36 results
Contributors
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- By Rose Teteki Abbey, K. C. Abraham, David Tuesday Adamo, LeRoy H. Aden, Efrain Agosto, Victor Aguilan, Gillian T. W. Ahlgren, Charanjit Kaur AjitSingh, Dorothy B E A Akoto, Giuseppe Alberigo, Daniel E. Albrecht, Ruth Albrecht, Daniel O. Aleshire, Urs Altermatt, Anand Amaladass, Michael Amaladoss, James N. Amanze, Lesley G. Anderson, Thomas C. Anderson, Victor Anderson, Hope S. Antone, María Pilar Aquino, Paula Arai, Victorio Araya Guillén, S. Wesley Ariarajah, Ellen T. Armour, Brett Gregory Armstrong, Atsuhiro Asano, Naim Stifan Ateek, Mahmoud Ayoub, John Alembillah Azumah, Mercedes L. García Bachmann, Irena Backus, J. Wayne Baker, Mieke Bal, Lewis V. Baldwin, William Barbieri, António Barbosa da Silva, David Basinger, Bolaji Olukemi Bateye, Oswald Bayer, Daniel H. Bays, Rosalie Beck, Nancy Elizabeth Bedford, Guy-Thomas Bedouelle, Chorbishop Seely Beggiani, Wolfgang Behringer, Christopher M. Bellitto, Byard Bennett, Harold V. Bennett, Teresa Berger, Miguel A. Bernad, Henley Bernard, Alan E. Bernstein, Jon L. Berquist, Johannes Beutler, Ana María Bidegain, Matthew P. Binkewicz, Jennifer Bird, Joseph Blenkinsopp, Dmytro Bondarenko, Paulo Bonfatti, Riet en Pim Bons-Storm, Jessica A. Boon, Marcus J. Borg, Mark Bosco, Peter C. Bouteneff, François Bovon, William D. Bowman, Paul S. Boyer, David Brakke, Richard E. Brantley, Marcus Braybrooke, Ian Breward, Ênio José da Costa Brito, Jewel Spears Brooker, Johannes Brosseder, Nicholas Canfield Read Brown, Robert F. Brown, Pamela K. Brubaker, Walter Brueggemann, Bishop Colin O. Buchanan, Stanley M. Burgess, Amy Nelson Burnett, J. Patout Burns, David B. Burrell, David Buttrick, James P. Byrd, Lavinia Byrne, Gerado Caetano, Marcos Caldas, Alkiviadis Calivas, William J. Callahan, Salvatore Calomino, Euan K. Cameron, William S. Campbell, Marcelo Ayres Camurça, Daniel F. Caner, Paul E. Capetz, Carlos F. Cardoza-Orlandi, Patrick W. Carey, Barbara Carvill, Hal Cauthron, Subhadra Mitra Channa, Mark D. Chapman, James H. Charlesworth, Kenneth R. Chase, Chen Zemin, Luciano Chianeque, Philip Chia Phin Yin, Francisca H. Chimhanda, Daniel Chiquete, John T. Chirban, Soobin Choi, Robert Choquette, Mita Choudhury, Gerald Christianson, John Chryssavgis, Sejong Chun, Esther Chung-Kim, Charles M. A. Clark, Elizabeth A. Clark, Sathianathan Clarke, Fred Cloud, John B. Cobb, W. Owen Cole, John A Coleman, John J. Collins, Sylvia Collins-Mayo, Paul K. Conkin, Beth A. Conklin, Sean Connolly, Demetrios J. Constantelos, Michael A. Conway, Paula M. Cooey, Austin Cooper, Michael L. Cooper-White, Pamela Cooper-White, L. William Countryman, Sérgio Coutinho, Pamela Couture, Shannon Craigo-Snell, James L. Crenshaw, David Crowner, Humberto Horacio Cucchetti, Lawrence S. Cunningham, Elizabeth Mason Currier, Emmanuel Cutrone, Mary L. Daniel, David D. Daniels, Robert Darden, Rolf Darge, Isaiah Dau, Jeffry C. Davis, Jane Dawson, Valentin Dedji, John W. de Gruchy, Paul DeHart, Wendy J. Deichmann Edwards, Miguel A. De La Torre, George E. Demacopoulos, Thomas de Mayo, Leah DeVun, Beatriz de Vasconcellos Dias, Dennis C. Dickerson, John M. Dillon, Luis Miguel Donatello, Igor Dorfmann-Lazarev, Susanna Drake, Jonathan A. Draper, N. Dreher Martin, Otto Dreydoppel, Angelyn Dries, A. J. Droge, Francis X. D'Sa, Marilyn Dunn, Nicole Wilkinson Duran, Rifaat Ebied, Mark J. Edwards, William H. Edwards, Leonard H. Ehrlich, Nancy L. Eiesland, Martin Elbel, J. Harold Ellens, Stephen Ellingson, Marvin M. Ellison, Robert Ellsberg, Jean Bethke Elshtain, Eldon Jay Epp, Peter C. Erb, Tassilo Erhardt, Maria Erling, Noel Leo Erskine, Gillian R. Evans, Virginia Fabella, Michael A. Fahey, Edward Farley, Margaret A. Farley, Wendy Farley, Robert Fastiggi, Seena Fazel, Duncan S. Ferguson, Helwar Figueroa, Paul Corby Finney, Kyriaki Karidoyanes FitzGerald, Thomas E. FitzGerald, John R. Fitzmier, Marie Therese Flanagan, Sabina Flanagan, Claude Flipo, Ronald B. Flowers, Carole Fontaine, David Ford, Mary Ford, Stephanie A. Ford, Jim Forest, William Franke, Robert M. Franklin, Ruth Franzén, Edward H. Friedman, Samuel Frouisou, Lorelei F. Fuchs, Jojo M. Fung, Inger Furseth, Richard R. Gaillardetz, Brandon Gallaher, China Galland, Mark Galli, Ismael García, Tharscisse Gatwa, Jean-Marie Gaudeul, Luis María Gavilanes del Castillo, Pavel L. Gavrilyuk, Volney P. Gay, Metropolitan Athanasios Geevargis, Kondothra M. George, Mary Gerhart, Simon Gikandi, Maurice Gilbert, Michael J. Gillgannon, Verónica Giménez Beliveau, Terryl Givens, Beth Glazier-McDonald, Philip Gleason, Menghun Goh, Brian Golding, Bishop Hilario M. Gomez, Michelle A. Gonzalez, Donald K. Gorrell, Roy Gottfried, Tamara Grdzelidze, Joel B. Green, Niels Henrik Gregersen, Cristina Grenholm, Herbert Griffiths, Eric W. Gritsch, Erich S. Gruen, Christoffer H. Grundmann, Paul H. Gundani, Jon P. Gunnemann, Petre Guran, Vidar L. Haanes, Jeremiah M. Hackett, Getatchew Haile, Douglas John Hall, Nicholas Hammond, Daphne Hampson, Jehu J. Hanciles, Barry Hankins, Jennifer Haraguchi, Stanley S. Harakas, Anthony John Harding, Conrad L. Harkins, J. William Harmless, Marjory Harper, Amir Harrak, Joel F. Harrington, Mark W. Harris, Susan Ashbrook Harvey, Van A. Harvey, R. Chris Hassel, Jione Havea, Daniel Hawk, Diana L. Hayes, Leslie Hayes, Priscilla Hayner, S. Mark Heim, Simo Heininen, Richard P. Heitzenrater, Eila Helander, David Hempton, Scott H. Hendrix, Jan-Olav Henriksen, Gina Hens-Piazza, Carter Heyward, Nicholas J. Higham, David Hilliard, Norman A. Hjelm, Peter C. Hodgson, Arthur Holder, M. Jan Holton, Dwight N. Hopkins, Ronnie Po-chia Hsia, Po-Ho Huang, James Hudnut-Beumler, Jennifer S. Hughes, Leonard M. Hummel, Mary E. Hunt, Laennec Hurbon, Mark Hutchinson, Susan E. Hylen, Mary Beth Ingham, H. Larry Ingle, Dale T. Irvin, Jon Isaak, Paul John Isaak, Ada María Isasi-Díaz, Hans Raun Iversen, Margaret C. Jacob, Arthur James, Maria Jansdotter-Samuelsson, David Jasper, Werner G. Jeanrond, Renée Jeffery, David Lyle Jeffrey, Theodore W. Jennings, David H. Jensen, Robin Margaret Jensen, David Jobling, Dale A. Johnson, Elizabeth A. Johnson, Maxwell E. Johnson, Sarah Johnson, Mark D. Johnston, F. Stanley Jones, James William Jones, John R. Jones, Alissa Jones Nelson, Inge Jonsson, Jan Joosten, Elizabeth Judd, Mulambya Peggy Kabonde, Robert Kaggwa, Sylvester Kahakwa, Isaac Kalimi, Ogbu U. Kalu, Eunice Kamaara, Wayne C. Kannaday, Musimbi Kanyoro, Veli-Matti Kärkkäinen, Frank Kaufmann, Léon Nguapitshi Kayongo, Richard Kearney, Alice A. Keefe, Ralph Keen, Catherine Keller, Anthony J. Kelly, Karen Kennelly, Kathi Lynn Kern, Fergus Kerr, Edward Kessler, George Kilcourse, Heup Young Kim, Kim Sung-Hae, Kim Yong-Bock, Kim Yung Suk, Richard King, Thomas M. King, Robert M. Kingdon, Ross Kinsler, Hans G. Kippenberg, Cheryl A. Kirk-Duggan, Clifton Kirkpatrick, Leonid Kishkovsky, Nadieszda Kizenko, Jeffrey Klaiber, Hans-Josef Klauck, Sidney Knight, Samuel Kobia, Robert Kolb, Karla Ann Koll, Heikki Kotila, Donald Kraybill, Philip D. W. Krey, Yves Krumenacker, Jeffrey Kah-Jin Kuan, Simanga R. Kumalo, Peter Kuzmic, Simon Shui-Man Kwan, Kwok Pui-lan, André LaCocque, Stephen E. Lahey, John Tsz Pang Lai, Emiel Lamberts, Armando Lampe, Craig Lampe, Beverly J. Lanzetta, Eve LaPlante, Lizette Larson-Miller, Ariel Bybee Laughton, Leonard Lawlor, Bentley Layton, Robin A. Leaver, Karen Lebacqz, Archie Chi Chung Lee, Marilyn J. Legge, Hervé LeGrand, D. L. LeMahieu, Raymond Lemieux, Bill J. Leonard, Ellen M. Leonard, Outi Leppä, Jean Lesaulnier, Nantawan Boonprasat Lewis, Henrietta Leyser, Alexei Lidov, Bernard Lightman, Paul Chang-Ha Lim, Carter Lindberg, Mark R. Lindsay, James R. Linville, James C. Livingston, Ann Loades, David Loades, Jean-Claude Loba-Mkole, Lo Lung Kwong, Wati Longchar, Eleazar López, David W. Lotz, Andrew Louth, Robin W. Lovin, William Luis, Frank D. Macchia, Diarmaid N. J. MacCulloch, Kirk R. MacGregor, Marjory A. MacLean, Donald MacLeod, Tomas S. Maddela, Inge Mager, Laurenti Magesa, David G. Maillu, Fortunato Mallimaci, Philip Mamalakis, Kä Mana, Ukachukwu Chris Manus, Herbert Robinson Marbury, Reuel Norman Marigza, Jacqueline Mariña, Antti Marjanen, Luiz C. L. Marques, Madipoane Masenya (ngwan'a Mphahlele), Caleb J. D. Maskell, Steve Mason, Thomas Massaro, Fernando Matamoros Ponce, András Máté-Tóth, Odair Pedroso Mateus, Dinis Matsolo, Fumitaka Matsuoka, John D'Arcy May, Yelena Mazour-Matusevich, Theodore Mbazumutima, John S. McClure, Christian McConnell, Lee Martin McDonald, Gary B. McGee, Thomas McGowan, Alister E. McGrath, Richard J. McGregor, John A. McGuckin, Maud Burnett McInerney, Elsie Anne McKee, Mary B. McKinley, James F. McMillan, Ernan McMullin, Kathleen E. McVey, M. Douglas Meeks, Monica Jyotsna Melanchthon, Ilie Melniciuc-Puica, Everett Mendoza, Raymond A. Mentzer, William W. Menzies, Ina Merdjanova, Franziska Metzger, Constant J. Mews, Marvin Meyer, Carol Meyers, Vasile Mihoc, Gunner Bjerg Mikkelsen, Maria Inêz de Castro Millen, Clyde Lee Miller, Bonnie J. Miller-McLemore, Alexander Mirkovic, Paul Misner, Nozomu Miyahira, R. W. L. Moberly, Gerald Moede, Aloo Osotsi Mojola, Sunanda Mongia, Rebeca Montemayor, James Moore, Roger E. Moore, Craig E. Morrison O.Carm, Jeffry H. Morrison, Keith Morrison, Wilson J. Moses, Tefetso Henry Mothibe, Mokgethi Motlhabi, Fulata Moyo, Henry Mugabe, Jesse Ndwiga Kanyua Mugambi, Peggy Mulambya-Kabonde, Robert Bruce Mullin, Pamela Mullins Reaves, Saskia Murk Jansen, Heleen L. Murre-Van den Berg, Augustine Musopole, Isaac M. T. Mwase, Philomena Mwaura, Cecilia Nahnfeldt, Anne Nasimiyu Wasike, Carmiña Navia Velasco, Thulani Ndlazi, Alexander Negrov, James B. Nelson, David G. Newcombe, Carol Newsom, Helen J. Nicholson, George W. E. Nickelsburg, Tatyana Nikolskaya, Damayanthi M. A. Niles, Bertil Nilsson, Nyambura Njoroge, Fidelis Nkomazana, Mary Beth Norton, Christian Nottmeier, Sonene Nyawo, Anthère Nzabatsinda, Edward T. Oakes, Gerald O'Collins, Daniel O'Connell, David W. Odell-Scott, Mercy Amba Oduyoye, Kathleen O'Grady, Oyeronke Olajubu, Thomas O'Loughlin, Dennis T. Olson, J. Steven O'Malley, Cephas N. Omenyo, Muriel Orevillo-Montenegro, César Augusto Ornellas Ramos, Agbonkhianmeghe E. Orobator, Kenan B. Osborne, Carolyn Osiek, Javier Otaola Montagne, Douglas F. Ottati, Anna May Say Pa, Irina Paert, Jerry G. Pankhurst, Aristotle Papanikolaou, Samuele F. Pardini, Stefano Parenti, Peter Paris, Sung Bae Park, Cristián G. Parker, Raquel Pastor, Joseph Pathrapankal, Daniel Patte, W. Brown Patterson, Clive Pearson, Keith F. Pecklers, Nancy Cardoso Pereira, David Horace Perkins, Pheme Perkins, Edward N. Peters, Rebecca Todd Peters, Bishop Yeznik Petrossian, Raymond Pfister, Peter C. Phan, Isabel Apawo Phiri, William S. F. Pickering, Derrick G. Pitard, William Elvis Plata, Zlatko Plese, John Plummer, James Newton Poling, Ronald Popivchak, Andrew Porter, Ute Possekel, James M. Powell, Enos Das Pradhan, Devadasan Premnath, Jaime Adrían Prieto Valladares, Anne Primavesi, Randall Prior, María Alicia Puente Lutteroth, Eduardo Guzmão Quadros, Albert Rabil, Laurent William Ramambason, Apolonio M. Ranche, Vololona Randriamanantena Andriamitandrina, Lawrence R. Rast, Paul L. Redditt, Adele Reinhartz, Rolf Rendtorff, Pål Repstad, James N. Rhodes, John K. Riches, Joerg Rieger, Sharon H. Ringe, Sandra Rios, Tyler Roberts, David M. Robinson, James M. Robinson, Joanne Maguire Robinson, Richard A. H. Robinson, Roy R. Robson, Jack B. Rogers, Maria Roginska, Sidney Rooy, Rev. Garnett Roper, Maria José Fontelas Rosado-Nunes, Andrew C. Ross, Stefan Rossbach, François Rossier, John D. Roth, John K. Roth, Phillip Rothwell, Richard E. Rubenstein, Rosemary Radford Ruether, Markku Ruotsila, John E. Rybolt, Risto Saarinen, John Saillant, Juan Sanchez, Wagner Lopes Sanchez, Hugo N. Santos, Gerhard Sauter, Gloria L. Schaab, Sandra M. Schneiders, Quentin J. Schultze, Fernando F. Segovia, Turid Karlsen Seim, Carsten Selch Jensen, Alan P. F. Sell, Frank C. Senn, Kent Davis Sensenig, Damían Setton, Bal Krishna Sharma, Carolyn J. Sharp, Thomas Sheehan, N. Gerald Shenk, Christian Sheppard, Charles Sherlock, Tabona Shoko, Walter B. Shurden, Marguerite Shuster, B. Mark Sietsema, Batara Sihombing, Neil Silberman, Clodomiro Siller, Samuel Silva-Gotay, Heikki Silvet, John K. Simmons, Hagith Sivan, James C. Skedros, Abraham Smith, Ashley A. Smith, Ted A. Smith, Daud Soesilo, Pia Søltoft, Choan-Seng (C. S.) Song, Kathryn Spink, Bryan Spinks, Eric O. Springsted, Nicolas Standaert, Brian Stanley, Glen H. Stassen, Karel Steenbrink, Stephen J. Stein, Andrea Sterk, Gregory E. Sterling, Columba Stewart, Jacques Stewart, Robert B. Stewart, Cynthia Stokes Brown, Ken Stone, Anne Stott, Elizabeth Stuart, Monya Stubbs, Marjorie Hewitt Suchocki, David Kwang-sun Suh, Scott W. Sunquist, Keith Suter, Douglas Sweeney, Charles H. Talbert, Shawqi N. Talia, Elsa Tamez, Joseph B. Tamney, Jonathan Y. Tan, Yak-Hwee Tan, Kathryn Tanner, Feiya Tao, Elizabeth S. Tapia, Aquiline Tarimo, Claire Taylor, Mark Lewis Taylor, Bishop Abba Samuel Wolde Tekestebirhan, Eugene TeSelle, M. Thomas Thangaraj, David R. Thomas, Andrew Thornley, Scott Thumma, Marcelo Timotheo da Costa, George E. “Tink” Tinker, Ola Tjørhom, Karen Jo Torjesen, Iain R. Torrance, Fernando Torres-Londoño, Archbishop Demetrios [Trakatellis], Marit Trelstad, Christine Trevett, Phyllis Trible, Johannes Tromp, Paul Turner, Robert G. Tuttle, Archbishop Desmond Tutu, Peter Tyler, Anders Tyrberg, Justin Ukpong, Javier Ulloa, Camillus Umoh, Kristi Upson-Saia, Martina Urban, Monica Uribe, Elochukwu Eugene Uzukwu, Richard Vaggione, Gabriel Vahanian, Paul Valliere, T. J. Van Bavel, Steven Vanderputten, Peter Van der Veer, Huub Van de Sandt, Louis Van Tongeren, Luke A. Veronis, Noel Villalba, Ramón Vinke, Tim Vivian, David Voas, Elena Volkova, Katharina von Kellenbach, Elina Vuola, Timothy Wadkins, Elaine M. Wainwright, Randi Jones Walker, Dewey D. Wallace, Jerry Walls, Michael J. Walsh, Philip Walters, Janet Walton, Jonathan L. Walton, Wang Xiaochao, Patricia A. Ward, David Harrington Watt, Herold D. Weiss, Laurence L. Welborn, Sharon D. Welch, Timothy Wengert, Traci C. West, Merold Westphal, David Wetherell, Barbara Wheeler, Carolinne White, Jean-Paul Wiest, Frans Wijsen, Terry L. Wilder, Felix Wilfred, Rebecca Wilkin, Daniel H. Williams, D. Newell Williams, Michael A. Williams, Vincent L. Wimbush, Gabriele Winkler, Anders Winroth, Lauri Emílio Wirth, James A. Wiseman, Ebba Witt-Brattström, Teofil Wojciechowski, John Wolffe, Kenman L. Wong, Wong Wai Ching, Linda Woodhead, Wendy M. Wright, Rose Wu, Keith E. Yandell, Gale A. Yee, Viktor Yelensky, Yeo Khiok-Khng, Gustav K. K. Yeung, Angela Yiu, Amos Yong, Yong Ting Jin, You Bin, Youhanna Nessim Youssef, Eliana Yunes, Robert Michael Zaller, Valarie H. Ziegler, Barbara Brown Zikmund, Joyce Ann Zimmerman, Aurora Zlotnik, Zhuo Xinping
- Edited by Daniel Patte, Vanderbilt University, Tennessee
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- Book:
- The Cambridge Dictionary of Christianity
- Published online:
- 05 August 2012
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- 20 September 2010, pp xi-xliv
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Chapter 35 - Multiple pregnancy following IVF
- from Section 4: - Early pregnancy after infertility treatment
- Edited by Botros R. M. B. Rizk, University of South Alabama
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- Book:
- Ultrasonography in Reproductive Medicine and Infertility
- Published online:
- 07 September 2011
- Print publication:
- 25 March 2010, pp 291-298
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Summary
Ovarian volume decreases significantly in each 10-year period of a woman's fertile life. The ovarian size decreases in women greater than 40 years old. The volume of each ovary is calculated by measuring in three perpendicular directions and applying the formula for an ellipsoid. Using the largest cross-sectional sagittal view of the ovary, the mean ovarian diameter could be calculated from measurement of two perpendicular diameters. The combination of transvaginal ultrasound and pulsed color Doppler is increasingly used in gynecology to assess the hemodynamic changes in various physiological and pathological situations of the pelvic organs. Only one study has compared the predictive value of antral follicle count (AFC) measurement made using both two-dimension and three-dimension ultrasound in determining the outcome of response to ovarian stimulation as measured by the number of follicles that develop, the number of oocytes retrieved, and the pregnancy rate following assisted reproductive technologies (ART).
Contributors
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- By Mona Aboulghar, Mostafa Abuzeid, Valentine Akande, Carolyn J. Alexander, Gautam N. Allahbadia, Vicki Arguello, Nabil Aziz, Osama M. Azmy, Shawky Z. A. Badawy, Susan L. Baker, Tony Bazi, Nicole Brooks, Robin Brown, William W. Brown, Maria Cerrillo, Rebecca Chilvers, Angela Clough, Willie Cotten, Alan H. DeCherney, Aygul Demirol, Richard Palmer Dickey, Essam S. Dimitry, Maria Dimitry, Tiffany Driver, Alaa El-Ebrashy, Kareem El-Nahhas, Amr Etman, Aimee Eyvazzadeh, Juan A. Garcia-Velasco, Tarek A. Gelbaya, Seth Granberg, Timur Gurgan, Gurkan Levent, Suleyman Guven, Lars Hamberger, Andrew C. Harbin, Wayne J. G. Hellstrom, Micah J. Hill, James Hole, Yakoub Khalaf, John C. LaFleur, Deborah Levine, Iwan Lewis-Jones, Edward A. Lyons, Diana M. Marcus, Samuel F. Marcus, Mohamed F. M. Mitwally, Hany F. Moustafa, Manubai Nagamani, Luciano G. Nardo, Mary G. Nawar, Moshood Olatinwo, Lia Ornat, Sheri Owens, Kathy B. Porter, Jose M. Puente, Puscheck Elizabeth, Rizk Botros, Christine B. Rizk, Christopher B. Rizk, Hassan N. Sallam, Dimitrios Siassakos, Youssef Simaika, Stuart J. Singer, Brad Steffler, Annika Strandell, Sherri K. Taylor, Antoine Watrelot, Matts Wikland, Tony G. Zreik
- Edited by Botros R. M. B. Rizk, University of South Alabama
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- Book:
- Ultrasonography in Reproductive Medicine and Infertility
- Published online:
- 07 September 2011
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- 25 March 2010, pp ix-xii
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40 - IVF in the Medically Complicated Patient
- from PART III - ASSISTED REPRODUCTION
- Edited by Botros R. M. B. Rizk, University of South Alabama, Juan A. Garcia-Velasco, Hassan N. Sallam, Antonis Makrigiannakis, University of Crete
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- Infertility and Assisted Reproduction
- Published online:
- 04 August 2010
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- 15 September 2008, pp 371-374
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Summary
This chapter discusses the outcome of in vitro fertilization (IVF) in medically complicated patients. A confounding factor for IVF pregnancies is the increased number of multiple pregnancies and the relatively increased number of high-risk pregnancies among women with chronic medical problems. Cancer patients present particular challenges to the IVF unit. Standard IVF protocols are used for controlled ovarian hyperstimulation in human immunodeficiency virus (HIV) discordant couples. The main concerns about IVF and malignant disease relate to the issue of the potential delay in the starting of the patient's chemotherapy or of any possible effect of hormonal changes on the cancer. Obesity might affect the outcome of IVF and pregnancy, but with careful management, a good outcome can be achieved. It has been suggested that systemic lupus erythematosus (SLE) may reduce the success of IVF-ET. The presence of antinuclear antibodies may reduce the implantation rate in IVF patients.
7 - Terminology of Errors of Morphogenesis
- Enid Gilbert-Barness, University of South Florida and University of Wisconsin Medical School, Diane Debich-Spicer, University of South Florida
- Foreword by John M. Opitz, University of Utah
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- Embryo and Fetal Pathology
- Published online:
- 23 February 2010
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- 31 May 2004, pp 207-226
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Summary
MALFORMATION
A malformation is a qualitative, structural end result of a disturbance of embryogenesis leading to a (congenital) defect of an organ, body part, or body region. Such defects can be mild or severe, common or rare. They arise either during blastogenesis (first 4 weeks of development) or during organogenesis (2nd half of embryogenesis, weeks 5-8). Defects of blastogenesis tend to be severe, to be frequently lethal, and to involve several parts of the developing organism sharing a common inductive molecular pathway (polytopic anomalies; i.e., DiGeorge anomaly) (Figure 7.1 and Tables 7.1 to 7.5). Defects of organogenesis tend to involve single structures (monotopic anomalies) – i.e., isolated polydactly, cleft palate, distal hypospadias, etc. Regardless of how mild or common in the population, malformations are never normal. Mild malformations (cleft uvula or xiphisternum, agenesis of palmaris longus muscle or of upper lateral incisors, spina bifida occulta of L5) are common in the population and tend to be dominantly inherited.
Developmental Fields
Developmental (or embryogenic or morphogenetic) fields are the parts of the embryo that react as a unit in response to normal inductive, teratogenic, or mutational causes (Tables 7.6 and 7.7). During early blastogenesis the entire pluripotent embryo is the primary field. A midline, axis formation and the initial events of gastrulation are its most important morphogenetic characteristics. Progenitor fields (Davidson) arise in the primary field and represent upstream expression domains of combinations of molecular inductive systems including transcription factors (e.g., HOX, SOX, TBX genes), growth factors (FGF, BMPs), and secreted morphogens (i.e., SHH).
19 - Genito-Urinary System
- Enid Gilbert-Barness, University of South Florida and University of Wisconsin Medical School, Diane Debich-Spicer, University of South Florida
- Foreword by John M. Opitz, University of Utah
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- Embryo and Fetal Pathology
- Published online:
- 23 February 2010
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- 31 May 2004, pp 513-545
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Summary
MALFORMATIONS
Horseshoe Kidney
A horseshoe kidney is a single, midline, horseshoe-shaped kidney.
The kidney is formed by an interaction between the ureteric bud and the metanephric blastema (Figures 19.1 to 19.3). If the ureteric buds are located more medially than normal or if the inducible metanephric blastema is continuous at the lower pole, then a fused horseshoe kidney may develop.
The horseshoe kidney is usually at a lower level than normal kidneys. Its renal pelves are displaced anteriorly and its ureters usually course across the anterior surfaces of the kidney. Dysplastic development may occur in the fused portion of the kidney.
The ureters may be duplicated or angulated, so that obstruction, which leads to hydronephrosis, occurs.
Ectopic Kidney
A kidney is ectopic when it is in the pelvis and not in its usual location. Ureter duplication is a double ureter that can be unilateral or bilateral. Ectopic kidney and ureter duplication usually are not functionally important in the prenatal period. Their frequency is increased in chromosome aneuploidies.
Renal Agenesis
In bilateral renal agenesis, both kidneys and ureters are absent (Table 19.1).
Bilateral renal agenesis is rare, occurring in 1/3,000 to 1/4,000 live borns (Figure 19.4). Unilateral agenesis occurs in 1/1,000 newborns; it is more common in males.
It is postulated that renal agenesis is caused by the failure of the ureteric bud to develop. The ureteric bud normally induces the metanephric blastema to become a kidney.
16 - Cardiovascular System Defects
- Enid Gilbert-Barness, University of South Florida and University of Wisconsin Medical School, Diane Debich-Spicer, University of South Florida
- Foreword by John M. Opitz, University of Utah
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- Embryo and Fetal Pathology
- Published online:
- 23 February 2010
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- 31 May 2004, pp 428-469
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Summary
PRENATAL DIAGNOSIS
With the advent of ultrasound and its application to the human fetal heart,prenatal diagnosis and management of structural heart disease and cardiacdysrhythmia is possible (Figure 16.1). Congenital heart disease is relatively uncommonin the general population, and not every pregnancy can or should be examined with fetal echocardiography. Only those pregnancies with recognized risk factors for cardiac disease and those with an abnormal four-chamberview on level I obstetrical sonograms should be evaluated.
TECHNIQUE OF FETAL ECHOCARDIOGRAPHY
The fetal heart is most easily examined by ultrasound transabdominally at 18-24 weeks gestation, when a nonfixed fetal position, incompletely calcifiedbones, and abundant amniotic fluid make cardiac imaging easier (Table 16.1). Transvaginal images show excellent cardiac detail as early as 14 weeks gestation. Transvaginal imaging is invasive, however, and carries a small potential risk, it should be used when transabdominal imaging is inadequate. Transabdominal ultrasound uses a relatively high-frequency transducer to examine the heart and great vessels segmentally. It uses M-mode, two-dimensional, pulsewave, and color flow Doppler to delineate the cardiac anatomy, fetal hemodynamics, and patency of the fetal circulatory pathways. Anormal fetal echocardiogram does not eliminate the potential for congenital heart disease. Lesions that may not be identified prenatally include mild semilunar valve obstruction, atrial septal defect, small ventricular defect, and partial anomalous venous return. In addition, coarctation of the aorta is a significant lesion that is difficult to diagnose.
The early fetal heart can be dissected under a dissecting microscope in the same manner as the heart of anolder fetus or a newborn (illustrated in Chapter 3).
18 - Gastrointestinal Tract and Liver
- Enid Gilbert-Barness, University of South Florida and University of Wisconsin Medical School, Diane Debich-Spicer, University of South Florida
- Foreword by John M. Opitz, University of Utah
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- Embryo and Fetal Pathology
- Published online:
- 23 February 2010
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- 31 May 2004, pp 490-512
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Summary
ESOPHAGEAL ATRESIA (SEE ALSO CHAPTER 17)
Esophageal atresia results in a complete separation of the esophagus into upper and lower segments. This is often accompanied by communication of either segment or both with the trachea resulting in tracheoesophageal fistula (TEF). It is accompanied by polyhydramnios in which the fetus is unable to swallow amniotic fluid.
The incidence is from 1/800 to 1/5,000 live births.
Pathogenesis
At approximately 4 weeks of development, a diverticulum grows caudally from the ventral wall of the foregut to form the trachea and esophagus. Tracheoesophageal folds forma tracheoesophageal septum, which separates the trachea from the esophagus at the 5th week of embryonic development.
If there is failure of normal septum formation, it results in a TEF with two disconnected segments of the esophagus.
Esophageal atresia is usually sporadic, although there have been about 80 reports of familial atresia with TEF. It also may occur in trisomy 18 or 21.
In over 80% of cases, the upper esophageal segment ends blindly and the lower segment communicates with the trachea (TEF). In approximately 10%, there is isolated atresia of the esophagus; in 1-3%, the upper segment joins the trachea; in 5%, both segments join the trachea. In the region of the fistula, the trachea is often narrow, and tracheal cartilage may be hypoplastic or absent. (See Chapter 17.)
The most frequently associated malformations are gastrointestinal defects, with about one-half associated with an imperforate anus. Cardiovascular malformations, such as persistent ductus arteriosus, VSD, ASD, right-sided aortic arch, dextrocardia, and urogenital defects, such as renal agenesis and hydronephrosis may be associated.
Acknowledgments
- Enid Gilbert-Barness, University of South Florida and University of Wisconsin Medical School, Diane Debich-Spicer, University of South Florida
- Foreword by John M. Opitz, University of Utah
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20 - Congenital Tumors
- Enid Gilbert-Barness, University of South Florida and University of Wisconsin Medical School, Diane Debich-Spicer, University of South Florida
- Foreword by John M. Opitz, University of Utah
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Summary
Congenital tumors are often composed of persistent embryonal or fetal tissues, suggesting a failure of proper cytodifferentiation or maturation during early life. Neuroblastoma develops from neural crest cells that migrate into the gland during embryonic and fetal life. Normally, these cells mature to ganglion cells.
Morphologic features of embryonic neoplasms include retinoblastoma, peripheral primitive neuroectodermal tumor (PNET), hepatoblastoma, yolk sac tumor of the testis, and embryonal rhabdomyosarcoma. Some teratomas show proliferation ofembryonic tissues that fail tomature. Anumberof tumors in the young are associated with congenital malformations and growth disturbances.
Some embryonic tumors have a benign course despite a malignant microscopic appearance such as stage IV-S neuroblastoma, congenital fibrosarcoma, and nephroblastomatosis. These tumors may undergo cytodifferentiation and spontaneous regression. Malignant neoplasms are seldom seen in the newborn and only infrequently are responsible for neonatal death or spontaneous abortion. Chromosomal abnormalities associated with childhood tumors are shown in Table 20.1.
VASCULAR TUMORS
Hemangiomas are the most common tumors of the skin and soft tissues in infants (Figure 20.1).
Benign Hemangiomas
Capillary hemangioma usually manifests at birth, grows steadily for 68 months, then stabilizes, and eventually regresses, although complete disappearance may take several years. It is composed of capillaries separated by stroma. It may present as a raised subcutaneous nodule that blanches under pressure. Because childhood hemangiomas are tumors that evolve in time, a capillary hemangioma is thought to originate from a more primitive form.
15 - Skeletal Abnormalities
- Enid Gilbert-Barness, University of South Florida and University of Wisconsin Medical School, Diane Debich-Spicer, University of South Florida
- Foreword by John M. Opitz, University of Utah
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Summary
OSTEOCHONDRODYSPLASIAS
Bone is formed from collagen. Bone dysplasias predominantly involve one type of collagen (Figure 15.1). Terms used in the description of bone dysplasias according to the defect in collagen are shown in Table 15.1.
The normal growth plate or physis consists of four zones:
resting cartilage;
proliferative cartilage;
hypertrophic cartilage;
zone of provisional calcification.
The revised international classification of osteochondrodysplasias encompasses those disorders that are perinatally lethal and/or amenable to prenatal diagnosis (Table 15.2). Prenatal diagnosis has been made in most of the lethal forms of ostechondrodysplasia (Table 15.3). The osteochondrodysplasias include the infant or fetus with dwarfism. Most are lethal. For most convenience in diagnosis they can be divided into the following groups:
■ Osteochondrodysplasias with platyspondyly
■ Osteochondrodysplasias with short trunk
■ Short rib osteochondrodysplasias
■ Osteochondrodysplasias with defective bone density
■ Miscellaneous group
Osteochondrodysplasias with Platyspondyly (Table 15.4)
Although the trunk of the infants in this group is not significantly short, the vertebral bodies in the radiograph are markedly flattened. Histopathologically the physeal growth zones are usually disorganized and may be retarded, but the resting cartilage is mostly unremarkable.
24 - Metabolic Diseases
- Enid Gilbert-Barness, University of South Florida and University of Wisconsin Medical School, Diane Debich-Spicer, University of South Florida
- Foreword by John M. Opitz, University of Utah
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Summary
Most metabolic disorders due to inborn errors of metabolism are inherited as autosomal recessive traits; some are X-linked. A few are dominant traits. Mitochondrial enzymes are coded by both the maternal nuclear genome and by the mitochondrial DNA. Some disorders can be detected by newborn screening (Table 24.1). Placental changes (Table 24.2) may be present and suggest a lysosomal storage disease. Skin fibroblasts, conjunctiva, intestinal biopsy, peripheral nerve, muscle, bone marrow and amniocytes may be used in the diagnoses of metabolic disease (Table 24.3). Vacuolated lymphocytes (Table 24.4) also may be seen in a number of storage diseases.
AMINO ACID DISORDERS
A number of disorders of amino acid metabolism have been described including phenylketonuria, tyrosinemia, alkaptonuria, homocystinuria, lysinemia, and cystinosis (Figures 24.1 and 24.2 and Tables 24.5 and 24.6). These disorders are rarely observed in the fetus or newborn infant.
MUCOPOLYSACCHARIDOSES
These disorders are distinguished by storage of glycosaminoglycans (GAG) (mucopolysaccharides) and glycolipids in the lysosomes of different cell types, including fibroblasts, macrophages, white blood cells, parenchymal cells of liver, kidneys, brain and other organs, and neurons, and by excretion of mucopolysaccharide in the urine (Table 24.7).
When the tissue is fixed in GAG-insoluble fixatives such as alcohol, the accumulated material shows intense metachromasia (purple-blue staining) with toluidine blue and stains with Alcian blue, weakly with periodic acid-Schiff (PAS), and is impregnated with colloidal iron. Lipid may be abundant.
Hurler disease is characterized by coarse features, prominent supraorbital ridges, depressed nasal bridge and dysostosis multiplex (Figures 24.3 to 24.5). Beaking of the vertebral bodies may be apparent in the fetus and newborn.
Frontmatter
- Enid Gilbert-Barness, University of South Florida and University of Wisconsin Medical School, Diane Debich-Spicer, University of South Florida
- Foreword by John M. Opitz, University of Utah
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Appendices
- Enid Gilbert-Barness, University of South Florida and University of Wisconsin Medical School, Diane Debich-Spicer, University of South Florida
- Foreword by John M. Opitz, University of Utah
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Summary
APPENDIX 1. CYTOGENETIC TERMINOLOGY
Aneuploid. An unbalanced state that arises through loss or addition of whole or pieces of chromosomes; always considered deleterious.
Chromosome. The location of hereditary (genetic) material within the cell. This hereditary material is packaged in the formof a very long, double-stranded molecule of DNA surrounded by and complexed with several different forms of protein. Genes are found arranged in a linear sequence along chromosomes, as is also a large amount of DNA of unknown function.
Confined placental mosaicism. A viable mutation in trophoblast or extraembryonic progenitor cells of the inner cell mass resulting in dichotomy between the chromosomal constitution of the placenta and the embryo or fetus.
Deletion. Pieces of chromosomes are missing in persons having 46 chromosomes.
Diploid (2n). The whole set of 46 chromosomes in a somatic cell.
Duplications. Extra pieces of chromosomes occur in individuals with 46 chromosomes.
Endomitosis. Duplication of the chromosomeswithout accompanying spindle formation or cytokinesis, resulting in a polyploid nucleus.
4 - Ultrasound of Embryo and Fetus: General Principles
- Enid Gilbert-Barness, University of South Florida and University of Wisconsin Medical School, Diane Debich-Spicer, University of South Florida
- Foreword by John M. Opitz, University of Utah
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Summary
ABSTRACT
The area of obstetric ultrasonography has undergone rapid and dramatic evolution over the past three decades. Initial imaging studies were limited to rudimentary evaluations of fetal position and identification of amniotic fluid pockets to the current state of the art, which offers the potential for three-dimensional image reconstructions and targeted Doppler sonographic interrogation of the heart and cerebral vascular structures. Because of the rapid pace of change within the field, several professional organizations offer guidance about routine performance of obstetric ultrasound. In the United States, the American College of Obstetrics and Gynecology (ACOG), the American College of Radiology (ACR), and the American Institute of Ultrasound in Medicine (AIUM) have offered guidelines for obstetric sonography, while in the British Commonwealth, the Royal College of Obstetrics and Gynecology (RCOG) of England, and the Society of Obstetrics and Gynecology of Canada (SOGC) offer recommendations and guidance. Potential resources include the following publications: ACOG, Practice Bulletin 27; ACOG, Technical Bulletin 187, Ultrasonography In Pregnancy (12/93) (http://www.acog.org); ACR, Standard for the Performance of Antepartum Obstetrical Ultrasound (http://www.acr.org); AIUM, Standards for Performance of the Antepartum Obstetrical Ultrasound Examination (http://www.aium.org); RCOG, Ultrasound Screening for Fetal Anomalies and the Value of Ultrasound in Pregnancy (http://www.rcog.org.uk); SCOG, Guidelines of Ultrasound as Part of Routine Prenatal Care (8/99), Obstetrics/Gynecologic Ultrasound (7/97) (http://www.sogc.medical.org).
3 - Fetal Autopsy
- Enid Gilbert-Barness, University of South Florida and University of Wisconsin Medical School, Diane Debich-Spicer, University of South Florida
- Foreword by John M. Opitz, University of Utah
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- Embryo and Fetal Pathology
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Summary
The normal anatomy of the adult and child are similar; however, the perinatal autopsy is significantly different. The variety and complexity of the congenital anomalies found in perinatal and fetal autopsies is endless and the prosector must be prepared to spend the necessary time demonstrating these anomalies. This detailed procedure can be altered to preserve any anomaly encountered without deforming the body itself. Most of the anomalies found in this population never survive to adulthood. Together with the clinical information this meticulous examination provides the necessary information to educate the families about future pregnancies.
PLACENTAL CHANGES AFTER FETAL DEATH
After the intrauterine death of the fetus, the placenta remains vital until it is expelled. However, changes occur that resemble vascular insufficiency but are diffuse, affecting fetal structure and all villi (Figure 3.1). Focal lesions suggest a preexisting abnormality (Tables 3.1).
Fetal death results in complete interruption of the fetal circulation. Vascular spaces within the villi are empty and collapsed. Within weeks, ingrowth of fibroblasts ultimately completely obliterate the vessels. Thrombosis does not occur and if present indicates preexistent pathology.
Calcificationmay be observed in addition to fibrosis as a postmortemchange within villi. It presents as fine granules deposited along the basal membrane of the trophoblast, sometimes almost in linear fashion. The fine granules contrast with the coarse deposits that sometimes occur in villi during physiological maturation. After fetal death, there are excessive syncytial knots that are diffuse. Primary vascular insufficiency is usually focal.
12 - Fetal Hydrops and Cystic Hygroma
- Enid Gilbert-Barness, University of South Florida and University of Wisconsin Medical School, Diane Debich-Spicer, University of South Florida
- Foreword by John M. Opitz, University of Utah
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Summary
Minor hydrops is common, particularly in premature infants. Severe hydrops is generalized edema of 7.5 mm subcutaneous edema in a third-trimester fetus with an effusion of at least one body cavity, usually accompanied by polyhydramnios and edema of the placenta.
POLYHYDRAMNIOS
Amniotic fluid volume is approximately 800 mL at term. The volume is increased by fetal urine and is simultaneously removed by fetal swallowing. Fetal anomalies that interfere with swallowing are associated with polyhydramnios, while a decrease of fetal renal function and production of urine result in oligohydramnios. The volume of amniotic fluid falls rapidly after 40weeks gestation to about 400 mL at 42 weeks and 200 mL at 44 weeks. Polyhydramnios is the presence of an excess of 1,500 mL of amniotic fluid at term and is present in up to 1% of pregnancies.
Causes of polyhydramnios
I. Maternal
A. Diabetes and gestational diabetes
II. Fetal anomalies
A. Anencephaly
B. Esophageal atresia
C. Small intestinal obstruction
D. Diaphragmatic hernia
E. Central nervous system malformations
F. Chromosomal defects
III. Placenta
A. Chorangioma
FETAL HYDROPS (FH)
Hydrops fetalis (HF) has a mortality rate in excess of 90% (Tables 12.1 to 12.5).
Intrauterine diagnosis of hydrops by ultrasound may allow successful treatment and reversal in selected cases, but the majority die without an established causative diagnosis.
13 - Central Nervous System Defects
- Enid Gilbert-Barness, University of South Florida and University of Wisconsin Medical School, Diane Debich-Spicer, University of South Florida
- Foreword by John M. Opitz, University of Utah
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Summary
Central nervous system (CNS) defects are the most common developmental defects both at birth and in spontaneously aborted conceptuses. The incidence is from 1 to 65 per 1,000 births.
The incidence of neural tube defects in embryos fromspontaneous abortions is about 10 times higher than in newborns. In aborted embryos, CNS defects are usually components of chromosomal syndromes that are lethal early in development and thus are seen less commonlyin aborted fetuses that have fewer chromosome anomalies. Most fetal specimens with CNS defects, therefore, are obtained from terminated pregnancies after prenatal detection of an isolated CNS defect.
NEURAL TUBE FORMATION
Neurulation occurs between days 20 and 30 of embryonic development (Stages 9-12) (Figures 13.1 to 13.3 and Table 13.1). Failure of the neural folds to fuse during this period results in a permanent open neural tube defect. Five sites of closure have been proposed. However, careful study of a series of staged human embryos has shown only two de novo sites of fusion: in the rhomboencephalon that proceeds rostrally and caudally, and in the prosencephalon that fuses caudally. It is debated whether failure of closure is due to a deficiency in the axial cephalic mesoderm or in the neuroepithelium itself, but in either case the result is an eversion of the cephalic neural tube and absence of the cranium in anencephaly.
The first sign of neurulation is the appearance of the neural plate in Stage 8. The neural folding process begins at Stage 9.
11 - Intrauterine Growth Retardation
- Enid Gilbert-Barness, University of South Florida and University of Wisconsin Medical School, Diane Debich-Spicer, University of South Florida
- Foreword by John M. Opitz, University of Utah
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- Embryo and Fetal Pathology
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Summary
Estimation of fetal maturity is the most accurate method of estimating gestation age by ultrasonographic measurements of crown-rump length during the first trimester. From the first trimester through 34 weeks, the biparietal diameter is accurate to within 10 days. Other measurements used in the 2nd and 3rd trimesters include fetal abdominal diameter and femur length.
Low birth weight (LBW) is a worldwide problem usually defined as birth weight <2,500 g, irrespective of gestational age. It is associated with increased perinatal morbidity and is used as a marker of increased neonatal risk. It is not an ideal marker of fetal growth and development and combines both prematurity and various degrees of growth retardation.Morbitity is associated with LBW and growth retardation. Twenty-one million LBW infants are born each year internationally, 90% in developing countries.
Insulin growth factor (IGF) II is essential for organogenesis and early fetal growth. IGF-I is essential for late fetal growth. IGF-I is low in intrauterine growth retardation (IUGR) infants.
Proportion of LBWs varies by type of society:
■ 3–12% rates of LBW infants occur in developed countries, 60% premature, 40% growth retarded
■ 12–40% rates of LBW in developing countries, 20% premature, 80% growth retarded
There is a high rate of perinatal morbidity in growth-retarded infants:
■ perinatal depression is 3 times more likely
■ hypoglycemia is 4–6 times more likely
■ hypothermia is 5 times more likely
■ meconium aspiration is 13 times more likely
■ fetal distress in labor is 6 times more likely
Contents
- Enid Gilbert-Barness, University of South Florida and University of Wisconsin Medical School, Diane Debich-Spicer, University of South Florida
- Foreword by John M. Opitz, University of Utah
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- Embryo and Fetal Pathology
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- 23 February 2010
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