Any intrapartum death of a previously healthy fetus should be presumed to be a result of asphyxia until proven otherwise. Almost every organ system has the potential to become damaged as a result of this condition including brain tissue causing neonatal seizures and cerebral palsy. There is an estimated 10% overall mortality rate.
chorioamnionitis- inflammation of the chorion and amnion (membranes surrounding the fetus) secondary to infection. Signs and symptoms include maternal fever and tachycardia, uterine tenderness and foul smelling vaginal discharge. When bacteria is found in the amniotic fluid, there is an increased incidence of maternal and neonatal sepsis. Premature rupture of membranes increases the likelihood of chorioamnionitis as the bacteria from the lower genital tract ascends to infect the amniotic cavity. With a positive diagnosis, antibiotics should be administered promptly as well of the induction of labor. Prognosis for the neonate is mostly dependent on the gestational age and lung maturity at time of delivery.
chromosome deletion- the loss of a portion of DNA from a chromosome that may be any length. Many small deletions are clinically undetectable, while others may make the difference for different blood groups or for the conditions of cystic fibrosis or a-thalassemia.
chromosome duplication- a genetic condition where there is inappropriate duplication of certain areas of DNA on a chromosome. This type of genetic defect is found to cause certain clinical disorders, including the condition of familial hypercholesterolemia.
chromosome- Klinefelter’s syndrome-a syndrome resulting from the trisomy of the sex chromosomes, in this case 47, XXY. These males are tall and thin with long extremities, and secondary sexual characteristics remain underdeveloped. They are always infertile and a majority of these patients have learning difficulties as well as poor psychosocial adjustment.
chromosome marker- version of a gene that can occupy a particular locus or position on a chromosome. These markers can be followed through easily classifiable alleles.
chromosome ring - a rare chromosome that is formed as a result of its ends having been deleted and the broken arms united to form a ring.
chromosome ring 21- a rare chromosomal anomaly that is associated with mental retardation and dysmorphic features. It is uncommonly familial, however when it is, it is associated with a normal phenotype. In unaffected female carriers, there is an increased risk of having children with Down’s syndrome.
chromosome tetraploid- condition where there are four sets of chromosomes instead of two (92, XXXX or 92, XXYY). This condition is incompatible with life and the fetus is spontaneously aborted early in the pregnancy.
chromosomal translocation- an event that involves the exchange of segments of chromosomes between nonhomologous chromosomes (chromosomes that do not contain the same order of gene positions). A translocation involving chromosome 21 creates the risk of producing a child with Down’s syndrome.
chromosome triploidy- a condition that occurs when there are three sets of chromosomes instead of two. The extra set can be paternal (e.g. 69, XXY) or maternal (e.g. 69, XXX). Most abort in the first trimester and may account for up to 10% of all first trimester abortuses. Those that survive into the second trimester my demonstrate intrauterine growth retardation, oligohydramnios (diminished amniotic fluid), facial clefting, abnormalities of the hands and feet, and cranial abnormalities including holoprosencephaly, hydrocephalus and agenesis of the corpus callosum.
chromosome trisomy- a state of having three of a given chromosome instead of the usual pair which is associated with advanced maternal age. Only three have been found in post-natal survival (13, 18, 21), and each are associated with growth and mental retardation as well as congenital anomalies.
chromosome/trisomy 13- a rare occurrence in live births which is usually lethal by six months. Clinical characteristics include growth retardation, central nervous system malformations including holoprosencephaly, severe mental retardation, absence of the eyes, cleft lip and palate, polydactyly, rocker-bottom feet, and congenital heart and urogenital defect. Advanced maternal age is a risk factor.
chromosome/trisomy 14- a rare trisomy that is associated with malignancy.
chromosome/trisomy 15- a rare trisomy, usually aborted in the first trimester. In live births, it manifests in severity depending on the degree of mosaicism as dysmorphism of the nose, anomalies of the hands and feet and hematological malignancies.
chromosome/trisomy 16- the most common trisomy in abortuses, but is not seen in live births.
chromosome/trisomy 18- a rare condition in live born infants but is estimated that about 95% of fetuses with this chromosomal abnormality abort spontaneously. Survival postnatally is usually only a few months. Features of this condition include mental retardation, failure to thrive and sever congenital malformations of the heart. Ears are low-set, there are rocker-bottom feet, the jaw is receding and the fists are clenched with the second and fifth digits overlapping the third and fourth. As with most trisomies, advanced maternal age is a risk factor.
chromosome/trisomy 21 (Down’s Syndrome)- the most common chromosomal disorder occurring in about one in 800 live births with an elevated risk occurring in children or fetuses of mothers older than 35. Clinical features include characteristic eyes, short stature, flat nasal bridge, low-set ears, protruding tongue, single crease in palm (“simian crease”), a wide gap between the first and second toes and mental retardation. Congenital heart disease is very common as are gastrointestinal anomalies (duodenal atresia and tracheoesophageal fistula), and there is a steep increase in the risk of leukemia. About half of these patients survive beyond 50 years, and there is a premature senility similar to Alzheimer’s disease that occurs in a large percentage of people with Down’s. This disease is well known to be associated with advanced maternal age and can be screened for by the triple screen test (low alpha-fetoprotein, low unconjugated estriol, and elevated human chorionic gonadotropin ) and later confirmed by diagnostic amniocentesis with chromosomal analysis.
chromosome/trisomy 22- the most frequent trisomy in spontaneous abortions after trisomy 16. Patients with this trisomy can survive if it is expressed in its mosaic form, however, they always have many physical anomalies including microcephaly, heart defects, craniofacial dysmorphisms, hypoplasia of the fingers as well as mental retardation. This chromosomal event is associated with advanced maternal age.
chromosome/trisomy 8- this trisomy often demonstrates agenesis of the corpus callosum in the brain causing holoprosencephaly, cardiac malformations and facial dysmorphisms. There is also an association with hematological and solid tumors.
chromosome- Turner’s syndrome-females with the karyotype 45,X instead of 46, XX resulting in a syndrome that includes short stature, gonadal dysgenesis (streak ovaries), infertility, unusual facies, webbing of the neck, widely spaced nipples, increased risk of cardiovascular and renal anomalies and a deficiency in spatial abilities and motor organization, although intelligence is usually normal. There is a very high incidence of this chromosomal abnormality in spontaneous abortions, but it seems to be very compatible with postnatal survival.
congenital adrenal hyperplasia- an autosomal recessive disorder (requiring inheritance of two genes to manifest disease) where an enzyme deficiency in the adrenal gland (most often 21-hydroxlase) causes virilization of females secondary to the overproduction of androgenic hormones. In utero exposure of the female fetus to high levels of these adrenal androgens results in an infant with ambiguous genitalia, however, the ovaries, fallopian tubes and uterus are unaffected A male infant usually appears normal at birth. In about half of affected individuals, there is also life-threatening salt wasting. Treatment is both medical and surgical including administration of glucocorticoids and correction of the ambiguous genitalia.
congenital heart disease- cardiovascular malformations that occur in approximately 1% of all live births. The etiology is unclear, and only 5-10% can be explained by maternal infection, toxic exposure, or chromosomal abnormalities. There are many different forms that this condition can take which include malformations of the great arteries, heart valves, outflow tracts (aorta and pulmonary arteries), and septa (walls between the chambers of the heart). Many fetuses with severe cardiac defects may die in utero. Treatment for an affected infant depends on the type of defect and usually includes surgery such as grafts, flaps shunts and even heart transplant.
cord accident- an event such as prolapse or rupture of the umbilical cord that causes the temporary or permanent disruption of blood flow to the fetus prior to birth or during delivery. This is a grave situation as the flow of oxygenated blood is blocked from the fetus. Prolapse of the cord may occur with excessively long cords or with malpresentation of the fetus during delivery. Rupture of a short cord may cause acute fetal blood loss. Contemporary fetal monitoring helps to initiate prompt management.
true knot- this is caused by entanglement of the cord that occurs in less than 1% of all deliveries. In an otherwise normal umbilical cord, it is not thought to be the direct cause of fetal death. Therefore, further investigation should be employed in the event of fetal loss.
vasa previa- velamentous insertion of the cord where the unprotected vessels pass over the cervical os (opening) creating a condition with a greater risk of fetal vessel rupture. Once diagnosed, prompt abdominal delivery should be performed.
velamentous insertion of cord- condition where vessels of the umbilical cord insert between the amnion and chorion layers instead of in their normal insertion. This state incurs a greater risk of rupture of fetal vessels, which should prompt expedient abdominal delivery. The occurrence of this velamentous insertion is higher in multiple pregnancies.
diabetes- glucose intolerance caused by autoimmune pancreatic dysfunction with low/absent production of insulin (type I) or by tissue resistance to insulin (type II) both causing hyperglycemia. These may be present prior to pregnancy or may be caused or unveiled during pregnancy. Prior or “overt” diabetes carries with it greater morbidity and mortality for the mother and fetus than does “gestational” diabetes and use to be the cause for much infertility. Depending on the degree of glycemic control at conception and during early embryogenesis, there is still a risk for spontaneous abortion, half of which are associated fetal anomalies, intrauterine fetal demise, intrauterine growth retardation, congenital anomalies including cardiovascular, neural tube defects, caudal regression syndrome, macrosomia (fetus weighing greater than 4000 gm) with traumatic delivery, and delayed organ maturity. There is an increased risk for neonatal hypoglycemia within minutes of birth due to an over stimulated fetal pancreas as a result of in utero exposure to maternal hyperglycemia. For the mother, there is an increased risk of polyhydramnios, preeclampsia, ketoacidosis and infection. Overt diabetes during pregnancy may or may not have an adverse effect on retinopathy, neuropathy or nephropathy already established from the preexisting diabetes. Gestational diabetes develops as an over response of the normal occurrence of insulin resistance during pregnancy with hyperglycemia. It has a greater incidence in obese women and typically occurs later in gestation. Interestingly, over half of the women will develop overt diabetes later in life, and there is the thought that their offspring have increased risk for obesity and diabetes as well. There is not the same risk for fetal anomalies as there is for overt diabetes since the hyperglycemia does not usually occur during embryogenesis. However, there is still the risk of having a macrosomic infant, which increases the risk of morbidity and mortality secondary to shoulder dystocia. Gestational diabetes also carries the risk for neonatal hypoglycemia, as well as for unexplained stillbirth. Detection of diabetes during pregnancy is first done by the one-hour glucose tolerance test followed by the three hour glucose tolerance test for borderline one-hour tests. Treatment is through diet, exercise and lastly insulin as hyperglycemia increases as the gestation progresses. There is a very high recurrence for subsequent pregnancies.
diaphramatic hernia- condition that may occur in utero in the developing fetus where part or all of the bowel is able to enter the thoracic (chest) cavity through an enlarged hole in the diaphragm. The bowel contents take up space, thus inhibiting growth of the lungs which
results in pulmonary hypoplasia and pulmonary hypertension, both of which cause neonatal cyanosis. This disorder manifests a scaphoid (sunken) abdomen, respiratory distress and bowel sounds in the chest on auscultation. Treatment is respiratory support and surgery.
DiGeorge’s syndrome- a disease that is caused by congenital absence of the parathyroid and thymus glands due to abnormal development early in organogenesis. It is classified as a sporadic syndrome complex of unknown etiology and is associated with micrognathia (underdeveloped chin), as well as aortic arch anomalies. The disease may present with hypocalcemia secondary to absence of parathyroid hormone, as well as increased susceptibility to infection from diminished T-cell production due to lack of thymus gland..
dilated cardiomyopathy- often called congestive cardiomyopathy, this disorder can be categorized into three groups: myocarditis, primary (familial), and drug-induced. Myocarditis is related to viral infections such as the coxsackie virus and is usually diagnosed during an episode of heart failure. An echocardiogram shows a very large and dilated heart. Patients are given diuretics and digitalis and usually recover completely.
eclampsia- this is the condition of pre-eclampsia with the addition of grand mal seizures. Patients with severe pre-eclampsia are at greater risk, but eclampsia does occur in mild forms as well. Management includes oxygen, intravenous fluids with dextrose, antihypertensive drugs (hydralazine), magnesium sulfate to decrease the hyperreflexia and prevent further convulsions, and delivery once the urine output increases.
ectopic pregnancy- a gestation that implants outside of the endometrial cavity, most often in the fallopian tubes, causing a serous hazard to the woman’s health. Risk factors identified include prior or current history of pelvic inflammatory disease (PID), history of therapeutic abortion, tubal ligation, prior ectopic, intrauterine device (IUD), and DES exposure. The overall incidence is high, occurring in approximately one in 200 pregnancies. Symptoms of the condition include amennorrhea, vaginal bleeding, abdominal pain, referred shoulder pain, and if ruptured, often a shock-like picture. Diagnosis is initiated by maternal blood test for levels of b-hCG abnormal for those of an intrauterine pregnancy. Ultrasound is next employed to identify the location of the sac, and surgical laparoscopy or laparotomy are performed to remove the gestation. Non-surgical methods (methotrexate) have gained popularity and may be infused intravenously for several days or directly into the gestational sac.
extreme prematurity- preterm infants have much more morbidity and mortality than full term infants due to their underdevelopment. Because not all of the maternal antibodies have crossed the placenta which provide immunity for the infant, neonates born before 32 weeks are at a six-fold increase of becoming septic. These infants also usually cannot coordinate the mechanisms for oral feeding, so need to be fed through a nasal or oral gastric tube. Immaturity of the gastrointestinal tract may precipitate gastoesophageal reflux, gastric stasis, abdominal distention and ileus, inability to defecate, reflux and aspiration, as well as intolerance to certain elements of milk. Extremely early newborns, especially those weighing under 750g are also at increased risk for neonatal hypoglycemia, retinopathy and blindness, hearing loss, hydrocephalus, microcephaly, mental retardation, cerebral palsy, chronic pulmonary insufficiency, necrotizing enterocolitis with subsequent short bowel syndrome, intraventricular hemorrhage and seizures, growth failure and learning disabilities.
factor V leiden- (activated protein C resistance)- this is an inherited state of hypercoaguability where one is prone to venous thrombosis (clotting). In pregnancy, it has been found to be the cause of recurrent abortions, and it is thought to be associated with the development of preeclampsia.
fetal demise- (intrauterine fetal death- IUFD)- death of the fetus defined as after 20 weeks gestation but before onset of labor. The estimated occurrence is approximately 1% of all pregnancies with about half having an unknown etiology. Identified causes include placental and cord complications, maternal hypertension or medical condition, congenital anomalies of the fetus and intrauterine infection. Signs include absence of fetal movement, uterus small for dates, absence of fetal heart tones, but not necessarily a negative pregnancy test as the placenta may continue to produce b-hCG. Definitive diagnosis is made by ultrasound. Approaches to management is usually includes induction of labor to ease the emotional component of the loss as well as to reduce the chance of intrauterine infection or disseminated intravascular coagulation (DIC) and shock. However, most women would go into spontaneous labor within a couple of weeks. If etiology is not apparent, further investigation should follow including maternal blood tests, fetal chromosomal studies and bacterial and viral cultures.
fetal distress- a condition that occurs when a fetus is unable to maintain biochemical homeostasis and becomes acidotic and hypoxic as a result of intrapartum asphyxia. Causes include problems with the umbilical cord (vasa previa, nuchal cord, prolapse), placenta (infarction, abruption), fetus (anemia, infection) or mother (hyper or hypotension, anemia, heart disease, seizure activity, pulmonary disease). This condition is screened by electronic fetal monitor demonstrating abnormal heart rate patterns. Management is dependent on the cause, but change of maternal position, oxygen therapy, and close monitoring of maternal and fetal conditions are routinely employed.
fetal hydrops- (see “hydrops fetalis”, immune)
fetal-maternal hemorrhage- the presence of fetal red blood cells in the maternal circulation which can be identified by a specific test (Kleihauer-Betke) that detects fetal hemoglobin. With this test and the mother’s hematocrit, the amount of fetal blood loss can be calculated. Large bleeds are uncommon and are associated with a placental lesion such as a chorioangioma. If there is a placental abruption due to trauma, there is an increased risk of this type of hemorrhage.
fetal sacrococcygeal teratoma- a teratoma is a tumor arising from several different cell lines and contains many types of tissue. A sacrococcygeal teratoma is the most common teratoma in newborns, occurring in females more than males. Dimensions may be very large but can be fully removed through surgery which should be performed on the first day of life to reduce the chance of development into malignancy. Diagnosis is by ultrasound and complications include dystocia (difficult birth), non-immune hydrops, polyhydramnios (excess amniotic fluid), and bleeding from tears. It is not typically accompanied by other anomalies.
Goldenhar’s syndrome- a syndrome of malformations including the face, tongue, soft palate and ears which may or may not have an associated deafness. It is caused by disruption early in embryogenesis of unknown etiology.
Grave’s disease- an autoimmune disease caused by receptor antibodies causing hyperthyroidism. In pregnancy, these antibodies can cross the placenta with the potential of causing neonatal thyrotoxicosis in 1% of newborns born of women with Grave’s disease. This is usually a transient state, however, it carries a significant risk of mortality. Intrapartum, the fetus may demonstrate growth retardation. The disease actually improves for the woman during pregnancy but may exacerbate in the postpartum period. Labor, infection, cesarian section or non-compliance with medications may precipitate “thyroid storm” or intense thyrotoxicosis with a 25% rate of maternal mortality. New-onset Grave’s disease is difficult to diagnose during pregnancy, as signs and symptoms of hyperthyroidism include those seen in the hyperdynamic circulatory state of a normal pregnancy. Total serum levels of thyroid hormones (specifically T4) are measured to make the diagnosis. Treatment during pregnancy is a bit different as radioactive iodine is contraindicating while gestating, but the other medical (PTU or Tapazole) or surgical options are utilized. PTU, however, does cross the placenta and carries a one to five percent risk of creating fetal goiter and hypothyroidism.
group B strep (GBS) sepsis- a type of streptococcal bacteria that is considered a part of the normal gastrointestinal flora of humans and can be found in the vagina, cervix, throat, skin and urethra. If a woman carries GBS in her vagina during pregnancy, there may be transmission to the infant at delivery. Other risk factors for transmission include preterm labor and delivery, prolonged labor, preterm rupture of membranes, intrapartum fever, and low birth weight infants. This organism is the most common cause of neonatal sepsis in the United States. The infection can be broken up into early onset and late onset; early usually presents within 48 hours as repiratory distress, pneumonia and often meningitis secondary to vertical transmission. Antibiotics must be initiated immediately, but despite expedient efforts, there is a very high mortality, especially in preterm infants. Late onset is usually acquired in the neonatal nursery and presents by four weeks of life, most often as meningitis. Effective measures to decrease this life-threatening infection for infants is mass screening of pregnant women and initiation of antibiotics during labor, as antibiotic administration prior to labor and delivery has not shown to prevent transmission.
HELLP syndrome- an acronym that stands for Hemolysis, Elevated Liver enzymes, and Low Platelets which form a syndrome that in an uncommon variant of preeclampsia, differing in that it occurs more often in multiparous (having had more than one baby) women, women over 25 years old and gestations less than 36 weeks. Hypertension may be absent. Diagnosis is made by clinical signs as well as thorough maternal blood tests. Management of this condition includes delivery if greater than 34 weeks or evidence of fetal lung maturity as well as signs of deteriorating health of either the mother or fetus. Elements of this syndrom usually correct themselves shortly after delivery, but stabilizing the coagulopathy and providing supportive measures are usually employed.
hydrops fetalis- abnormal accumulation of fluid in the tissue (edema/anasarca) and body cavities (pericardial/pleural effusions and ascites) of the fetus as well as excess amniotic fluid (polyhydramnios). Diagnosis is made by a thorough history from the mother covering race, occupation, infectious exposures and obstetrical, medical and family history. Blood work should entail a complete blood count, chemistry, protein, genetics and viral and bacterial cultures. A comprehensive ultrasound should also be performed assessing the fetus’ anatomy and well being. This condition is treated according to the etiology. When associated with structural heart disease, this conditions is almost always fatal, as is a chronic or progressive course. In addition to fetal loss, other severe sequellae include prematurity secondary to polyhydramnios and bilateral pulmonary hypoplasia as a result of growth interference by the fluid that occupied the pleural cavity during development. Maternal complications include hypoproteinemia, edema, hypertension, pregnancy-induced hypertension, and uterine overdistension secondary to polyhydramnios (excess amniotic fluid) with the associated dangers of abruption, cord prolapse and post-partum hemmorhage.
-immune- hydrops caused by maternal circulating antibodies against the fetal red blood cells resulting in anemia of the fetus with subsequent tissue hypoxia and heart failure. The antibodies are formed in response to maternal exposure to fetal blood cells in a prior pregnancy, delivery or abortion. The most common antibody is to the Rh antigen on the fetal cells, and the immune response (and thus the hydrops) can be prevented by administration of Rh immune globulin at 28 weeks and in the immediate postpartum period. Treatment of this form of hydrops includes in utero fetal transfusion.
-non-immune- uncommon during a viable pregnancy but found commonly in first and second trimester spontaneous abortions. There are many causes of this condition which can be separated into fetal, maternal and placental etiologies. Fetal causes include anatomic anomalies (cardiovascular, thoracic, gastrointestinal, urinary tract), chromosomal abnormalities (45X, trisomy 13, 18, and 21), infection (CMV, parvovirus B19, toxoplasmosis, syphillis, coxsackie, rubella, listeria), anemia (secondary to a-thalassemia, G6PD deficiency, maternal-fetal hemmorhage, twin-to-twin transfusion), or metabolic disorders. Maternal causes include severe diabetes mellitus, anemia, or hypoproteinemia, and placental causes include choroangioma, venous thrombosis, cord torsion or knot.
hyperemesis gravidarum- a condition defined by intractable nausea and vomiting that has an estimated incidence of 1% of all pregnancies occuring most frequently in white women in a first pregnancy. Diagnosis is by history and physical exam. The illness is self-limiting and outcome is generally good, however it may be complicated by metabolic deterioration as a result of dehydration and electrolyte loss. Treatment includes psychosocial support and counseling, dietary modifications and lastly antiemetic drugs when other approaches have failed.
hypoplastic left heart syndrome- a syndrome that includes the in utero underdevelopment of the left ventricular chamber in the heart that pumps oxygenated blood to the brain and body. Fetuses with these congenital anomalies do well in utero, however, post parturition their condition quickly declines demonstrating heart failure, low cardiac output , cyanosis and acidosis. Treatment requires surgery otherwise early neonatal death will ensue. Options include a two step operation (the second at about two years of age) or a cardiac transplantation.
hypoplastic lung syndrome (pulmonary hypoplasia)- a congenital disorder that ultimately causes pulmonary hypertension and pulmonary insufficiency and presents as respiratory distress in the neonate. This condition may be due to decreased amniotic fluid, a substance that is needed to prevent constriction of the fetus by the uterus which inhibits lung growth, any bone disorders where the chest wall is small and bony preventing proper development, diaphragmatic hernias and pleural effusions in hydops fetalis which act as space occupying lesions in the chest cavity thus inhibiting appropriate development of the lungs, and neuromuscular diseases that prevent normal fetal breathing movement which are also needed for lung growth and maturation. Treatment includes admission to the neonatal intensive care unit, intubation and treatment with steroids and surfactant.
incompetent cervix- a condition when the cervix is unable to hold a pregnancy by prematurely dilating. Causes are anatomical, usually secondary to trauma from a rapid dilation during a pregnancy termination or currettage, as well as functional where the cervix is anatomically indistinguishable from a normal cervix yet is associated with pregnancy loss. In subsequent preganancies, a suture or cerclage is placed through the cervix in the first trimester to prevent premature dilation and pregnancy loss.
intrauterine growth retardation (IUGR)- a condition defined by a neonatal birth weight less than the tenth percentile for any given gestational age. Risk factors include previous low birth weight infants, short maternal stature as well as weight less than 100 pounds, narcotic, alcohol and cigarette use, chronic hypertension, pregnancy induced hypertension, threatened abortion, intrauterine infection and congenital malformation of the fetus. The fetus is at risk for meconium aspiration, asphyxia, hypoglycemia and mental retardation. Diagnosis is made by ultrasound which includes precise measurements of fetal head and abdominal circumference, femur length, as well as an estimated fetal weight which are all dependent on accurate dating. Intrapartum management consists of bedrest and correction of underlying cause. Prognosis is good if there is no underlying chromosomal disruption, congenital anomaly or infection, but a neonatal team must be on hand as the neonate is at risk for hypoglycemia, hypothermia and respiratory distress.
intraventricular hemmorhage- a condition usually occuring in the first three days of life that is more prevalent in preterm and very low birthweight infants and is a common cause of neonatal seizures. The pathogenesis of the bleeds is unknown although there are many theories such as weak blood vessels and unstable blood pressure of the neonate. Diagnosis is confirmed by ultrasound through the anterior fontanelle, and treatment includes supportive care, blood transfusions and shunts to decrease the intracranial pressure.
LCHAD- a defect in mitochondrial fatty acid oxidation involving the enzyme long chain 3-hydroxyacyl-coA dehyrogenase. In the pregnant woman with this disease or who is a carrier of this gene, there is an increased risk of severe preeclampsia or acute fatty liver changes of pregnancy. In the neonate, this disease manifests as hypoglycemia, hepatopathy, hypotonia, cardiomyopathy, retinopathy and hypoparathyroidism. Treatment is through dietary modification.
luteal phase defect- the luteal phase is a time frame in the ovary that begins with the onset of the luteinizing hormone midcycle surge that initiates ovulation and ends with the first day of menses. This phase is concurrent with the secretory phase of the endometrium (dynamic lining of the uterine cavity) which is the time when this lining prepares itself for implantation of a fertilized egg. Progesterone is the hormone that dominates these two concurrent periods. A defect during the luteal phase is a cause of infertility that may be suggested by an abnormal increase in basal body temperature, a history of spontaneous abortion or demonstration of poor cervical mucous. Endometrial biopsy with careful histologic examination, providing that the exact dating of the menstrual cycle is known, can make the diagnosis.
meconium aspiration syndrome- a syndrome that occurs usually in full-term infants that causes neonatal cyanosis and repiratory distress through mechanical obstruction, inflammation from chemical pneumonitis and pulmonary hypertension. Meconium in the amniotic fluid signifies fetal distress, and it is common in infants born in the breech presentation. Aspiration of this fluid can happen in utero, but more commonly occurs immediately after delivery. Many of these infants will develop a pneumonia or pneumothorax. Treatment is supportive care as well as mechanical ventilation. Prevention is through careful fetal monitoring, close observation of the fluid that comes out during birth and immediate suctioning of the oropharynx before delivering the infant’s body. After full delivery, deeper and more aggressive suctioning should be instituted. Some doctors practice saline infusion into the amniotic cavity prior to delivery with the belief taht this may reduce the incidence of aspiration.
meningitis- this is the inflammation of the tissue layer that surrounds the brain and spinal cord which may be caused by bacteria, viruses or uncommonly by fungi. The three most common bacterial organisms that cause meningitis in the neonatal period includegroup B strep, Listeria monocytogenes and E. coli, which usually result from late-onset sepsis. Despite antibiotics, there is still a high mortality for these infants, especially if born preterm. Among the survivors of bacterial meningitis, there is a high incidence of neurological abnormalities. The most common viruses causing neonatal meningitis are rubella, CMV, herpes, coxsackie and echo virus, typically from intra-uterine transplacental infection.
microcephaly- “small head” or one that is more than three standard deviations below the mean size due to any process that causes brain growth to stop in the perinatal period. Etiologies include chromosomal, genetic, infectious (congenital rubella, CMV, herpes simplex, toxoplasmosis and syphilis), toxic (maternal radiation or alcohol), or vascular (intrauterine or neonatal hypoxia/ischemia). One treatable cause of this disorder is premature closure of the skull sutures associated with hyperthyroidism. Microcephalic children are usually free of other anomalies but do have impaired intellectual development.
miscarriage-this is the lay public’s term for a spontaneous event that ends a pregnancy. This event is called “abortion” in medical terminology and is defined as the unplanned, spontaneous loss of a pregnancy before the fetus can survive outside the mother or if the fetus is less than 500g or 20 weeks gestation. There are several types of abortion: threatened, inevitable, incomplete, complete, missed, recurrent. Threatened abortion is a pregnancy that is complicated by vaginal bleeding before 20 weeks gestation with a closed cervix. Approximately 25% of pregnancies are threatened abortions, and 50% of these go on to completely abort. An inevitable abortion is a pregnancy complicated by vaginal bleeding, cramping and dilation. The pregnancy is eventually lost. An incomplete abortion consists of vaginal bleeding, dilation and passage of some products of conception. A complete abortion is defined by passage of all products of conception, decreased uterine contractions, closed cervix and a negative pregnancy test. A missed abortion occurs when a fetus has died but is retained in the uterus for some weeks. Recurrent abortion is defined as three successive abortions, although most clinicians consider two successive first trimester or one second trimester loss reason for investigation. blighted ovum- an abortion where there is no visible fetus in the sac.
molar pregnancy- “gestational trophoblastic neoplasia” (GTN) is a condition that comes in several forms varying in levels of severity. Benign hydatidiform mole (subdivided into complete and partial according to genetic makeup), invasive mole and malignant choriocarcinoma. Cause of molar pregnancy is unknown and the pathophysiology is defective fertilization. Interestingly, incidence in the Far East is much greater than in the United States. Risk of a second molar pregnancy is approximately 40 times greater after the first. Symptoms of a molar pregnancy include a uterus large for dates, irregular/heavy bleeding, hyperthyroid-type symptoms, occasional hyperemesis gravidarum or preeclampsia. Diagnosis is by high levels of b-hCG, confirmed by an ultrasound that shows a “snow storm” appearance. In benign hydatitiform moles, the complete mole is comprised of an empty egg (no maternal genetic material) that was fertilized, so only contains paternal chromosomes, whereas the partial moles consist of an egg with genetic material fertilized by two sperm. A partial mole is associated with a developing fetus, symptoms are usually less severe and there is a lower malignant potential. Invasive moles demonstrate persistent b-hCG despite molar evacuation. They rarely metastasize, so hysterectomy is usually curative. Half of malignant choriocarcinomas follows a molar pregnancy,and the other half proceed a spontaneous or induced abortion or an ectopic pregnancy. Symptoms mimic many other diseases and malignancies, so unless it follows a molar pregnancy, it is usually not suspected. Malignant choriocarcinoma metastasizes and is treated with chemotherapy (radiation therapy if mets to the brain or liver). This disease is divided into good and bad prognostic features (such as mets to the brain or liver, very high b-hCG titres, occurrence after a full-term delivery) predicting chance of survival. Cure is possible in most instances of cases with good prognostic features.
monoamniotic twins- twins that share an amniotic cavity without membranes to separate them. They may also share a chorion (“monochorionic”) with the possibility of having two umbilical cords or sharing one cord that is forked. The monoamniotic condition represents the process where there was very late cleavage (splitting) of the fertilized. In fact, the later the cleavage, more parts will be shared by the embryos including body parts termed which would produce “conjoined twins”. This type of pregnancy has the risks of any multiple pregnancy including intrauterine growth retardation, preterm birth, congenital anomalies and velementous insertion of the cord, but it carries the additional risk of cord entanglement since there are no separating membranes between the fetuses.
multicystic (polycystic) kidneys- this is an inherited disease which affects both kidneys and comes in two forms: autosomal recessive (requires inheritance of two genes for expression) referred to as “infantile,” and autosomal dominant (requiring only one gene for expression) referred to as “adult” polycystic kidney disease. The infantile form is characterized by enlargement of the kidneys from the many cysts throughout. This can be diagnosed in utero by ultrasound. Due to oligohydramnios (too little amniotic fluid) from poorly functioning fetal kidneys, pulmonary hypoplasia occurs as the lungs need this fluid to properly develop, and this is the cause of much of the morbidity and mortality. Hepatic (liver) fibrosis also occurs with this form of the disease and also contributes to the high degree of morbidity and mortality. The adult type typically occurs in the fourth or fifth decade of life, but can present in early childhood or even infancy. This form is associated with a strong family history, hepatic, splenic and pancreatic cysts, as well as with cerebral aneurysms.
multiple gestation- defined as any pregnancy where there is more than one embryo or fetus. This is considered a complication of pregnancy because it carries with it a much higher morbidity and mortality for the fetuses as well as for the mother. The etiologies of this phenomenon is through the splitting of an already fertilized egg or through the fertilization of more than one egg, the first being term monozygotic or identical and the second called dizygotic or fraternal. Dizygotic fetuses have separate fetal membranes (chorion and amnion), but the placentas may be separate or fused. Monozygotic fetuses may be the result of cleavage of the egg at several stages during early embryogenesis, where the later the breaking occurs, the more parts of the membranes, cord or even the fetuses (“conjoined”) are shared. Monozygosity also creates the risk of twin-twin transfusion, placental vascular anastomosis (connections between the arterial and venous circulation) and fetal or umbilical cord malformations. Both types of multiple gestations are associated with preterm labor and delivery and all of the morbidity and mortality associated with these processes. There is also maternal complications of multiple gestations such as anemia, hypertension, postpartum uterine atony, postpartum hemorrhage, and preeclampsia and eclampsia. The prevalence of multiple gestation varies according to race, heredity, maternal age, and the use of fertility agents where 10-30% of pregnancies are multiple depending on the type of therapy used. Diagnosis is confirmed through ultrasound, but signs and symptoms include excessive maternal weight gain and fetal movemen, and more than one fetal heart rate found during auscultation. Management includes measures that will prolong the gestation such as bedrest and tocolytic therapy to prevent preterm labor, close fetal monitoring by ultrasound, and steroids to increase fetal lung maturity if preterm labor ensues. The mode of delivery is dependent on the presentation of the fetuses.
necrotizing enterocolitis (nec)- a medical emergency that usually occurs in the premature infant who is receiving oral feedings. Symptoms usually begin in the first week of life and include abdominal tenderness and distention, rectal bleeding and a shock-like appearance as well as positive blood cultures in less than half of the patients. Diagnosis is by x-ray, and treatment includes antibiotics, nasogastric decompression, and parenteral (through the veins) nutrition. A grave consequence of NEC is intestinal perforation which requires surgical exploration.
neonatal sepsis- this is severe systemic illness of the newborn that can be acquired in utero or during delivery which presents as early or late onset, or alternatively can be acquired after birth in the nursery. Important organisms include group B strep, staph aureus and epidermidis and listeria. Early onset sepsis from in utero exposure usually occurs in premature infants which presents as grunting, tachypnea and cyanosis at birth. The disease manifests as respiratory failure, shock, meningitis, necrosis of the functional units of the kidneys, peripheral gangrene, hypoxia and hypotension. Risk factors includes vagial colonization with the causative organism (eg. group B strep), preterm or prolonged rupture of membranes, chorioamnionitis, male sex or black race and preterm birth. Treatment includes antibiotics, mechanical ventilation and medication to keep the blood pressure up. Late-onset neonatal sepsis occurs after the first week of life, usually in a healthy full-term infant. This variation presents as lethargy, poor feeding, hypotonia, apathy, seizures, bulging fontanelles, fever and bacteremia which may result in focal infection (such as urinary tract infection or osteomyelitis) from seeding through the blood. Treatment is the same as for early-onset. Acquired sepsis usually occurs in preterm infants who are exposed to pathogens, typically multi-drug-resistant organisms, in the neonatal intensive care unit, as these infants often have indwelling catheters, endotracheal tubes and central venous lines which are excellent conduits for infection. Sepsis in these infants can present in many way, including pneumonia, meningitis, cellulitis and diarrhea. Treatment is with antibiotics that are effective against resistant organisms.
neural tube defect- one of the most common human malformations that may include the cranium and/or the spinal cord. There is a wide range in severity from lethal (anencephaly) to aymptomatic (spina bifida occulta). It is diagnosed by measuring the amniotic fluid level of alpha-fetoprotein as well as a through a comprehensive ultrasound after 16 weeks gestation. Etiologies of this group of defects include teratogens, single gene mutations, or chromosomal abnormalities.
anencephaly- this is the most severe neural tube defect where the cranial vault is absent or severely underdeveloped and the brain is replaced by hemorrhagic tissue. Physical feature include a small thick and flat skull base.
holoprosencephaly- condition where there is a single undivided hemisphere rather than the normal two hemispheres. This is due to agenesis of the corpus callosum in the brain, and it is often accompanied by facial dymorphology including: cyclopia, hypoplastic eyes, agnathia, otocephaly and facial clefts. Many fetuses with this condition also have a chromosomal disturbance, most often trisomy 13 or 18..
hydrocephaly- condition where there is an enlargement of the ventricles in the brain that house the cerebral spinal fluid (CSF). The etiology is through obstruction of CSF along its course, often as a result of congenital malformations of the brain, brainstem or bones of the skull. Increased intracranial pressure is a manifestation of this condition which eventually causes neurological problems such as ataxia, spasticity, atrophy of the optic nerve and endocrine dysfunction. Treatment is both medical and surgical which includes drugs that decrease the production of CSF and shunts that bypass the obstuctive site.
spinabifida- this is a subgroup of the neural tube defects that also has a wide range of severity. It is caused by failure of closure of the neural tube during development that leaves an exposed area of tissue. The most severe is myelomeningocele, which is a mass of tissue that contains herniated spinal cord and its covering (meninges). Lesser in severity is meningocele which is a herniated mass containing only meninges, followed by the least severe, and often asymptomatic spina bifida occulta which is a vertebral defect without an associated herniation.
Niemman Pick disease- this is a disease that falls under the category of lysosomal storage diseases caused by an enzyme deficiency (sphingomyelin). It is autosomal recessive requiring inheritance of two genes to manifest the disease. Presentation may occur as early as in utero as hydrops fetalis or late into adulthood. Manifestations of this disease include intellectual retardation, seizures, loss of muscle tone, enlargement of the liver and spleen, and jaundice. Diagnosis can be confirmed by enzyme analysis on blood leukocytes (white blood cells) or skin fibroblast, by investigation of bone marrow, as well as by chorionic villus sampling (CVS) in the first trimester of pregnancy.
omphalocoele- herniation of abdominal contents into the umbilical cord caused by a midline ventral defect. This condition is associated with other major malformations (cardiac, gastrointestinal, genitourinary, musculoskeletal, central nervous system), as well as chromosomal disruptions. The associated condition determines the prognosis, but there is approximately 90% survival if the omphalocele is isolated. Incidence is probably underestimated because of unaccounted fetal demise, but it occurs in about one in four to five thousand live births. Fetuses with large omphaloceles may benefit from cesarian sections to avoid injury to the herniated sac. Diagnosis is initiated by detection of increased levels of maternal serum a-fetoprotein and is confirmed by ultrasound. Shortly after delivery, there is a gradual surgical reduction of the visceral contents back into the abdominal cavity with a silastic silo to cover the external gut in the interim. Complete reduction is not performed all at once to avoid excess intraabdominal pressure and respiratory distress. Parental nutrition is begun until the infant’s gastrointestinal tract becomes functional.
partial molar pregnancy- (please see “molar pregnancy”)
parvo virus- 5th’s disease- a DNA virus that can cause erythema infectiosum in children or hydrops fetalis in utero. There is only 1% estimated chance of fetal infection in infected mothers, and there is no evidence of teratogenesis. Infected pregnant women may present with a rash that should prompt
placental abruption (abruptio placentae)- a separation of a normally implanted placenta creating a hematoma (tumor of blood) that causes further separation. Ultimately, there is destruction of placental tissue in the involved area, thus decreasing the amount of tissue involved in respiratory gas exchange. Causes of abruption include trauma, maternal hypertension, cigarette smoking, increased parity (number of previous pregnancies), and cocaine abuse. Symptoms include abdominal pain, uterine contractions and tenderness and vaginal bleeding which is not proportional to the severity of the condition. Diagnosis is made by ultrasound. The pregnant woman should be hospitalized with vital signs taken often, and an external fetal monitor should be placed. Complications include shock, damage to distant organs and loss of the fetus.
pneumothorax- a situation when there is an accumulation of air in the pleural space which may result from leakage of air from the lungs or airway, or more commonly from external trauma. Depending on the size, pneumothorax causes problems such as repiratory distress which may present as cyanosis with physical exam signs of unilater absent breath sounds, tracheal deviation, distended neck veins, and tympany to percussion of the involved side. Mechanical ventilation, asthma, cystic fibrosis, as well as other disorders such as Marfan’s syndrome predispose to this condition. Diagnosis is confirmed by x-ray, and treatment may require a chest tube if the air collection is large, needle aspiration or no treatment. Infants born with repiratory distress as a result of prematurity who need mechanical ventilation are at risk for pneumothorax as well as bronchopulmonary dysplasia from the high concentrations of external oxygen.
posterior urethral valve obstruction- though uncommon, the most common cause of bladder outlet obstuction in male infants. This condition causes dilation of the urethra and kidneys and hypertrophy of the bladder walls. If the condition is severe in utero, oligohydramnios (too little amniotic fluid) is present which causes pulmonary hypoplasia. If less severe, it may present in the male infant as a urinary tract infection, weak urinary stream and failure to thrive. Diagnosis is through ultrasound, and treatment includes decompression and valve ablation. Prognosis is good, but it depends upon whether the obstruction of the valve was severe in utero and subsequent degree of pulmonary insufficiency.
preterm labor and delivery- defined as occuring after 20 weeks and before 37 weeks gestation with a changing cervix, preterm labor and delivery are associated with increased perinatal morbidity and mortality. Fifty percent of preterm labor and delivery are unexplained, but the other half are associated with previous preterm labor and delivery, first trimester bleeding, urinary tract infections, multiple gestations, uterine anomalies, polyhydramnios, incompetent cervix and medical reasons for induction such as preeclampsia, uncontrolled third trimester bleeding with placenta previa or abruptio placenta . Low socioeconomic background of the mother seems to be an associated risk factor. Prevention includes identification of high-risk patients and early recognition of preterm contractions so that preterm labor can be stopped. Depending on the etiology, treatment of preterm labor includes placement in the left lateral decubitus position, close monitoring of both the mother and fetus through ultrasound, intravenous hydration, cervical cultures, blood work, urinalysis and tocolytic therapy to stop contractions if appropriate. Tocolytics include ritodrine, terbutaline, magnesium sulfate, protaglandin synthesis inhibitors and calcium channel blockers. Tocolysis delays delivery usually for more than 72 hours, enough time to administer glucocorticoid or thyroid releasing hormone that will enhance pulmonary maturity of the fetus and decrease the incidenc of neonatal respiratory distress syndrome. Preterm delivery needs careful assessment as the fetus often demonstrates malpresentation and is at greater risk for cord prolapse or compression. Because the head of a very preterm infant is proportionally much bigger than its body, breech delivery imposes the risk of head entrapment. Depending on the gestational age at birth, the infant is at increased risk of becoming septic, feeding problems, necrotizing enterocolitis, neonatal hypoglycemia, retinopathy, repiratory distress syndrome, intraventricular hemmorage, seizures, sepsis, cerebral palsy and mental retardation or learning disabilities.
renal agenesis- failure of development of one or both of the kidneys. Bilateral renal agenesis causes oligohydramnios (lack of amniotic fluid which is made mostly of fetal urine). With lack of fluid, there is fetal compression by the uterus which causes flat facies, clubfoot and pulmonary hypoplasia as lung development is dependent on amniotic fluid. This congregation of features is called Potter syndrome, and these infants usually die of pulmonary insufficiency in the first week of life. Unilateral renal agenesis is often associated with reproductive tract abnormalities, for example uterine anomalies such as uterus didelphys, due to the close interaction of these two systems during early fetal development. The existing kidney does a very good job at compensating with none or a minimal decrease in renal function, so there is a normal life expectancy if the anomaly is not associated with other syndromes such as VATER or Turners.
salpingitis isthmica nodosa- also called “tubal diverticulum”, this condition is not caused by infection, but rather by the direct invasion of the muscular layer of the tube into the epithelial layer. This creates a higher chance for tubal (ectopic) pregnancy from disruption of transport of the fertilized ovum, rather than from mechanical obstruction.
severe toxemia of pregnancy/ preeclampsia/ pregnancy-induced hypertension (PIH)- a condition that usually occurs in the third trimester, but as late as 6 weeks postpartum, characterized by pathologic edema (fluid in the tissues of the hands and face vs. legs and feet), hypertension and proteinuria. It most often affects younger patients in their first pregnancies and demonstrates a spectrum of severity judged by parameters of the hypertension and proteinuria. There are many proposed etiologies but none that is universally accepted. In addition to the above signs, there may be visual disturbances, hyperreflexia and low platelets. Management includes hospitalizaton, bedrest in the left lateral position to increase uterine blood flow, salt restriction, induction of labor if greater than 36 weeks gestation, antihypertensive medications (hydralazine) if the blood pressure is above 160/100 and anticonvulsant therapy (magnesium sulfate) administration during labor and delivery to prevent seizures. Caution must be exercised not to lower the blood pressure too quickly to avoid decreased uteroplacental blood flow. There are no long-term maternal sequellae as long as there has been no cerebrovascular accident, a risk with any severe hypertensive episode. Sequellae to the infant are greater, especially if born pretem, as there is associated intrauterine growth retardation, fetal distress and possible long-term central nervous system effects.
short rib polydactyl syndrome (SRPS)- an autosomally recessive syndrome (requiring inheritance of two genes in order to manifest the disease) that comes in several forms, all of which demonstrate an infant having short ribs and polydactyly (extra digits on the hands or feet). This sydrome is typically incompatible with life as there are also many viseral (internal organ) anomalies that accompany the syndrome. Diagnosis is by ultrasound which often reveals a hydropic infant.
shoulder dystocia- dystocia means difficult childbirth but is used to indicate dysfunctional labor or one that does not progress normally. It may be caused by disproportionate size of the fetus to the pelvis as is the case in shoulder dystocia when the fetus’ head comes out during delivery, but progression of the delivery unexpectedly stops. Several maneuvers (McRoberts) must quickly be initiated to allow the anterior shoulder to pass from under the pubic symphysis which is what is keeping the infant from being fully delivery. Another maneuvre is added if the preceding one does not work, beginning with downward pressure on the suprapubic region, followed by flexion of the maternal thighs against the abdomen, episiotomy, pressure on the infant’s scapula to turn the shoulder, insertion of the hand into the vagina to pull the posterior arm across the chest, and lastly fracture of one or both of the infant’s clavicles. There is definite potential for brachial plexus damage in the infant during these maneuvers, but the general health of the baby is in grave danger if they are not performed.
Staphlococcal("Staph") infection- this organism is part of the normal human flora including the nares (nostrils) of many asymptomatic people and may be transmitted through nasal discharge, hands and general contact. Newborns are very susceptible to this organism, althoguh it is common in children and adults as well. It can affect almost every system including the skin as scalded skin syndrome or impetigo, the lungs as pneumonia, the muscles as abcesses, in the bones and joints as osteomyelitis and arthritis, the central nervous system as meningitis and abcesses, the heart as endocarditis, abcesses and pericarditis, the kidneys as abcesses, the intestinal tract in the form of food poisening, as well as systemically as sepsis. Treatment includes antibiotics as well as incision and drainage of loculated collections of infected fluid. Staph toxin is also the cause for toxic shock syndrome which most often occurs in women using tampons and is characterized by abrupt onset, high fever, headache, vomiting, diarrhea, myalgias (muscle aches), hypotension, rash and shock. Mortality is about 3%..
subchorionic hemorrhage- hemorrhage that occurs between the chorion (outermost fetal membrane) and the decidual layer of the endometrium that carries with it an increased risk of spontaneous abortion, intrapartum fetal demise, stillbirth, abruptio placenta and preterm labor, especially with larger bleeds. The etiology of this type of hemorrhage is unknown.
sudden infant death syndrome (SIDS)- the unexpected death of an infant less than one year of age that cannot be explained. In the United States, it is the most common cause of death in the first year of life carrying an incidence of approximately one to two per 1000 live births. Risk factors include being of African American or Native American descent, having a young, single impoverished mother, or a mother who abuses drugs, being premature, having a sibling who died of SIDS and winter months. The pathology demonstrates hypoxia (lack of oxygen), and there are many proposed mechanisms including abberations in respiratory control and cardiac arrythmias, but not one theory is widely accepted.
Tay Sach’s disease- an autosomal recessive disease (requiring inheritance from both parents) where there is a deficiency of an enzyme leading to the destruction of neurons. There is an approximately three percent carrier frequency in Ashkenazi Jews causing an incidence of about one in 3600 of their births. The disease is fatal in early childhood and is characterized by neurological degeneration including severe mental retardation and physical deterioration, including blindness that begin at about six months of age.
twin-to-twin transfusion syndrome- a phenomenon that occurs as the result of an arterial-venous connection in the placenta, typically of monochorionic pregnancies, which leads to donation of blood from one twin that empties into the recipient twin. Due to this chronic shunting of blood, the donor twin demonstrates growth retardation, microcardia, hypovolemia, hypotension and anemia, whereas the recipient twin may develop edema (fluid collection in tissues), cardiomegaly, hypervolemia, hypertension, and congestive heart failure. A key on ultrasound is oligohydramnios (too little amniotic fluid) in the donor twin’s amniotic cavity and polyhydramnios (excess amniotic fluid) in that of the recipient. This condition carries a significant morbidity and mortality, especially of the recipient twin. Treatment includes....
uterine anomalies- anatomical disturbances, either congenital or acquired, that are associated with pregnancy loss as well as with cervical incompetence. Uterine fibroids are acquired abnormalities which tend to occur in women in their late thirties as well as more often in black women. Surgical removal will increase the likelihood of carrying a pregnancy to term. Congenital anomalies usually occur as a consequence of malfusion during development and result in varying degrees of septation. The etiology is unknown but it is believed to be from teratogens (eg. DES exposure) in utero and/or genetic inheritance. Evaluation of these anomalies requires laparoscopy and hysteroscopy.
vanishing twin syndrome- death of one twin who was identified earlier in the pregnancy by ultrasound but is not found later in the pregnancy. There is an increase incidence of cerebral palsy in the surviving twin.
VATERS syndrome- an acronym that describes the association of Vertebral defects, Anal atresis, Trach-Esophageal fistula, and Radial limb dysplasia. The etiology of this syndrome is unknown, and it falls under the category of sporadic syndrome complexes. Polyhydramnios secondary to tracheoesophageal fistula should cause intrapartum suspicion of this syndrome. After birth, coughing, choking and cyanosis will occur due to the fistula, so surgical repair is necessary. Congenital heart disease, usually ventricular septal defects, often accompanies this syndrome as does unilateral renal agenesis .
viral infection-
CMV- this is a DNA virus that can be transmitted through blood transfusion, organ transplant, sexual contact, transplacentally, during delivery, as well as through breast feeding, saliva and urine. Over one half of pregnant women demonstrate seropositivity for CMV indicating that they have previously been infected and that the virus could be in latency. Subclinical infection is the usual course, however, a mono-like illness may ensue. During pregnancy, a fetus may become infected even when the mother is asymptomatic, with ten to twenty percent of the neonates exhibiting a congenital syndrome including non-immune hydrops, intrauterine growth retardation, chorioretinitis, microcephaly, cerebral calcifications, hydrocephaly and enlargement of the liver and spleen. The severity of this syndrome is not dependent on when in the pregancy a woman incurred the infection, and there is a much lower fetal risk when the infection in the mother is a recurrent one. Many infants are asymptomatic at birth, but eventually develop mental retardation, psychomotor delay and progressive hearing loss. There is no treatment for this virus, but ultrasound and amniotic fluid culture can help to diagnose fetal infection.
listeria- a bacteria which is obtained from unpasteurized milk and is found in chickens, pigs and even in the fecal flora of humans that may cause listeriosis. This is a very rare illness that is usually mild and self-limiting during pregnancy, however, it may cause preterm labor or chorioamnionitis. Transplacental infection can occur which may result in spontaneous abortion, intrauterine fetal demise, and sepsis, meningitis, conjunctivitis and respiratory infection in the newborn, as well as neonatal death. An infected placenta demonstrates characteristic small areas of necrosis and abscesses. Ampicillin and gentamicin can be administered during pregnancy.
volvulus- this is an event that occurs when the small intestine is not fixed in the abdomen leading to twisting of the bowel which causes disruption to the blood supply, ischemia and infarction. Abdominal apin, vominting, diarrhea and bloody stools are symptoms of this condition, and bowel perforation with peritonitis is a grave complication. A midgut volvulus is a surgical emergency.
ACOG Technical Bulletin: "Substance Abuse." No 194, July 1994.
Arnold, Joan Hagan and Gemma, Penelope Buschman, A Child Die: A Portrait of Family Grief, Second Edition. Philadelphia: The Charles Press, 1994.
Bell, GL and Lau, K., Perinatal and Neonatal Issues of Substance Abuse. Pediatric Clinics of North America 42 (2): 261-281, 1995.
Benson, Judi and Falk, Agneta, The Long Pale Corridor: Contemporary Poems of Bereavement. Newcastle upon Tyne: Bloodaxe Books, Ltd., 1996.
Bluenfeld-Kosinski, Renate, Not of Woman Born: Representations of Caesarean Birth in Medieval and Renaissance Culture. Ithica: Cornell University Press, 1990.
Blum, Jeffrey, Ph.D., Living with Spirit in a Material World.New York: Ballantine Books, 1981.
Cacciatore, Joanne, Dear Cheyenne: A Journey into grief. Peoria: Mothers in Sympathy and Support , 1996.
Faldet, Rachel and Fitton, Karen, Our Stories of Miscarriage: Healing with Words. Minneapolis: Fairview Press, 1997.
Fertig, Mona, A Labor of Love: An Anothology of Poetry on Pregnancy and Childbirth. Winlaw: Polestar Press, Ltd., 1989.
Hawkes, Jacquetta and Woolley, Sir Leonard, History of Mankind, Prehistory and the beginnings of civilization. vol. 1, New York: Harper and Row, 1963.
Hacker, NF and Moore, JG, Essentials of Obstetrics and Gynecology. 2nd Ed. Philadelphia: W.B. Saunders, 1992.
Hickerson, Nancy Parrott, Linguistic Anthropology. Orlando:Harcourt Brace Jovanovich College Publishers, 1980.
Kluge, Eike-Henner W, The Practice of Death. New Haven: The Yale University Press, 1975.
Kohn, Ingrid, M.S.W. and Moffitt, Perry-Lynn, A Silent Sorrow: Pregnancy Loss.New York: Delacorte Press, 1992.
Lafser, Christine O'Keeffe, An Empty Cradle, A Full Heart: Reflections for mothers and fathers after miscarriage, stillbirth, or infant death. Chicago: Loyola Press, 1998.
Lammert, Cathi and Friedeck, Sue, Angelic Presence: Short stories of solace and hope after the loss of a baby. Salt Lake City: Richard Paul Evans, Publishing,1997.
Little BB and Van Beveren TT: Placental Transfer of Selected Substances of Abuse. Seminars in Perinatology 20(2): 147-53, 1996.
Lothrop, Hannah, Help, Comfort and Hope after Losing Your Baby in Pregnancy or the First Year, Tuscon: Fisher Books, 1997.
Mueller, Lisel, Alive Togethe: New and Selected Poems. Baton Rouge: Louisanna State University Press, 1986.
Murray, Thomas H., The Worth of a Child. Berkeley: The University of California Press, 1996.
Otten, Charlotte, The Virago Book of Birth Poetry. London: Virago Press Ltd., 1993.
Wheeler, SF: Substance Abuse During Pregnancy. Primary Care 20 (1): 191-207, 1993.
Rich, Laurie A., When Pregnancy Isn't Perfect. New York: Penguin Group,1993.
Tiger, Lionel, Optimism: The Biology of Hope. New York: Simon and Shuster, 1979.
Aristotle, Poetics. Translated into English by Gerald F. Else. Ann Arbor: The University of Michigan Press, 1970.
Kristen Aversa, Medical Student, Yale University School of Medicine
Karen Aresco, parent and caregiver
Brenda Beard, R.N., Nurse, Labor and Delivery Suite, Yale New Haven Hospital, Co-Director Maternity Bereavementt Services, Yale New Haven Hospital
Julia Bishop-Hahlo, R.N., Newborn Special Care Unit Yale-New Haven Hospital
Frank H. Boehm, M.D., Professor and Director of Maternal/Fetal Medicine, Vanderbilt University Medical Center
Leslie Carligio, MS, Certified Genetic Counselor, Yale Perinatal Unit, Yale- New Haven Hospital
Jennifer Caufman, parent
Adina Chelouche, Instructor, Department of Obstetrics and Gyjecology, Yale University School of Medicine
Joshua Copel, M.D., Professor of Obstetrics and Gynecology, Yale University School of Medicine, Director of Obstetrics, Yale New Haven Hospital
Anuja Dokrus, M.D., Ph.D., Fellow in Reproductive Endocrinology, Department of Obstetrics and Gynecology, Yale University School of Medicine
Neal Elgersma Jr., parent
Steven Fleischman, Resident in Obstetrics and Gynecology, Yale Universuty School of Medicine, Yale New Haven Hospital
Laurel Jonason R.N., BSN , Nurse, Newborn Special Care Unit, Co-Director, Perinatal Bereavement Services, Yale New Haven Hospital
David Jones, M.D, Associate Professor, Department of Obstetrics and Gynecology, Section of Maternal and Fetal Medicine, Yale University School of Medicine
Ande L. Karimu, M.D., Resident, Department of Obstetrics and Gynecology, Yale-New Haven Hospital
Harvey Kliman, M.D.,Ph.D., Placental Pathologist, Department of Obstetrics and Gyneoclogy, Yale University School of Medicine
David Lima, M.D., Instructor, Department of Obstetrics and Gynecology, Yale University School of Medicine
Sarah Marder, M.D., Assistant Professor of Obstetrics and Gynecology, University of Pennsylvania School of Medicine
Linda McDonald, parent
Sheryl McMahon, parent
Giancarlo Mari, Asssitent Professor of Obstetrics and Gynecology, Yale University School of Medicine
Carmen and Justin Murphy, parents
Kunle Odunsi, M.D., Ph.D., Chief Resident , Department of obstetrics and Gynecology, Yale New Haven Hospital
Rotimi Odutayo, M.D. Department of Obstetrics and Gynecology , Queen's University, Kingston, Ontario, Canada ,
Tanja Pejovic, M.D., Ph.D, Resident, Department of Obstetrics and Gynecology, Yale-New Haven Hospital
Brian and Sue Roquemore, parents
Paolo Rinaudo, M.D, Resident, Department of Obstetrics and Gynecology, Yale New Haven Hospital
Rene Rylander, Parent
Debra Kasowitz-Sachs, Parent
Andrea Seigerman, MSW, LCSW, Senior Clinical Social Worker, Department of Social Services, yale New Haven Hospital
Lisabeth Marie Smith, caregiver
Jacob Tangir, M.D., Resident, Department of Obstetrics and Gynecology, Yale-New Haven Hospital
Leena Vaisanen, M.D., Ph.D., Faculty of Medicine, University of Oulu, Oulu, Finland
Louise Ward, R.N., Nurse, Labor and Delivery Suite, Yale New Haven Hospital, Co-Director Maternity Bereavement Services, Yale New Haven Hospital
Ashley Wivel, Medical Student, Yale University School of Medicine
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[1] M. Gordon, A Moral Choice, The Atlantic Monthly 265, Issue 4 (April), pp.78 in Walburga von Raffler-Engel, The Perception of the Unborn Across the Cultures of the World (Toronto: Hogrefe and Huber Publishers, 1994) 105.
[2] Czeslaw Milosz, The Witness of Poetry, (Cambridge: Harvard University Press, 1983) 25.
[3] G.S Rousseau, Medicine and The Muses
[4] W. F. Bynum and Roy Porter, Literature and Medicine During the 18th Century
[5] Irwin Edman, The World, The Arts and the Artist (New York: W.W.Norton and Company, Inc., 1928) 30.
[6] Mary Jane Moffat, In The Midst of Winter (New York: Vintage Books, Division of Random House,Inc.,1992)xxiv.
[7] Rita Dove, in John Fox, Poetic Medicine, The Healing Art of Poem-Making(New York: Jeremy P. Tarcher/Putnam, 1997) 4.
[8] Lisel Mueller commenting on Yehudi Amichai; Stephen Kuusisto, Deborah Tall and David Weiss, The Poet's Notebook (New York: W.W. Norton and Company, 1995) 215.
[9] Moffat , In The Midst of Winter, xxiv.
[10] “Poetry is rhythmical. Rhythm secures the heightening of physiological consciousness so as to shut out sensory perception of the environment. In the rhythm of dance, music or song we become self conscious instead of conscious. The rhythm of a heartbeat and breathing and physiological periodicity negates the physical rhythm of the environment." Christopher Caudwell in Melvin Rader, A Modern Book of Aesthetics, (New York: Holt Rinehart and Winston, Inc.,1965) 154.
[11] D.H. Lawrence, in Stewart L. Udall, The Quiet Crisis, 1963, 1.
[12] Randall White, Dark Caves, Bright Visions: Life in Ice Age Europ e(New York: The American Museum of Natural History, W. W. Norton and Company) 19.
[13] White, Dark Caves, Bright Visions, 14.
[14] White, Dark Caves, Bright Visions, 19.
[15] White, Dark Caves, Bright Visions, 19.
[16] Rader, A Modern Book of Esthetics, 155.
[17] Edman, The World, The Arts and the Artist, p.30.
[18] Edman, The World, The Arts and the Artist, p.30
[19] Emanule Feldman, Biblical and Post-Biblical Defilement and Mourning: Law as Theology,(New York: Yeshiva University Press, KTAV Publishing House, Inc.,1977) 3.
[20] Dr. Palmer Findley, The Story of Childbirth (New York: Doubleday and Co., 1934) 2.
[21] Personal Observation: American Museum of Natural History, New York.
[22] Ralph S. Solecki , Shanidar, The First Flower People (New York: Alfred A. Knopf, 1971 ) 247.
[23] Edward Burnett Tylor in Randall White, Dark Caves, Bright Visions: Life in Ice Age Europe, 14.
[24] Marija Gimbutas, The Language of The Goddess (San Francisco: HarperCollins Publishers, 1991) 316.
[25] Gimbutas, The Language of The Goddess, 316.
[26] Gimbutas, The Language of The Goddess, xvii.
[27] Gimbutas, The Language of The Goddess, 213.
[28] Leroi-Gourhan in White, Dark Caves, Bright Visions, 157.
[29] Douglas J. Davies , Death, Ritual and Belief, The Rhetoric of Funerary Rites (London: Cassell, 1997) 133.
[30] Bernardo T. Arriaza, Beyond Death, The Chinchorro Mummies of Ancient Chile, (Washington: Smithsonian Institution Press, 1995) 139.
[31] Douglas J. Davies , Death, Ritual and Belief, The Rhetoric of Funerary Rites, 132-133.
[32] Richard Deurer, (January,1997) Egypt and Art [WWW page] http://m2.aol.com/egyptart/hathor.html)
[33] The Papyrus of Ani, (1240 bc) Translated by E.A. Wallis Budge (New York: Dover Publications, 1967)
[34] Findley, The Story of Childbirth, 155.
[35] Findley, The Story of Childbirth, 274.
[36] Darrel W. Amundsen, Medicine, Society and Faith in the Ancient and Medieval Worlds (Baltimore: The Johns Hopkins University Press ) 52.
[37] Darrel W. Amundsen, Medicine, Society and Faith In The Ancient and Medieval Worlds, 52.
[38] John M. Rist, Human Value: A Study in Ancient Philosophical Ethics cited in Amundsen, Medicine, Society, and Faith In The Ancient and Medieval Worlds, 52.
[39] Heliodorus, An Ethiopian Romance, 61.
[40] Findley, The Story of Childbirth, 274.
[41] Findley, The Story of Childbirth, 165.
[42] Christopher Daniell, Death and Burial in Medieval England, 1066-1550, (London: Routledge 1997) 124-125.
[43] Daniell, Death and Burial in Medieval England, 125-126.
[44] Daniell, Death and Burial in Medieval England, 127.
[45] Rabbi Debra Orenstein, Life Cycles, Jewish Women on Life Passages and Personal Milestones, Volume 1 (Woodstock: Jewish Lights Publishing, 1994) 37.
[46] Colin Murray Parkes, Pittu Laungani and Bill Young, Death and Bereavement Across Cultures (London: Routledge, 1997) 194.
[47] Parkes, Death and Bereavement Across Cultures, p.194.
[48] Elie Wiesel, The Nobel Lecture: Hope, Despair and Memory, in the Nobel Peace Prize 1986 (New York: Summit Books and Boston Universiry, 1986)21.
[49] Thomas A. Dooley, M.D., The Night They Burned The Mountain (New York: Signet Books, 1960) 32.
[50] Lisel Meuller, in Stephen Kuusisto, Deborah Tall, and David Weiss The Poets Notebook, Excerpts form the Notebooks of Contemporary American Poets (New York: W.W. Norton and Company, 1995) 215
[51] Douglas J. Davies , Death, Ritual and Belief, The Rhetoric of Funerary Rites, 1.
[52] Irwin Edman, The World, The Arts and the Artist, 30.
[53] Irwin Edman, The World, The Arts and the Artist,.51.
[54] Lisel Meuller, in Stephen Kuusisto, Deborah Tall, and David Weiss The Poets Notebook, Excerpts form the Notebooks of Contemporary American Poets, 215.
[55] Lisel Mueller, personal communication.
[56] Francis Ridley Havergal in Michele Durkson Clise, Memento, Solace for Grieving, (Boston: Little Brown and Company, 1995) 5.
[57] Michael R. Berman, M.D., Hygeia, An Online Journal for Pregnancy and Neonatal Loss, [www page]. 1998. Available from http://www.hygeia.org.
[58] SHARE, Source of Help in Airing and Resolving Experiences, a paradigm for perinatal support groups, was funded in 1977.
[59] Lucian Pye, Communications and Political Development (Princeton: Princeton
University Press, 1963) 4.
[60] Mark Poster, The Mode of Information (Chicago: The University of Chicago Press, 1990) 116.
[61] Michael R. Berman, M.D., Hygeia, An Online Journal for Pregnancy and Neonatal Loss, [www page]. 1998. Available from http://www.hygeia.org.
[62] Editors Note: This abstract is excerpted by permission of the author from her academic dissertation. I learned of her work when she contacted me through HygeiaÒ and cite it here for it sensitively embodies the truths and emotions of perinatal and childhood loss. Leena Vaisanen , Abstract of Family Grief and Recovery Process when a Baby Dies(Oulu: Oulu Univeristy Press, 1996)
[63] Excerpted, with permission of the author, from The Tennesseean, Nashville, Tennessee, November 27, 1992.
[64] I have included two papers on the placenta because of its importance in fetal well-being and disease.
[65] Editors Note:This information presents an extremely comprehensive summary
of the pervasive complication of pregnancy, premature rupture of the fetal
membranes or PROM. Although it is written with many medical terms,
all readers will derive a benefit from its presentation here in this manner
[66] Toppozada M, Sallam N, Gaffar A, al. c. Role of repeated stretching in the
mechanism of timely rupture of the membranes. . American Journal of Obstetrics and Gynecology 1970; 108:243.
[67] Kanayama N, Terao T, Y. K. Collagen types in normal prematurely ruptured
amniotic membranes. . American Journal of Obstetrics and Gynecology 1985; 153:899.
[68] Vadillo-Ortega F, Gonzalez-Avilla G, Karclimen S, al. e. Collagen metabolism in premature rupture of amniotic membranes. Obstetrics and Gynecology 1990;75:84.
[69] Naeye R. Factors that predispose to premature rupture of membranes. Obstetrics and Gynecology,1982;60:93
[70] Harger JH, Hsing A, Tuomola R, al. e. Risk factors for preterm premature rupture of fetal membranes: A multicenter case-control study. . American Journal of Obstetrics and Gynecology 1990; 163:130
[71] Hadley C, Main D, Gabbe S. Risk factors for preterm premature rupture of fetal membranes. . American Journal of Perinatology 1990;7:374.
[72] Mead PB. Management of the patient with premature rupture of the membranes. Clinics in Perinatology 1980;7:243 - 255.
[73] Garite TJ, Freeman RK, Linzey EM, Braly PS, Dorchester WL. Prospective
randomized study of corticosteroids in the management of premature rupture of the membranes and the premature gestation. . American Journal of Obstetrics and Gynecology 1981; 141:508 - 5 15.
[74] Garite Til Freeman RK. Chorioanmionitis in the preterm gestation. Obstetrics and Gynecology 1982;54:539.
[75] Bibbs RS, Blanco JD, St. Clair PJ, al. e. Quantitative bacteriology of arymiotic fluid from patients with clinical intra-amniotic infection at term. Journal of Infectious Diseases 19 82; 145: 1.
[76] Gunn CC, Mishell DR, Morton DG. Premature rupture of the fetal membranes. . American Journal of Obstetrics and Gynecology 1970; 106:469
[77] Rutherford SE, Phelan JP, Smith CV, Jacobs N. The four quadrant assessment of anmiotic fluid volume: An adjunct to antepartum fetal heart rate testing. Obstetrics and Gynecology 1987;70:353.
[78] Gabbe SG, Ettinger BB, Freeman RK, al. e. Umbilical cord compression
associated with amniotomy: Laboratory observations. American Journal of Obstetrics and Gynecology 1976; t 26:3 53.
[79] . Moberg Li, Garite Ti. Antepartum fetal heart rate testing in preterm PROM.
Seventh annual meeting of the Society of Perinatal Obstetricians. Lake Buena, FL: 1987.
[80] Vintzileos AM, Campbell WA, Nochimson DJ, Weinbautn PJ. Degree of
oligohydramnios and pregnancy outcome in patients with premature rupture of the membranes. Obstetrics and Gynecology 1985;66:162.
[81] Itoh K, Itoh H. A study of cartilage development in pulmonary hypoplasia. Pediatric Pathology 1988; 8:65.
[82] Rotschild A, Ling EW, Puterman ML, al. e. Neonatal outcome after prolonged preterm rupture of the membranes. Am J Obstet Gynecol 1990; 162:46.
[83] Nimrod C, Varela-Gittings F, Machin G, al. e. The effect of very prolonged membrane rupture on fetal development. . American Journal of Obstetrics and Gynecology 1984; 148:540.
[84] Vergani P, Ghidini A, Locatelli A, al. e. Risk factors for pulmonary hypoplasia in second trimester PROM. American Journal of Obstetrics and Gynecology 1994; 170:1359.
[85] Nimrod C, Davies D, lwanick S, al. e. Ultrasound prediction of pulmonary
hypoplasia. Obstetrics and Gynecology 1986;68:495.
[86] Vintzileos AM, Campbell WA, Rodis JF, al. e. Comparison of six different
ultrasonographic methods for predicting lethal fetal pulmonary hypoplasia. American Journal of Obstetrics and Gynecology, 1989; 161:606.
[87] Keirse MJNC, Ohlsson A, Treffers PE, Kanhai HHH. Prelabour rupture of
membranes preterm. In: Chalmers 1, Enkin M, Keirse MJNC, ed. Effective care in pregnancy and childbirth. Oxford, UK: Oxford University Press, 1989: 666 - 693.
[88] Mercer BM, Arheart KL. Antimicrobial therapy in the expectant management of preterm premature rupture of membranes. Lancet 1995;346:1271.
[89] Crowley PA, Chalmers 1, C. KMJN, al. e. The effects of corticosteroid
administration before preterm delivery:" An overview of evidence from controlled trials. British Journal of Obstetrics and Gynaecology 1990;97:1 1.
[90] Crowley PA. Corticosteroids prior to preterm delivery. In: 1.3 ed. Oxford: Oxford database of perinatal trials, 1992.
[91] Bauer CR, Morrison C, et al. A decreased incidence of necrotizing
enterocolitis after prenatal glueocorticoid therapy. Pediatrics 1984;73 -682.
[92] Mead PB. Management of the patient with premature rupture of the membranes. Clinics in Perinatology 1980;7:243 - 255.
[93] Christensen KK, Ingemarsson 1, Leideman T, Solum H, Svenningsen N. Effect of ritodrine on labor after premature rupture of the membranes. Obstetrics and Gynecology 1980;55:155.
[94] Garite TJ, A. KK, Freeman RK, Nageotte MP. A randomized trial of ritodrine
tocolysis versus expectant management in patients with premature rupture of membranes at 25 to 30 weeks of gestation. American Journal of Obstetrics and Gynecology 1987; 157 - 3 8 8.
[95] Weiner CP, Renk K, Klugman M. The therapeutic efficacy and cost effectiveness of aggressive tocolysis for premature labor associated with premature rupture of the membranes. American Journal of Obstetrics and Gynecology 1988; 1 59:216.
[96] Levy DL, Warsof SL. Oral ritodrine and preterm premature rupture of membranes. Obstetrics and Gynecology 1985;66:621.
[97] Dunlop PDM, Crowley PA, Lamont RF, Hawkins DF. Preterm ruptured
membranes, no contractions. Journal of Obstetrics and Gynaecology 1986;7:92.
[98] . Hannah ME, Ohisson CM, Farine D, Hewson SA, al. e. Induction of labor
compared with expectant management for pretabor rupture of the membranes at term. New England Journal of Medicine 1996;334:1005.
[99] Garite Til Freeman RK. Chorioanmionitis in the preterm gestation. Obstetrics and Gynecol ogy 1982;54:539.
[100] Hughes EC (ed): Obstetric-Gynecologic Terminology. Philadelphia, FA Davis, 1972.
[101] Page EW, Christianson R (1976) The impact of mean arterial blood pressure in the middle trimester upon outcome of pregnancy. American Journal of Obstetrics and Gynecology 125:740.
[102] Talledo Oe, Chesley LC, Zuspan FP (1968) Renin-angiotesin system in normal and toxemic pregnancies. III. Differential sensitivity to angiotensin II and norepinephrine in toxemia of pregnancy. American Journal of Obstetrics and Gynecology 100:218.
[103] Gant NF, Daley GL, Chand S et al (1973): A study of angiotensin II Pressor response throughout primigravid pregnancy. Journal of Clinical Investigation 52:2682.
[104] Cunningham FG, Lindeheimer MD (1992): Hypertension in pregnancy. New England Journal of Medicine 326:927.
[105] Dadak C, Kefalides A, Sinzinger H, Weber G (1982): Reduced umbilical artery prostacyclin formation in complicated pregnancies. American Journal of Obstetrics and Gynecology 144:792.
[106] Moncada S, Palmer RMI, Higgs EA (1991): Nitic oxide: Physiology, pathophysiology, and pharmacology. Pharmacology Review 43:109.
[107] Chesley LC (1978): Hypertensive Disorders in Pregnancy. New York, Appleton-Century-Crofts.
[108] Redman CWG, Beilin LJ, Bonnar J (1976): Plasma urate measurement in predicting fetal death in hypertensive pregnancies. Lancet 1:1370.
[109] Pritchard JA, Cunningham FG, Mason RA (1976): Coagulation changes in eclampsia: their frequency and pathogenesis. American Journal of Obstetrics and Gynecology 124:855.
[110] Weinstein L (1982): Syndrome of hemolysis, elevated liver enzymes, and low platelet count: a severe consequence of hypertension in pregnancy. American Journal of Obstetrics and Gynecology 142:159.
[111] Sibai BM, Taslimi MM, El-Nazar A et al (1986) Maternal-perinatal outcome associated wuth the syndrome of hemolysis, elevated liver enzymes, and low platelets in severe preeclampsia-eclampsia American Journal of Obstetrics and Gynecology 155:501.
[112] Khong TY, De Wolf F, Robertson WB, Brosens I (1986): Inadequate maternal response to placentation in pregnancies complicated by pre-eclampsia and by small-gestational age infants. British Journal of Obstetrics and Gynecology 93:1049.
[113] Kitzmiller JL, Benirschke K (1973): Immunofluorescent study of placental bed vessels in pre-eclampsia. American Journal of Obstetrics and Gynecology 115:248.
[114] Pritchard JA, Stone SR (1967) Clinical and laboratory observations on eclampsia. American Journal of Obstetrics and Gynecology 99:754.
[115] Imperiale TF, Petrulis AS (1991): A meta-analysis of low-dose aspirin for the prevention of pregnancy-induced hypertensive disease. JAMA 266:261.
[116] Plouin PF, Chatqllier G, Breart G et al (1986) Frequency and perinatal consequences of hypertensive disease of pregnancy. Advances in Nephrology 57:69.
[117] Naeye RL, Friedman EA (1979): Causes of perinatal death associated with gestational hypertension and proteinuria. American Journal of Obstetrics and Gynecology 133:8.
[118] Tervila L, Goecke C, Timonen S (1973) Estimation of gestosis of pregnancy (ERH-gestosis). Acta Obstet Scand 52:235.
[119] Ballantyne, J.W., The problem of the postmature infant . Journal of Obstetrics and Gynaecology British Empire, 1902. 2(36): p. 521-544.
[120] Clifford, S.H., Postmaturity - with placenta dysfunction. Journal of Pediatrics, 1954. 44: p. 1.
[121] Hasseljo, R. and A.C. Auberg, Prolonged Pregnancy. Acta Obstetrics and Gynaecology of Scandinavia Supplementary, 1962. 61: p. 23-29.
[122] Lanman, J.T., Delays During Reproduction and their effects on the Embryo and Fetus. New England Journal of Medicine, 1968. 278: p.1092-1099.
[123] Bergsjo, P., ed. Postterm Pregnancy : Induction or Surveillance, 1985 in Progress in Obstetrics And Gynaecology, J.W. Studd. Vol.5. 1985, Churchill Livingstone: Edinburgh and London. 121-133.
[124] Crowley, P., Post Term Pregnancy : Induction or Surveillance, in Effective Care in Pregnancy and Childbirth, I. Chalmers , M. Enkins , and M.J.N. Kierse , Editors. 1989, Oxford University Press: Oxford. p.776-791.
[125] Crowley,776-791.
[126] Barss, V.A., F.D. Frigoletto, and F. Diamond, Stillbirth after nonstress testing. Obsterics and Gynecology, 1985. 65: p. 541.
[127] Boyd, M.E., R.H. Usher, and F.H. McLean, et al, Obstetric consequences of post-maturity American Journal of Obstetrics and Gynecology 1988. 158: p. 334.
[128] . WHO, Recommended definitions , terminology and format for statistical tables related to the perinatal period and use of a new certificate for cause of perinatal deaths . Acta Obstetrics and Gynecology Scandinavia, 1977. 56: p. 247-53.
[129] FIGO, FIGO news: List of gynecologic and obstetrical terms and definitions. International Journal of Gynecology and Obstetrics, 1976. 14: p. 570-6.
[130] Bakketeig, L. and P. Bergsjo, Postterm Pregnancy : Magnitude of the problem, in Effective care in Pregnancyand Childbirth, I. Chalmers, M. Enkin, and M. Kierse, Editors. 1989, Oxford University press: Oxford. p. 765-775.
[131] Crowley, 776-791.
[132]Saunders, N. and C. Paterson, Can We Abandon Naegele's rule, Lancet, 1991. 337: p. 600-1.
[133] Mittendorf, R., M.A. Williams, and C.S.e.a. Berkey, The length of uncomplicated human gestation. Obstetrics and Gynecology, 1990. 75: p. 929-32.
[134] Mere, H.B., Ultrasound Demonstration of an unusual fetal growth pattern in Indians. British Journal of Obstetrics and Gynaecology, 1981. 88: p. 260-3.
[135] Von Doring, G., Uber die Tragzeit post ovulation. geburtshilfe
Frauenheilkd, 1962. 22: p. 1191-4.
[136] Gardosi, J. and M. Mongelli, Risk Assessment Adjusted for Gestational Age In Maternal Serum Screening For Down's Syndrome. British Medical Journal, 1993. 306: p. 1509-11.
[137] Robinson, H.P. and J.E. Fleming, A Critical Evaluation Of Crown -Rump Length Measurement. British Journal Of Obstetrics And Gynaecology, 1975. 82: p. 702-10.
[138] Campbell, S. And G.B. Newman, Growth Of The Fetal Biparietal
Diameter During Normal Pregnancy. Journal Of Obstetrics And Gynaecology
Of The British Commonwealth, 1971. 78: p. 513-9.
[139] Hall, M.H., Definitions Used In Relation To Gestational Age. Paediatric Perinatal Epidemiology, 1990. 4: p. 123-8.
[140] Persson, P.H. And B.M. Weldner, Reliability Of Ultrasound Fetometry In Estimating Gestational Age In The Sevcond Trimester. Acta Obstetrics And Gynaecology Of Scandinavian 1986(65): p. 481-3.
[141] Mongelli, M. And B. Opatola, Duration And Variability Of Normal Pregnancy , Implication For Clinical Practice. Journal Of Reproductive Medicine 1995. 40(9): p. 645-8.
[142] Mongelli, M., M. Wilcox, And J. Gardosi, Estimating The Date Of Confinement : Ultrasonographic Biometry Versus Certain Menstrual Dates. American Journal Of Obstetrics And Gynecology 1996. 174(1): p. 278-81.
[143] WHO, Recommended definitions , terminology and format for statistical tables related to the perinatal period and use of a new certificate for cause of perinatal deaths . Acta Obstetrics and Gynecology Scandinavia 1977. 56: p. 247-53.
[144] Geirsson, R.T. and R.M.C. Busby-Earle, Certain dates may not provide a reliable estimate of gestational age . British Journal of Obstetrics and Gynecology 1991. 98: p. 108-9.
[145] Waldenstroem, U., O. Axelson, and S. Nilsson, A Comparison of the ability of a sonographically measured biparietal diameter and the last menstrual period to predict the spontaneous onset of labor. Obstetrics and Gynecology 1990. 76: p. 336-8.
[146] Geirsson, R.T. and R.M.C. Busby-Earle, Certain dates may not provide a reliable estimate of gestational age . British Journal of Obstetrics and Gynecology 1991. 98: p. 108-9.
[147] Mongelli, M., M. Wilcox, and J. Gardosi, Estimating the date of confinement : Ultrasonographic biometry versus certain menstrual dates. American Journal of Obstetrics and Gynecology 1996. 174(1): p. 278-81
[148] Hannah, M.E., Postterm pregnancy : Should all women have labor induced? A review of literature . Fetal Maternal Medicine Review 1993. 5: p. 3-17.
[149] Hannah, M.E., W.J. Hannah, and J. Hellman, et al., Induction of labor as compared with serial antenatal monitoring in postterm pregnancy . A randomized controlled trial . New England Journal of Medicine 1992. 326: p. 1587-92.
[150] Shime, J., et al., Prolonged pregnancy survellance of the fetus and the neonatal and the course of labor and delivery . American Journal of Obstetrics and Gynecology 1984. 148: p. 547-52.
[151] Sadovsky, E. and H. Yaffe, Daily fetal movement recording and fetal prognosis. Obstetrics and Gynecology 1973. 41: p. 845-50.
[152] Grant, A., et al., Routine fetal movement counting and risk of antepartum late death in normally formed singletons . Lancet 1989. ii: p. 346-49.
[153] Hannah, Postterm pregnancy : Should all women have labor induced? A review of literature, 3-17.
[154] Beischer, N.A., J.H. Evans, and L. Townsend, Studies in prolonged pregnancy. The incidence of prolonged pregnancy. American Journal of Obstetrics and Gynecology 1969. 103: p. 476-82.
[155] Moore, T.R. and J.E. Cayle, Amniotic fluid index in Normal human pregnancy American Journal of Obstetrics and Gynecology 1990. 162: p. 1168.
[156] Marks, A.D. and M.Y. Divon, Longitudinal study of the amniotic fluid index in postdates pregnancy . Obstetrics and Gynecology 1992. 79: p. 29-33.
[157] Trimmer, K.J., et al., Observations on the cause of oligohydramnios in prolonged pregnancy . American Journal of Obstetrics and Gynecology 1990. 163: p. 1900-3.
[158] Crowley, P., C. O'Herlihy, and P. Boylan, The value of ultrasound measurement of amniotic volume in the management of prolonged pregnancies. British Journal of Obstetrics and Gynecology 1984. 91: p. 444-8.
[159] Rutherford, S.E., et al., The four quadrant assessment of amniotic fluid volume: an adjunct to antepartum fetal heart rate testing. Obstetrics and Gynecology 1997. 70: p. 353.
[160] Martin, J.N., et al., Alternative approches to the management of gravidas with prolonged postterm pregnancies . Journal of Mississippi State Medical Association 1989. 30: p. 105-111.
[161] Mediaris, A.L. Postterm pregnancy: active induction (PGE2gel) not associated with improved outcomes compare to expectant management . A preliminary report . in Proceeding of 10th annual meeting of Society of Perinatal Obstetricians 1990. Houston, Texas, USA.
[162] Suikkari, A.M., et al., Prolonged pregnancy: induction or observation. Acta Obstetrics and Gynecology of Scandinavia 1983. 116(supplimentary): p. 58.
[163] Green, J.N. and R.H. Paul, The value of Amniocentesis in prolonged pregnancy . Obstetrics and Gynecology 1978. 51: p. 293-8.
[164] Katz, Z., et al., Nonaggressive management of postdate pregnancies. European Journal of Obstetrics , Gynecology and Reproductive Biology 1983. 15: p. 71-9.
[165] Knox, G.E., et al., Management of prolonged pregnancy: results of a prospective randomized trial . American Journal of Obstetrics and Gynecology 1979. 134: p. 376-81.
[166] Devoe, L.D. and J.S. Scholl, Post date pregnancy : Assessment of Fetal risk and obstetric management. Journal of Reproductive Medicine 1983.
[167] Small, J.L., J.P. Phelan, and S.V. Smith, et al, An active management approach to the postdate fetus with a reactive nonstress test in fetal heart rate decelerations . Obsterics and Gynecology 1967. 70: p. 636.
[168] Mohide, P. and M.J.N.C. Keirse, Biophysical assessment of fetal well-being . Effective care in pregnancy and childbirth, ed. I. Chalmers , M. Enkin, and M. Keirse. Vol. 1. 1989, Oxford , England:
Oxford University Press. 477-92.
[169] Fischer, R.L., et al., Doppler evaluation of umblical and uterine arcuate arteries in the the postdates pregnancies. Obstetrics and Gynecology 1991. 78: p. 363-8.
[170] Stokes, H.J., R.V. Roberts, and J.P. Newham, Doppler flow velocity waveform analysis in postdates pregnancies . Australian and New Zealand Journal of Obstetrics and Gynecology 1991. 81: p. 27-30.
[171] Keirse, M.J.N.C. and A.C.A. van Oppen, Preparing the cervix for induction of labour, in Effective care in pregnancy and childbirth, I. Chalmers , M. Enkin , and M. Keirse, Editors. 1989, Oxford University Press: Oxford. p. 988-1056.
[172] Vorherr, H., Placental insufficiency in relation to postterm pregnancy and fetal postmaturity . Evaluation of fetoplacental function : management of the postterm gravida . European Journal of Obstetrics ,Gynecology and Reproductive Biology 1974. 123: p. 67-100.
[173] Dyson, D.C., Fetal surveillace vs labor induction at 42 weeks in postterm gestation . Journal of Reproductive Medicine 1988. 33: p. 262-70.
[174] Freeman, R.K., et al., Utilization of contraction stress testing for primary fetal surveillance. American Journal of Obstetrics and Gynecology 1981. 140: p. 128-35.
[175] Cardozo, L.D., J. Fysh, and J.M. Pearse, Prolonged pregnancy: The management debate. British Medical Journal. 1986. 293: p. 1059-63.
[176] Bergsjo, P., et al., Comparison of induced versus non-induced labor in postterm pregnancy; A randomized prospective study. Acta Obstetrics and Gynecology of Scandinvia 1989. 68: p. 683-7.
[177] Goeree, R., M. Hannah, and S. Hewson, et al, Cost effectiveness of induction of labour versus serial antenatal monitoring in the Canadian multicenter postterm pregnancy trial. Canadian Medical Association Journal 1995. 152(9): p. 1445-50.
[178] Hannah, M.E., Management of postterm pregnancy. Journal of the Society of Obstetricians and Gynaecologists of Canada 1994. 4: p.1581-91.
[179] Cardozo, L.D., J. Fysh, and J.M. Pearse, Prolonged pregnancy: The management debate. British Medical Journal, 1986. 293: p. 1059-63.
[180] Roberts, L.J. and K.R. Young, The management of prolonged pregnancy - An analysis of women's attitudes before and after term. British Journal of Obstetrics and Gynaecology 1991. 98: p. 1102 06
[181] A personal eulogy at a memorial serivce for still born babies buried in a mass burial site.
[182] Octavia Paz in John Fox, Poetic Medicine, The Healing Art of Poem Making, (New York: Jeremy P. Tarcher/Putnam,1997) 48.
[183] Dooley, The Night They Burned The Mountain, 19.
[184] John Donne, Devotions upon Emergent Occasions, 1624.
[185] Elie Wiesel, A Song for Hope in Carol Rittner, R.S.M., Elie Wiesel, Between Memory and Hope, (New York: New York University Press, 1990) 208.