practical guide to high risk pregnancy and delivery

Practical Guide to High-Risk Pregnancy

and Delivery

A South Asian Perspective

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Practical Guide to High-Risk Pregnancy

and Delivery

A South Asian Perspective

Third Edition

Fernando Arias, MD, PhD, FACOGProfessor of Obstetrics and Gynecology

University of Toledo, College of Medicine, The Toledo HospitalDepartment of MaternalFetal Medicine, Toledo, Ohio, USA

Editors

Shirish N Daftary, MD, DGO, FICS, FIC, FICOGProfessor Emeritus and Former Medical Advisor, Nowrosjee Wadia Maternity Hospital, Mumbai, India;

Formerly Dean, Nowrosjee Wadia Maternity Hospital;Past President, Federation of Obstetrics and Gynaecological Societies of India;Former Jt. Associate Editor, Journal of Obstetrics and Gynaecology of India;

Past President, Indian College of Obstetrics and Gynaecology;Past Chairman, MTP Committee of FOGSI;

Vice President, Indian Academy of Juvenile and Adolescent Gynaecology & Obstetrics;Chairman, Indian College of Maternal and Child Health

Amarnath G Bhide, MD, DGO, DNB, DFP, MICOG, MRCOG (London)Consultant in MaternalFetal Medicine and Obstetrics, St. George's Hospital, London, UK;

Honorary Senior Lecturer, St. George's University of London;Scientific Editor, BJOG: An International Journal of Obstetrics and Gynaecology;

Formerly, Professor and Unit HeadNowrosjee Wadia Maternity Hospital, Mumbai, India

ELSEVIER

A division of

Reed Elsevier India Private Limited

Practical Guide to High-Risk Pregnancy and Delivery: A South Asian Perspective, 3/eArias, Daftary, and Bhide

ELSEVIERA division ofReed Elsevier India Private Limited

Mosby, Saunders, Churchill Livingstone, Butterworth Heinemann andHanley & Belfus are the Health Science imprints of Elsevier.

2008 ElsevierFirst edition 1984Second edition 1993Third edition 2008

All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmittedin any form or by any means, electronic, mechanical, photocopying, recording or otherwise, without the priorpermission of the publisher.

ISBN: 978-81-312-1155-7

Medical knowledge is constantly changing. As new information becomes available, changes in treatment, proce-dures, equipment and the use of drugs become necessary. The authors, editors, contributors and the publisher have,as far as it is possible, taken care to ensure that the information given in this text is accurate and uptodate.However, readers are strongly advised to confirm that the information, especially with regard to drug dose/usage,complies with current legislation and standards of practice.

Commissioning Editor: Sonali DasguptaManaging Editor (Development): Shabina NasimCopy Editor: Meenakshi KhannaProduction Executive: Ambrish Choudhary

Published by Elsevier, a division of Reed Elsevier India Private Limited,Sri Pratap Udyog, 274, Captain Gaur Marg, Sriniwaspuri, New Delhi-110065

Laser typeset by Chitra Computers, Delhi

Printed and bound at

In loving memory of

Dr Fernando Arias

June 11, 1943 August 7, 2007

To our families

Dr (Mrs) Sindhu Daftary, Dr Gaurang Daftary,

Dr Ameet, and (Mrs) Aanal Mehta Daftary

Shirish N Daftary

To our families

Mr Govind Bhide, Mrs Manik Bhide, Dr (Mrs) Priya Bhide,

(Miss) Anuradha Bhide, and (Miss) Malvika Bhide

Amarnath G Bhide

The second edition of this book was widely applauded by students in training and practitioners alike. It presented con-cisely the present-day trends in the management of pregnant women and provided guidance for the optimum care ofhigh-risk pregnancies. An update of this treatise has been long awaited. In appreciation of the popularity of the book,Professor Fernando Arias was persuaded to revive it and bring it back to the offices of practicing obstetricians alongwith added observations and experiences of Indian workers. The experiences of the senior Indian authoran obstetri-cian practicing the art for over 40 years, author of several works in the specialty, and a teacher at the Seth GS MedicalCollege and Nowrosjee Wadia Maternity Hospital, Mumbai for over 30 yearscombined with the expertise of the jointauthor who has been professor of Obstetrics and Gynecology at the Seth GS Medical College and Nowrosjee WadiaMaternity Hospital, Mumbai for many years and is presently a consultant in maternalfetal medicine at the well-knownSt. Georges Hospital, London, UK, have provided fresh inputs to update this book to suit the Indian subcontinent.

A separate chapter on Tropical Diseases in Pregnancy has been added keeping in mind Indian conditions. Data of rel-evance to India has been added at relevant places in all the chapters. The addition of Indian experiences at the end ofevery chapter lends additional information about the experiences of practitioners in India, which may be of relevanceto readers of the subcontinent.

Shirish N DaftaryAmarnath G Bhide

Preface to the Third Edition

Preface to the Third Edition vii

Section I

FETAL MEDICINE

1. Antepartum Care of the High-Risk Pregnancy 3

2. Prenatal Diagnosis of Chromosomal Abnormalities 32

3. Fetal Dysmorphology 62

4. Fetal Growth Restriction 105

5. Fetal Infections 135

6. Birth Asphyxia 172

Section II

OBSTETRICAL COMPLICATIONS

7. Preterm Parturition Syndrome 193

8. Preterm Labor 217

9. Premature Rupture of Membranes 240

10. Cervical Insufficiency 262

11. Prolonged Pregnancy 277

12. Multifetal Gestation 293

13. Bleeding During Pregnancy 323

14. Rh Alloimmunization 358

15. Abnormal Labor and Delivery 373

16. Hypertensive Disorders in Pregnancy 397

17. Diabetes and Pregnancy 440

18. Hematologic Disorders in Pregnancy 465

19. Abnormalities of the Urinary System During Pregnancy 489

20. Cardiac Disease and Pregnancy 506

Section III

TROPICAL DISEASES IN PREGNANCY

21. Tropical Diseases in Pregnancy 527

Index 553

Contents

Section I

FETAL MEDICINE

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CHAPTER OUTLINE

Identification of the High-Risk Patient Preconceptional Counseling Prenatal Care Determination of gestational age Prevention of abnormal maternal and fetal outcomes

Antepartum Fetal Surveillance Fetal movement count The nonstress test The contraction stress test The biophysical profile The modified biophysical profile Doppler velocimetry Fetal blood sampling

Indian Experience of Antepartum Surveillance Important Points References

A high-risk pregnancy is that with a significant probabil-ity for a poor maternal or fetal outcome. In some cases,these patients are recognized in the initial prenatal officevisit because they have a poor obstetrical history or awell-recognized medical complication. In other caseswomen become high-risk pregnancies because they devel-op unexpected complications in the course of otherwisenormal pregnancies. These patients with unexpected com-plications are in a vulnerable emotional position due tothe sudden loss of their expectations for a normal preg-nancy and the lack of preparedness for invasive testingand obstetrical interventions. High-risk patients requiresophisticated maternal and fetal surveillance and in manyoccasions difficult management decisions in order to opti-mize their outcome. This chapter provides (a) a descrip-tion of the available systems to identify women at highrisk for abnormal pregnancy outcomes, (b) a generaldescription of prenatal care focused in the prevention ofmorbid outcomes not analyzed in other chapters of thisbook, and (c) an overview of the methods used for fetalsurveillance in high-risk pregnancies, the rationale behindtheir use, the situations where their use is indicated, theirlimitations, their clinical usefulness, and their impact onthe maternal and fetal outcome.

IDENTIFICATION OF THE HIGH-RISKPATIENT

A high-risk pregnancy can be identified only if the womanhas access to prenatal care. Povertylimiting access to thehealth care systemand lack of ability of societies and gov-ernments to provide medical coverage to those unable topay for these services are powerful factors that preventaccess to prenatal care. Once the woman has access to pre-natal care, the second limiting factor preventing the identi-fication of those at risk is the quality of the prenatal care

Antepartum Care of the High-Risk Pregnancy

Andres Sarmiento R*

*Andres Sarmiento R, MD, Department of Obstetrics, Gynecologyand Reproductive Medicine, Universidad de los Andes andHospital Fundacion Santa Fe de Bogota, Bogota Colombia.

1

SECTION I FETAL MEDICINE4

itself, because in many cases the services provided are ofmarginal quality, and high-risk patients are not identified.

High-risk pregnancies are a small segment of the obstet-rical population that produces the majority of the maternaland infant mortality and morbidity. This denominationincludes women with chronic hypertension, pregestationaldiabetes, anemia, chronic lung disease, Rh alloimmuniza-tion, cardiac and renal disease, women at risk for congeni-tal abnormalities in the offspring, and other conditions(Box 1-1) that place the pregnancy at risk (Martin et al.,2003). Women with a poor obstetrical history (Box 1-2) arealso at high risk for abnormal outcomes.

To facilitate the identification of high-risk pregnancies,most prenatal records incorporate a list of high-risk fac-tors that should be systematically checked during the firstprenatal visit to find women at risk. Some of these systemsassign a numerical value to the high-risk factors, depend-ing on the potential severity of their effects on the preg-nancy or the accuracy of the risk factor in predicting outcome, resulting in a numerical score that is supposedto be a quantitative reflection of the severity of the prob-lems and their potential effects on the pregnancy. A poten-tial benefit of this quantitative estimation of risk is that itmay be useful to identify those cases that because of theseverity of their problems require prenatal care under thedirection of a specialist in Maternal Fetal Medicine. Thereare no adequate studies providing a basis for or demon-strating the benefits of referring women with high-riskfactors to the specialists in Maternal Fetal Medicine, andthe pattern of referral varies significantly between

communities. Some suggestions on this respect are foundin Box 1-3.

Unfortunately, most individual high-risk factors lack thenecessary qualities to be adequate predictive tools. Thereare several methods to assess the accuracy or strength of arisk factor. One of these methods compares the frequencyof a given outcome in patients with and without the riskfactor (likelihood ratio), and the higher its value thestronger the association with the adverse outcome.However, even risk factors strongly associated with agiven outcome may be poor predictors if the frequency ofthe outcome is low. For example, a cervical length of lessthan 1.5 cm is associated with preterm delivery within 7days with a likelihood ratio of 8.7 (Gomez et al., 2005).The predictive value of this measurement will be muchless in an unselected population with a frequency ofpreterm delivery of 11% than in a population at high riskwith a frequency of preterm birth of 35%.

Another method to assess the predictive value of ahigh-risk factor is by analysis of its sensitivity and speci-ficity. Sensitivity is the ability of the variable to identifypatients who have the abnormal outcome and specificityis the ability of the same variable to identify patients whodo not have the outcome. Most of the time when the sen-sitivity of a variable is high, the specificity decreases andthe number of false positives increases. For example, uter-ine contractions are a sign with high sensitivity to predictthe onset of preterm labor. However, the specificity ofuterine contractions is low, and a large number of womenwith contractions will not deliver preterm. ROC (receiver

BOX 1-2

Obstetrical high-risk factors

History of previous prolonged laborinstrumental assisteddelivery

History of previous obstructed labor/ruptureuterus/traumaticdelivery

History of postpartum hemorrhage (high parity status)/obstet-ric shock

History of puerperal sepsis Prior preterm birth (less than 36, less than 32, less than 28

weeks) History of birth asphyxia/neonatal convulsions/birth injuries Prior stillbirth Prior fetal growth restricted infant Second trimester pregnancy loss Prior neonatal death Prior infant with cerebral palsy Prior cesarean delivery Diagnosis of incompetent cervix in prior pregnancy History of preeclampsia before 32 weeks in prior pregnancy Prior fetus with chromosomal disorder or congenital anatomic

abnormalities Anatomic abnormality of the uterus History of cervical trauma

BOX 1-1

Partial list of medical conditions that place pregnancy at highrisk for a poor outcome

Malnutrition Anemia Chronic hypertension Diabetes Asthma Thrombophilia (history of DVT or PE) Cardiac disease Seizure disorder Family history of genetic disease Hemoglobinopathy Renal disease Psychiatric illness Lupus erythematosus and other connective tissue disorders Drug and alcohol abuse Smoking Rh alloimmunization Hepatitis B carrier Human immunodeficiency virus infection Syphilis Gonorrhea and Chlamydia infection Asymptomatic bacteriuria

CHAPTER 1 ANTEPARTUM CARE OF THE HIGH-RISK PREGNANCY 5

operating characteristic) analysis is a plot of sensitivity onthe y-axis versus 1 specificity (false positive results) onthe x-axis. It is useful to determine if the high-risk factordiscriminates better than chance alone and to find thethreshold value with greater sensitivity and less false pos-itive results which will be used to determine when the testis positive or negative.

For the individual patient and for the clinician takingcare of patients, the positive and negative predictive val-ues of the test are more significant and useful than theirsensitivity and specificity. Positive predictive value is theprobability that an individual who if tested positive isgoing to develop the condition he or she is being testedfor. Negative predictive value is the probability that a neg-ative test result truly predicts that the condition will notoccur. The predictive value of any test is affected by theprevalence of the condition in the general population. Atest may have a high sensitivity (ability to detect cases inthe general population) but a low positive predictive valueif that condition only affects a small segment of the pop-ulation. Since abnormal and particularly catastrophicpregnancy outcomes occur infrequently, the majority ofobstetrical tests are characterized by low positive and highnegative predictive values.

Another tool to determine the predictive value of high-risk factors is the univariable analysis where all the vari-ables significantly associated with a given outcome areused in a predictive model to determine which of them isthe strongest predictor. Another method, the multivari-able analysis, in particular logistic regression, performs astepwise evaluation of the relative contribution of eachvariable to the prediction model and allows the investiga-tor to determine if one or several of the variables underconsideration are independent or not of each other. Theseare refined statistical techniques used to measure the accu-racy of high-risk factors, laboratory tests and interven-tions in the prediction of outcomes. An excellent review ofmethods of clinical prediction is found in the article byGrobman and Stamilio (2006).

The use of individual or composite high-risk factorsdoes not allow an accurate prediction of women who aregoing to deliver preterm because of preterm labor withintact membranes or because of premature rupture ofmembranes early in gestation. Similarly, there are no riskfactors that predict with accuracy the occurrence ofpreeclampsia. This is unfortunate, because these two con-ditions, preterm delivery and preeclampsia affect close to15% of all pregnancies, particularly in nulliparouspatients, and the lack of adequate methods for their prediction and treatment poses a heavy burden on the discipline of Obstetrics.

PRECONCEPTIONAL COUNSELING

The best time to assess the potential impact of medical orobstetrical complications on the outcome of pregnancy isbefore pregnancy occurs. This is known as preconception-al counseling. Ideally a significant number of high-riskpregnancies can be identified before pregnancy occurs.When this happens, the woman will benefit considerablyfrom a meeting with the obstetrician to analyze her high-risk factors and the life style modifications that she mayadopt to maximize the outcome of pregnancy. In thecourse of this interview the following points should bemethodically reviewed by the obstetrician:

1. The relative importance of each one of the high-riskfactors identified through the history and examina-tion of the patient.

2. The potential effects that each risk factor may haveon the pregnancy.

3. The changes or effects that pregnancy may causeupon each risk factor.

4. The potential disability for the mother during preg-nancy and the length of such disability.

5. The tests that will be required to monitor maternaland fetal well-being during pregnancy.

6. The prognosis for the outcome of the pregnancy.

BOX 1-3

High-risk patients that may benefit from referral or consulta-tion with maternal fetal medicine

1. Women with conditions that may require invasive proce-dures for fetal diagnosis or treatment, such as: Rh alloimmunization Nonimmunologic fetal hydrops Fetal urinary tract obstruction Need for CVS

2. Women with severe medical complications affecting thepregnancy, such as: Insulin-dependent diabetes Artificial heart valves Cardiomyopathy Systemic lupus erythematosus Sickle cell disease/thalassemia Thromboembolic phenomena Seizure disorder

3. Women with recurrent poor obstetrical outcome, such as: Repetitive second trimester pregnancy losses Recurrent stillbirths Recurrent early preterm labor Recurrent early rupture of membranes

4. Women with severe obstetrical complications, such as: Preeclampsia/eclampsia with renal failure, pulmonary

edema Severe HELLP syndrome Suspected cervical incompetence after 20 weeks gesta-

tion Suspected twin-to-twin transfusion Multiple gestation of high order (3 and above)


7. The cost of the pregnancy particularly in terms of lossof revenue as a result of prolonged hospitalization andfrequent testing, and the need for help at home withother children and the monetary and emotional costsof dealing with the effects of prematurity.

The ideal medical condition benefiting from preconcep-tional counseling is maternal diabetes. It includes educationabout the effects of diabetes on pregnancy and the effects ofpregnancy on diabetes, advantages of rigorous metaboliccontrol, and the importance of maintaining a low precon-ceptional level of glycosylated hemoglobin to decrease theincidence of congenital malformations. Other conditionsthat may benefit greatly from preconceptional counselingare Rh alloimmunization, history of recurrent stillbirthsand patients at high risk for having fetuses with aneuploidy.Women with history of birth of a baby with neural tubedefect should be prescribed folic acid supplements for 3months prior to attempting subsequent pregnancy. In India,the practice of routine immunization of adolescents againstrubella is not yet universally prevalent. Hence in presentday practice, obstetricians are called upon to care forpatients suffering from rubella during pregnancy with itspotential to cause fetal malformations. Routine testing forrubella IgG antibodies prior to planning pregnancy is rec-ommended. All susceptible patients should be immunizedand advised against attempting pregnancy for the subse-quent 3 months. Lastly, because of the high prevalence ofthyroid disease in the sub-Himalayan region, the use ofiodized salt and the practice of screening all patients forthyroid disorders are recommended. Thyroid insufficiencyis an important cause of mental retardation in the offspring.

An important requirement of preconceptional counsel-ing is that it should be nondirective. For example, whenasked about the advisability of becoming pregnant, theobstetrician should provide information on the subject asfactual as possible and avoid to tell the patient what todo. The decision to become pregnant despite significantrisks is very personal and based on a multiplicity of vari-ables and considerations that are known only by thepatient and her partner.

Another important aspect of preconceptional counsel-ing is to give consideration to the financial burden associ-ated with the care of a high-risk pregnancy, particularly interms of working disability. Many parents are not awareof the potential impact on the family unit and the person-al cost that they assume when they get pregnant, specifi-cally in terms of time off work and the need for help withchildren and household duties when they are admitted tothe hospital or placed on bed rest at home.

PRENATAL CARE

Not too long ago the main objective of obstetrical prac-tice was the prevention of maternal mortality.

Improvements in the overall health conditions of women,obstetrical anesthesia, laboratory diagnosis, availability ofblood transfusion, and improvements in surgical tech-niques resulted in significant advances in achieving thisobjective, and in industrialized societies maternal mortal-ity became a rare event. Furthermore, maternal morbidityalso markedly decreased. The significant improvementsachieved in maternal outcomes were quickly followed bythe adoption of a second paradigm of obstetrical carewhich was to obtain the best possible fetal outcome.Progress in achieving the fetal objective of obstetrical carehas been amazingly rapid not only because of continuoustechnological developments but also due to the universaladoption of the concept of the fetus as a patient thatclearly established the dual responsibility of the obstetri-cian as provider of care not only for the mother but alsofor the fetus. It was found soon that a small proportion ofall pregnancies was responsible for the large majority ofpoor fetal outcomes, and in the last 30 years an explosionof knowledge about these pregnancies at risk has affectedall aspects of prenatal care and has been responsible forthe development of a new medical speciality in Maternaland Fetal Medicine.

One of the most significant achievements of the newdiscipline in Maternal and Fetal Medicine has been thediscovery and subsequent integration to obstetrical careof new methods for the surveillance of the high-risk preg-nancy. Unfortunately, many of these tests have beenadopted into the regular obstetrical care of low-risk preg-nancies without studies demonstrating their usefulness inthis particular population. This has increased the cost ofpregnancy care, burdened specialized laboratories withunnecessary tests, and has had little to do in improvingthe outcome of low risk women.

In summary, the main objective of prenatal care is theprevention and treatment of abnormal maternal and fetaloutcomes. Prenatal care offers a unique opportunity todetect pathological conditions affecting the pregnancyand implement interventions that may positively affectthese outcomes.

Determination of Gestational Age

An accurate determination of the gestational age and theexpected date of delivery (EDD) is fundamental to themanagement of high-risk pregnancies. Proper assignmentof the EDD is necessary in order to obtain and appropri-ately interpret laboratory tests, to plan and execute therapeutic maneuvers, and to determine the optimalmanagement in certain difficult situations.

It is generally accepted that the best method to determinegestational age is through neonatal evaluation. Unfortu-nately, neonatal evaluation is not useful to the obstetrician,and there are data suggesting that overestimation of


gestational age in very preterm babies and underestimationof gestational age in post-term pregnancies occurs frequent-ly when the neonate is evaluated by the Ballards method ascompared with early ultrasound examination (Alexander etal., 1992). Despite these deficiencies neonatal evaluation ofgestational age is the gold standard to determine theaccuracy of any other method.

Clinical dating

Clinical dating has limited value. Even women who con-ceive in the course of infertility protocols may have signif-icant errors in the estimation of their EDDs. Therefore, allpregnant women including those with reliable clinical cri-teria pointing to a given EDD should have ultrasoundexamination for confirmation of their gestational age.

The variables necessary for clinical estimation of gesta-tional age are the timing and characteristics of the lastmenstrual period (LMP), the findings on the initial pelvicexamination, the date on which fetal heart tones are firstheard, and the relation between the date of the first posi-tive pregnancy test and the menstrual history.

The patients menstrual history is considered adequatefor the purpose of establishing the EDD only if the LMPwas normal in duration and amount of flow, if the priormenstrual periods came at regular intervals, and if thepatient did not use oral contraceptives within 3 months ofher last period. Unfortunately, 30% of patients do not ful-fill those criteria, thus making estimation of the EDDbased on their LMPs unreliable. In a study of more than11,000 pregnancies at McGill University, it was shownthat LMP estimates were particularly inaccurate inpatients with preterm and post-term pregnancies (Krameret al., 1988).

The evaluation of uterine size has limited value foraccurate clinical dating. Among the many variables thatmake assessment of the uterine size unreliable are mater-nal obesity, observer experience, position of the uterus,amount of amniotic fluid, multiple gestation, presence ofuterine myomas, and fetal growth disorders. Studies havedemonstrated that physicians measurements tend tounderestimate the gestational age and have a preferencefor even numbers (Alexander et al., 1989).

The date on which fetal heart tones are first audiblewith Doppler ultrasound devices (10 weeks) or with stan-dard obstetrical stethoscopes (20 weeks) has also beenused to determine gestational age. Similar to other clinicalparameters to evaluate gestational age, the time at whichfetal heart sounds are first heard is an ineffective way toassess gestational age. It has value only when it agreeswith other clinical indicators and with the ultrasoundmeasurements.

In some patients, the time at which the first positivepregnancy test was obtained may be useful to establish the

EDD. The sensitivity of the available over-the-counterpregnancy tests allows the diagnosis of pregnancy at 45postmenstrual weeks. Thus, if a patient has a positivepregnancy test 45 weeks after her LMP the patientsdates become firmly established.

Dating by ultrasound

The ability to visualize with ultrasound different fetalanatomic landmarks and to follow their growth during ges-tation is one of the most important tools that the obstetri-cian has acquired for the evaluation of the fetus. Fetal bio-metry has made it possible to accurately determine the ges-tational age of the fetus and the adequacy of the fetalgrowth. The methods most commonly used to determinethe gestational age and EDD involve measurement of thecrownrump length (CRL) in the first trimester and thebiparietal diameter (BPD), head circumference (HC), femurlength (FL), humerus length (HL), and abdominal circum-ference (AC) in the second trimester. Cross-sectional or lon-gitudinal measurements of these variables are plotted inscattergrams and the data analyzed by polynomial regres-sion to obtain a curvilinear graph. By convention, the 5thand 95th percentiles above and below the curve are used tomeasure the normal dispersion or confidence limits aroundthe mean. The measurements obtained in a given patientcan be compared with the norms, and deviations from nor-mality can be recognized.

Fetal biometry has been fundamental for determining thegestational age and to follow the fetal growth, but this isnot without problems. One of these problems is inadequateinterpretation of fetal measurements which are thought toreveal an error in the patients gestational age when in factthey are indicative of abnormalities of the fetal growth,either fetal growth restriction (FGR) or a large for gesta-tional age fetus. This error may have serious implicationsbecause FGR may not be discovered until late stages, whenfetal hypoxia and acidosis may have already occurred, andalso because an undiscovered large for gestational ageinfant may have serious intrapartum problems. The oppo-site mistake may also occur and normal fetuses may be clas-sified as growth restricted and submitted to unnecessarytesting and intervention. Despite these problems, fetal bio-metry remains one of the most important tools for follow-ing the high-risk pregnancy patient.

Determination of gestational age by ultrasound hassimilar accuracy when performed between 1114 weeksof gestation and 1822 weeks of gestation. This wasdemonstrated in a study of 104 singleton, 81 twins, and33 triplet pregnancies conceived by in vitro fertilization(Kalish et al., 2004). After 22 weeks the margin of errorincreases, and it is necessary to obtain serial measure-ments 34 weeks apart to avoid a significant error. Thereliability of the EDD may be categorized as excellent,


good, or poor by using the set of clinical and ultrasoundcriteria shown in Box 1-4.

Crownrump length

Measurement of the CRL in the first trimester of pregnan-cy is the most accurate method to determine gestationalage. The image should show a longitudinal view of the

embryo and the calipers should be placed at the outeredge of the cephalic pole and the embryonic rump (Figure1-1). The measurements are more accurate when theembryo is visualized with high-frequency vaginal ultra-sound (Lasser et al., 1993). The CRL is accurate and pre-dicts the menstrual age with a variation of + 3 days whenit is obtained between 7 and 10 weeks. The variationincreases with gestation and is + 5 days between 10 and14 weeks. The practical implication of this information isthat between 7 and 10 weeks gestation, a discrepancy ofmore than 3 days between the gestational age calculatedfrom clinical information and the gestational age calculat-ed from the CRL indicates that the gestational age deter-mined by the CRL is the true gestational age and the EDDmust be changed. The same rule applies to a difference of

Table 1-1. Gestational age by crownrump length (615 weeks)

CRL Gestational CRL Gestational CRL Gestational CRL Gestational CRL Gestational(mm) age (mm) age (mm) age (mm) age (mm) age

(weeks) (weeks) (weeks) (weeks) (week)

3 5.9 21 8.7 39 10.8 57 12.3 75 13.64 6.1 22 8.9 40 10.9 58 12.3 76 13.75 6.2 23 9.0 41 11.0 59 12.4 77 13.76 6.3 24 9.1 42 11.1 60 12.5 78 13.87 6.4 25 9.2 43 11.2 61 12.6 79 13.98 6.5 26 9.4 44 11.2 62 12.6 80 14.09 6.9 27 9.5 45 11.3 63 12.7 81 14.1

10 7.1 28 9.6 46 11.4 64 12.8 82 14.211 7.2 29 9.7 47 11.5 65 12.8 83 14.212 7.4 30 9.9 48 11.6 66 12.9 84 14.313 7.5 31 10.0 49 11.7 67 13.0 85 14.414 7.7 32 10.1 50 11.7 68 13.1 86 14.515 7.9 33 10.2 51 11.8 69 13.1 87 14.616 8.0 34 10.3 52 11.9 70 13.2 88 14.717 8.1 35 10.4 53 12.0 71 13.3 89 14.818 8.3 36 10.5 54 12.0 72 13.4 90 14.919 8.4 37 10.6 55 12.1 73 13.4 91 15.020 8.6 38 10.7 56 12.2 74 13.5

From Hadlock FP, Shah YP, Kanon DJ, et al. Fetal crownrump length: reevaluation of relation to menstrual age (518 weeks) with high-resolution real-

time US. Radiology 1992; 182: 5015.

Figure 1-1. Crownrump length.

BOX 1-4

Reliability of the expected date of delivery

Excellent dates

1. Patients with adequate clinical information (known, normalLMP; 2830-day cycles; no recent use of oral contraceptives;uterine size in agreement with dates) plus ultrasound exami-nation between 16 and 24 weeks indicating that the fetalmeasurements are in agreement with the clinical estimationof gestational age.

2. Patients with inadequate or incomplete clinical informationbut with two ultrasound exams between 16 and 24 weeksshowing linear fetal growth and similar EDD.

Good dates

1. Patients with adequate clinical information (as definedabove) and one confirming ultrasound examination obtainedafter 24 weeks of gestation.

2. Patients with inadequate or incomplete clinical informationand two or more ultrasound exams showing adequate growthand similar EDD.

Poor dates Any clinical situation different from those listed above.


5 or more days for pregnancies between 10 and 14 weeksgestation. One of the implications of accurate determina-tion of gestational age by CRL is that the rate of induc-tion for post-term pregnancy is significantly less when thegestational age is based on CRL than when it is based onsecond trimester biometry (Bennett et al., 2004). A possi-ble source of error in the determination of gestational ageby using the CRL is the presence of an embryo with chro-mosomal abnormalities, because abnormal embryos maybe smaller than expected. Table 1-1 shows the gestationalage by CRL between 6 and 15 weeks of gestation.

Biparietal diameter

The BPD is the most accurate measurement to determinethe gestational age in the second trimester of pregnancy.In the majority of cases the BPD is relatively easy toobtain. It is measured in a transverse image of the head atthe level of the thalamus with the calipers placed in theouter edge of the skull surface near to the transducer andin the inner edge of the distal skull (Figure 1-2). Fetuses inbreech presentation may have a flattened head (dolicho-cephaly). If the fetal head looks flattened and elongated,

Table 1-2. Gestational age by BPD measurements

BPD Gestational age (weeks) BPD Gestational age (weeks)

(mm) 10th percentile 50th percentile 90th percentile (mm) 10th percentile 50th percentile 90th percentile

20 12 12 1221 12 12 1222 12.2 12.7 13.223 12.4 13.0 13.624 12.6 13.2 13.825 12.9 13.5 14.126 13.1 13.7 14.327 13.4 14.0 14.628 13.6 14.3 15.029 13.9 14.5 15.230 14.1 14.8 15.531 14.3 15.1 15.932 14.5 15.3 16.133 14.7 15.6 16.534 15.0 15.9 16.835 15.2 16.2 17.236 15.4 16.4 17.437 15.6 16.7 17.838 15.9 17.0 18.139 16.1 17.3 18.540 16.4 17.6 18.841 16.5 17.9 19.342 16.6 18.1 19.843 16.8 18.4 20.2 44 16.9 18.8 20.745 17.0 19.1 21.246 17.4 19.4 21.447 17.8 19.7 21.648 18.2 20.0 21.849 18.6 20.3 22.050 19.0 20.6 22.2 51 19.3 20.9 22.552 19.5 21.2 22.953 19.8 21.5 23.254 20.1 21.9 23.755 20.4 22.2 24.056 20.7 22.5 24.3 57 21.1 22.2 24.558 21.5 23.2 24.959 21.9 23.5 25.1

60 22.3 23.8 25.5 61 22.6 24.2 25.862 23.1 24.6 26.163 23.4 24.9 26.464 23.8 25.3 26.865 24.1 25.6 27.166 24.5 26.0 27.567 25.0 26.4 27.868 25.3 26.7 28.169 25.8 27.1 28.470 26.3 27.5 28.771 26.7 27.9 29.172 27.2 28.3 29.473 27.6 28.7 29.874 28.1 29.1 30.175 28.5 29.5 30.576 29.0 30.0 31.077 29.2 30.3 31.478 29.6 30.8 32.079 29.9 31.1 32.580 30.2 31.6 33.081 30.7 32.1 35.582 31.2 32.6 34.083 31.5 33.0 34.584 31.9 33.4 35.185 32.3 34.0 35.7 86 32.8 34.3 36.287 33.4 35.0 36.688 33.9 35.4 36.6 89 34.6 36.1 37.690 35.1 36.6 38.1 91 35.9 37.2 28.5 92 36.7 37.8 38.9 93 37.3 38.8 39.394 37.9 39.0 40.195 38.5 39.7 40.996 39.1 40.6 41.597 39.9 41.0 42.198 40.5 41.8 43.1

From Kurtz AB, Needleman L. Ultrasound assessment of fetal age. In: Cullen PW, ed. Ultrasonography in Obstetrics and Gynecology (2nd edn).

Philadelphia: Saunders, 1988: 4764.


it is necessary to measure the cephalic index which is theratio of the BPD divided by the occipitofrontal diameter(OFD). The cephalic index normal range is between 0.75and 0.85, and when the value is less than 0.75 the HCshould be used instead of the BPD to calculate the gesta-tional age. It is frequently difficult to obtain adequatevisualization of the transverse plane of the head when thefetal head is in occiput posterior position. In this case it isbetter to determine the gestational age using the femur orthe HL. Table 1-2 shows the gestational age by BPDbetween 12 and 40 weeks.

Head circumference

The HC is measured in the same transverse plane as used tomeasure the BPD and it is not altered by dolichocephaly orbrachycephaly of the fetal head. Most ultrasound machinesmeasure the HC by means of electronic calipers but it canbe calculated from the BPD and the OFD of the head, usingthe equation HC = BPD + OFD/2.

Femur length

The FL is an excellent parameter to calculate the gesta-tional age, because it is not significantly affected byalterations in the fetal growth. It is measured in the bonecloser to the transducer from the origin to the end of thebone shaft without including the femoral head or the dis-tal epiphysis (Figure 1-3). Table 1-3 shows the gestation-al age according to the FL.

Humerus length

The HL is another parameter, relatively easy to obtain,that is used for determination of the gestational age. It ismeasured in a similar way as the FL is measured.

Abdominal circumference

The AC is a less reliable parameter when used to determinegestational age because it is very sensitive to alterations in

fetal growth. For the same reason the AC is the mostimportant parameter in the estimation of fetal weight.The AC should be measured in a transverse plane at the

Figure 1-3. Femur length.

Table 1-3. Gestational age by femur length measurements

Gestational age Femur percentile(weeks) 5 50 95

12 4 8 1313 6 11 1614 9 14 1815 12 17 2116 15 20 2417 18 23 2718 21 25 3019 24 28 3320 26 31 3621 29 34 3822 32 36 4123 35 39 4424 37 42 4625 40 44 4926 42 47 5127 45 49 5428 47 52 5629 50 54 5930 52 56 6131 54 59 6332 56 61 6533 58 63 6734 60 65 69 35 62 67 7136 64 68 7337 65 70 7438 67 71 7639 68 73 7740 70 74 79

From Jeanty P, Cousaert E, Cantraine F, et al. A longitudinal study of fetal

limb growth. Am J Perinatol 1984; 1: 13644.

Figure 1-2. Biparietal diameter.


level of the intrahepatic course of the umbilical vein. Theribs should be present at the sides of the image and the

view should include the stomach bubble (Figure 1-4).When the umbilical vein is seen at its entrance in theabdomen, the plane is oblique and the measurement is notaccurate. Table 1-4 show the gestational age in relation toAC measurements.

Other parameters used to determine

gestational age

Other parameters are not commonly used to determinethe fetal gestational age. These include the length of thetibia, the radius, the ulna, the clavicle, the foot, the binoc-ular diameter, the sacrum and the transverse cerebellardiameter.

Determination of gestational age

Most ultrasound machines have incorporated into theirsoftware nomograms to calculate the gestational ageusing the BPD, HC, AC, FL, CRL, and HL. Some equip-ment includes nomograms for gestational age using thetransverse diameter of the cerebellum and the size of thegestational sac. The estimated gestational age calculatedfrom several of these variables is averaged and the resultexpressed as weeks and days of gestation. The EDD isthen calculated automatically. Most of the equipment alsocalculates the gestational age and the EDD from thepatients menstrual history and so discrepancies in thisinformation can be apparent to the examiner.

Prevention of Abnormal Maternal and Fetal Outcomes

The prevention of adverse maternal and fetal outcomesis the fundamental objective of prenatal care. The worseadverse outcomes are maternal and fetal death. Otherpoor outcomes are the birth of an infant with chromo-somal abnormalities or congenital defects and the birthof a premature infant. The birth of an asphyxiated infantthat later develops cerebral palsy is another tragic out-come. These outcomes have devastating consequencesfor the pregnant woman, her family and for society ingeneral. Unfortunately, the frequency of these outcomesis unacceptable, particularly in developing countries,and most investigators agree that it is necessary toimplement a multidisciplinary approach involving healthcare providers, community leaders, local governments,and the international community to have an impact onthis problem. This book is entirely dedicated to thedescription and analysis of conditions causing abnormalpregnancy outcomes. This chapter is limited to theanalysis of severe poor outcomes that are not covered inother chapters of the book, particularly maternal andfetal death.

Figure 1-4. Abdominal circumference.

Table 1-4. Gestational age by abdominal circumferencemeasurements

Gestational age (weeks) 2SD Mean +2SD

12 31 56 8113 44 69 9414 56 81 10615 68 93 11816 80 105 13017 92 117 14218 104 129 15419 116 141 16620 127 152 17721 139 164 18922 150 175 20023 161 186 21124 172 197 22025 183 208 23326 194 219 24427 204 229 25428 215 240 26529 225 250 27530 235 260 28531 245 270 29532 255 280 30533 265 290 31534 275 300 32535 284 309 33436 293 318 34337 302 327 35238 311 336 36139 320 345 37040 329 354 379

From Hadlock FP, Deter RL, Harrist RB, et al. Fetal abdominal circumfer-

ence as a predictor of menstrual age. Am J Roentgenol 1982; 139:

36770.


Maternal death

Maternal death is the worst possible outcome of pregnan-cy. In industrialized countries, access to prenatal care andavailability of legal abortion have been responsible for asignificant decrease in the frequency of maternal deaths toabout 8 per 100,000 live births. This is in dramatic con-trast to developing countries, like Ethiopia, where the fre-quency of maternal deaths has been calculated at 1528per 100,000 births (Jowett, 2000).

Worldwide figures are impressive and it has been esti-mated that one woman dies every minute from the effectsof pregnancy or childbirth (Tracy and Tomich, 2002).Maternal mortality rates (MMRs) have been lowered dra-matically in the developed world, but continue to remainappallingly high in the underdeveloped countries asshown in Table 1-5.

MMR in India continues to be unacceptably high;however, the MMR reveals wide regional variations asgiven in Table 1-6.

The low MMR achieved in Kerala (southern India) isthe result of high literacy rate, better nutrition, improvedstatus of women in society, and their demand for betterhealth care. In the lesser progressive states of northernIndia, MMR continues to remain high. The mean MMRfor India is 407 per 100,000 live births (Dutta, 2004). A great deal needs to be accomplished in the field ofmaternal health and welfare.

The Center for Disease Control (CDC) and theAmerican College of Obstetricians and Gynecologists(ACOG) have defined pregnancy-associated deaths asthose that occur during pregnancy or after 1 year of deliv-ery. Pregnancy-associated deaths are pregnancy-related ifthe death resulted from complications of pregnancy, wasthe result of a chain of events initiated by pregnancy, orwas due to an unrelated event aggravated by pregnancy orits management. If the cause of the death is not related topregnancy, it is considered nonpregnancy-related. TheInternational Classification of Diseases defines maternaldeath as the death of a woman while pregnant or after 42days (or 1 year for late maternal deaths) of delivery, irre-spective of the duration and site of the pregnancy, fromany cause related to or aggravated by pregnancy, but notfrom accidental or incidental causes.

It is clear from these figures that the frequency ofmaternal deaths is similar in industrialized countries.Also similar are the main causes of maternal death(Table 1-7). In order of frequency the most importantcauses of maternal death in industrialized countries arehypertensive disorders, thromboembolism, bleeding,and abortion (Khan et al., 2006). Approximately 10%of maternal deaths occur during labor, 60% during thefirst postpartum week, and 25% during the second post-partum week (Berg et al., 1996). Even minimal prenatalcare seems to be associated with a significant decrease inmaternal mortality, but this association disappears whenthe data are corrected by income and education attain-ment (Harper et al., 2003). In USA, pregnancy-relatedmortality occurs significantly more frequently inAfrican-American mothers.

Table 1-7. Causes of maternal death by geographical criteria

Developed countries: Hypertensive disorders 16.1% Embolism 14.9% Hemorrhage 13.4% Abortion 8.2%

Africa: Hemorrhage 33.9% Sepsis/infection 9.7% HIV/AIDS 6.2% Obstructed labor 4.1%

Asia: Hemorrhage 30.8% Anemia 12.8% Sepsis/infection 11.6% Obstructed labor 9.4%

Latin America and the Caribbean: Hypertensive disorders 25.7% Hemorrhage 20.8% Obstructed labor 13.4% Abortion 12.0%

Table 1-5. Global perspective of MMR

S. Developed MMR/ Developing MMR/No. countries 100,000 LB countries 100,000 LB

1. USA 9.1 India 4072. Scandinavia 7.4 Pakistan 5803. United Kingdom 9 Bangladesh 8504. Japan 9.1 Nepal 12405. Canada 4 Sri Lanka 26 6. Germany 10 Myanmar 2707. Hong Kong 5 Malaysia 698. Singapore 6 China 95

LB = live births

Table 1-6. MMR in different parts of India (mean MMRfor India: 407/10,000 LB)

Indian state MMR Indian state MMR

Andhra Pradesh 436 Karnataka 250Assam 544 Kerala 67Bihar 470 Madhya Pradesh 498Gujarat 189 Maharashtra 236Haryana 236 Orissa 738Himachal Pradesh 356 Punjab 269Rajasthan 625 Tamil Nadu 76Uttar Pradesh 704 West Bengal 264


According to the last WHO systematic review, hyperten-sive disorders are the most frequent cause of death in devel-oped countries and in Latin America and the Caribbean(Khan et al., 2006). In India, the leading direct causes ofmaternal mortality are hemorrhage, sepsis, preeclampsiaand eclampsia, unsafe abortion, and obstructed labor. Todecrease maternal deaths secondary to preeclampsia/eclampsia/HELLP syndrome in developing countries, it isnecessary to increase access to prenatal care. Since access tocare is not a limiting factor in industrialized nations, mater-nal mortality secondary to preeclampsia may be related toinadequate diagnosis and therapy. It is also important thatdeath as a result of hypertension during pregnancy is agerelated and occurs more frequently in older women than inthose aged < 25 years. The reader will find more informa-tion about this subject in the chapter on hypertension dur-ing pregnancy.

Prevention of maternal death due to thromboembolicdisease requires search for all known thrombophiliasbefore or at the beginning of prenatal care. Unfortunately,these tests are expensive and have limited positive predic-tive value. A single laboratory test capable of detectingmultiple thrombophilias would be ideal for the screeningof the obstetrical population. A test with these character-istics, thrombin generation, has been used prospectively ina nonpregnant population at high risk for recurrentvenous thromboembolism and was found to be a gooddiscriminator between patients at high and low risk ofrecurrent deep vein thrombosis (Hron et al., 2006). A sig-nificant number of cases of thromboembolic disease dur-ing pregnancy can be prevented by the liberal use of pneu-matic compression stockings in women who rest in bedfor prolonged periods of time, such as those with threat-ened preterm labor, preeclampsia, and premature ruptureof the membranes. Prophylactic heparinization with low-dose fractionated or unfractionated heparin in womenwith risk factors for thromboembolization will also beuseful to decrease the incidence of this problem. The read-er will find more information about this subject in thechapter about hematologic complications of pregnancy.

In industrialized countries where patient access to careis not a limiting factor, the majority of maternal deathsdue to bleeding are preventable and are due to substan-dard care (de Swiet, 2000). Despite multiple advances indiagnostic tools, blood banking, interventional radiology,drug therapy, mechanical devices, and surgical techniquesfor bleeding control, women continue to die from obstet-rical hemorrhage. Obviously, there is a problem with theapplication of technology and with adequate use ofresources in cases of obstetrical hemorrhagean areawhere continuous education of health care providers mayhave a significant effect. The interested reader will findmore information about this subject in the chapter aboutbleeding during pregnancy.

Maternal death secondary to infection exhibited a sig-nificant decrease with the availability of legal abortionbut is on the rise again. This trend is more apparent indeveloping countries with a high frequency of infectionsby the human immunodeficiency virus (HIV). In industri-alized countries, overwhelming sepsis caused by antibiot-ic-resistant bacteria is responsible for a significant propor-tion of infection-related deaths.

Maternal death secondary to abortion is still a signifi-cant problem in developing and industrialized countries.According to the last WHO systematic review, 8.2% ofmaternal deaths in developed countries are secondary toabortiona figure that is only surpassed by Latin-American and Caribbean nations with an incidence of12% (Khan et al., 2006) and 13% in India. In contradis-tinction, the frequency of maternal deaths secondary toabortion is 3.9% in Africa and 5.7% in Asia. This is analarming problem that can be explained partially by thelack of availability of legal abortion in developing coun-tries but has no adequate explanation in industrializedcountries where abortion is legal. Direct obstetric causesrelate to maternal deaths resulting from complications ofpregnancy, labor, puerperium due to interventions, omis-sions, or incorrect treatments, or from a chain of eventsresulting from any of the above.

In summary, maternal death is an untenable publichealth problem that requires priority attention. Mostmaternal deaths directly or indirectly related to pregnancyare preventable, but this requires significant social and gov-ernmental efforts to eliminate poverty and restrictions tohuman rights and individual efforts from health careproviders, taking care of pregnant women to keep up withthe methods to identify women at risk and to aggressivelytreat those complications that may result in maternal death.

Stillbirth

Stillbirth is a fetal death occurring after 20 weeks gesta-tion or when the fetus weighs more than 500 g. The still-birth rate in USA in 2002 was 6.4 per 1000 births. Blackwomen have more than twice the rate of stillbirth thanthat of Caucasian females (Silver, 2007). A stillbirth is amajor obstetrical catastrophe at any gestational age butthe emotional pain and distress caused by this eventincreases in direct relation to the duration of pregnancy.

Some of the risk factors associated with fetal death arethe presence of maternal medical complications, advancedmaternal age, Black race, low socioeconomic status, obe-sity, high cigarette use, history of prematurity, and adverseoutcome in a prior pregnancy (Huang et al., 2000; Froenet al., 2001; Vintzileos et al., 2002a; Kahn et al., 2003;Fretts, 2005). Few of these high-risk factors can be modi-fied during prenatal care. However, their identificationmakes it possible to follow these women with frequent


clinical and laboratory assessments in the hope of pre-venting an abnormal outcome. One study of 98 stillbirths(Chibber, 2005) identified several risk factors for fetaldeath. The most frequent were nulliparity, multiparity(more than five pregnancies), low socioeconomic status,maternal age less than 18 or greater than 40 years, pre-conceptional weight greater than 70 kilograms (155 lbs),less than three prenatal office visits, and late prenatalcare. These are factors that cannot be modified duringprenatal care and have only prognostic importance. Arecent systematic review (Fretts, 2005) identified 15 riskfactors for stillbirth. The 3 occurring most frequentlywere preconceptional obesity, socioeconomic status, andadvanced maternal age. These are variables that cannot becorrected during prenatal care.

In Latin-American countries the lack of prenatal careincreases four times (RR 4.26, 95% CI 3.844.71) therisk of fetal death (Conde-Agudelo et al., 2000). In USAabsence of prenatal care increases the relative risk (RR) offetal death 2.9 times in the African-American and 3.4times in the Caucasian population. Prenatal care decreas-es the possibility of fetal death even if other high-risk fac-tors are present (Vintzileos et al., 2002b). The absence ofprenatal care also affects the RR of neonatal death whichincreases 1.4 times for African-American and 1.5 timesfor Caucasians (Vintzileos et al., 2002b). As little as oneprenatal visit improves the outcome of pregnancy andmay decrease the risk of perinatal death by 20%(Mondestin et al., 2001).

The known causes of stillbirth are fetal, placental, andmaternal (Table 1-8). However, the etiology of between25 and 40% of stillbirths remains unknown despite care-ful search for an explanation. At present only approxi-mately 25% of stillbirths can be prevented. The mostimportant preventable category is placental insufficiency,which may be secondary to abnormal placentation,thrombophilia, or other factors. Placental insufficiency is

also the main cause of stillbirth when medical conditionssuch as hypertension or diabetes affect the mother andwhen the obstetrical history reveals placental insufficien-cy in a prior pregnancy. For this reason the large majori-ty of tests for antepartum fetal surveillance are designedto investigate the possibility of placental insufficiency andthe fetal response to hypoxia.

The relative frequency of the causes of stillbirth is dif-ferent depending on the gestational age when the fetaldeath occurs. Between 24 and 28 weeks the most commoncauses of fetal death are infection, abruptio placenta, con-genital fetal abnormalities, and unexplained fetaldeath. Between 28 and 36 weeks the most common rea-sons are unexplained, FGR, and abruptio placenta.After 37 weeks the most common etiologies are unex-plained, FGR, and abruption but the frequency ofunexplained stillbirths increases markedly when com-pared with the 2836 weeks group (Fretts, 2005).

The role of the obstetrician in the prevention of still-birth starts with the identification of patients at risk forthis outcome: advanced maternal age, obesity, high ciga-rette use, low socioeconomic status, late and limited pre-natal care, and women with medical complications suchas diabetes, hypertension, connective tissue disorder, thy-roid gland dysfunction, cardiac or renal disease, andsevere asthma (Huang et al., 2000; Froen et al., 2001). Allof these patients should have a first trimester screening foraneuploidy and a second trimester quad screening for theprediction of pregnancy outcome. Women with elevatedconcentrations of serum alpha-fetoprotein (MSAFP) inthe second trimester of pregnancy unexplained by sonog-raphy are at increased risk for fetal death, FGR,preeclampsia, and premature rupture of membranes(Waller et al., 1991; Simpson et al., 1995). The risk ishigher if the MSAFP concentration is greater than 3 mul-tiples of the mean (MoM), but women with MSAFPbetween 2.0 and 3.0 MoMs are also at high risk. Womenwith low concentrations of MSAFP, equal or less than0.25 MoMs, are also at risk for fetal loss (Burton, 1988).Unexplained elevations of maternal serum hCG (humanchorionic gonadotropin) in the second trimester are alsoassociated with poor pregnancy outcomes, includingpreeclampsia, growth restriction, preterm delivery, andfetal death. The association is strongest when the hCGconcentration is equal to or greater than 4.0 MoMs, butvalues equal to or larger than 3.0 MoMs are of concern(Gonen et al., 1992; Towner et al., 2006). Low unconju-gated estriol, undetectable or less than 0.15 MoMs, is alsoassociated with fetal death, growth restriction, placentalsulfatase deficiency, and SmithLemliOpitz syndrome(Kowalczyk et al., 1998; Schoen et al., 2003). Increasedmaternal serum concentration of inhibin A in the secondtrimester is associated with the development of severepreeclampsia (Kim et al., 2006).

Table 1-8. Etiology of stillbirth

Fetal Multifactorial genetic defects 16% Aneuploidy 5% Other genetic defects 2% Fetal infection 5%

Placenta Placental insufficiency 14% Abruptio placenta 12% Cord accidents 4% Fetomaternal bleeding 5%

Maternal Diabetes 3% Hypertension 5% Other maternal diseases 3%

Unknown 25%


Women with risk factors for stillbirth and abnormalvalues of one or several analytes in the second trimesterquad screening require careful and systematic follow-upclinically and with serial ultrasound examinations. Theultrasound follow-up of the fetal growth is importantbecause the incidence of stillbirth in fetuses small forgestational age is 46.8 per 1000 live birth as comparedwith 4 per 1000 in fetuses growing appropriately. Uterineand umbilical Doppler should be measured starting at 24weeks of gestation and further fetal evaluation dictated bythe result of these exams and the pattern of fetal growthby ultrasound examination. Early delivery may be neces-sary if there is clear evidence of fetal compromise.

Post-term pregnancy is a condition associated withstillbirth. The incidence of fetal deaths is more than dou-ble when the gestational age is 40 weeks or more as com-pared with pregnancies between 38 and 40 weeks. Theincrease in mortality associated with post-term pregnancyis quite evident when the stillbirth rate is calculated cor-rectly, using the number of undelivered fetuses as thedenominator rather than the number of live births (Divonet al., 2004). Preventative intervention consists of deliverywhen the pregnancy reaches 40 weeks if the cervix is ripeand delivery at 41 weeks in all other cases.

It is important to investigate the cause of a stillbirth. Ifthe cause of a fetal death can be identified, the family willhave answers about the possibility of recurrence and theavailability of medical treatment to prevent recurrence.There is no universally accepted evaluation plan to deter-mine the cause of stillbirth, but it is widely accepted thatpathological examination of the placenta, fetal autopsy,and karyotype are the most important elements of thatassessment. The usefulness of the KleihauerBetke test forfetalmaternal hemorrhage, anticardiolipin antibodies,thrombophilia, and TORCH titer is limited.

Neonatal death

Neonatal death is another catastrophic outcome that inmany occasions is a direct consequence of antepartumand intrapartum conditions. The incidence of neonataldeaths in USA is approximately 4.5 per 1000 live births.There are significant regional variations in the neonataldeath rate that are a reflection of the quality of neonatalcare. The neonatal mortality figures are much better forinfants born in hospitals with Newborn Intensive careUnits (NICU) than in hospitals with no NICU or smallcommunity NICUs (Cifuentes et al., 2002). There areracial differences as well and the neonatal mortality forBlack infants is more than twofold greater than that inCaucasians. The Center for Vital Statistics of the UnitedStates classifies infant deaths as all those that occur with-in 1 year of birth. Neonatal deaths are subdivided intoearly neonatal (06 days), late neonatal (727 days), and

postneonatal (28 days to 11 months). Early neonataldeaths constitute 80% of all neonatal deaths and lateneonatal most of the remaining 20%.

The most frequent causes of neonatal deaths in USAare congenital malformations and chromosomal disorders(37%), prematurity (18.2%), complications of pregnancy,labor and delivery (15.4%), maternal complications ofpregnancy (8.2%), placental and cord abnormalities(5.5%), and intrauterine hypoxia or birth asphyxia(2.9%). The number of neonatal deaths secondary toantepartum and intrapartum asphyxia has decreased sub-stantially in USA. Similarly, with the generalized use ofantepartum glucocorticoids and neonatal surfactant thenumber of respiratory deaths associated with prematurityhas also markedly decreased. The overwhelming majorityof neonatal deaths worldwide occur in developing coun-tries, with the largest neonatal mortality rates in sub-Saharan Africa and south-central Asia. The main causesof neonatal mortality in developing countries are prema-turity, infection, and birth asphyxia.

Obstetrical prevention of neonatal mortality is a com-plex task. The largest contributors in USA are congeni-tal malformations. The effect of these conditions onneonatal mortality can be reduced by early diagnosisand pregnancy termination. Also, some of these condi-tions (neural tube defects) can be prevented with ade-quate ingestion of folic acid in the periconceptional peri-od. Prevention of prematurity has been unsuccessful sofar. However, a frequent contributor to preterm birth isthe significant increase in multifetal gestations due to theuse of ovulation-inducing agents and assisted reproduc-tive techniques. A serious and generalized effort to avoidiatrogenic multifetal gestations will have an impact onneonatal mortality rates.

The perinatal mortality rates (PNMRs) in countries ofthe Indian subcontinent (India, Pakistan, and Bangladesh)are three- to fivefold higher than in the developed coun-tries. Lack of antenatal care, lack of patient compliance,lack of facilities for prenatal fetal health monitoring andinstitutional care, and deficient neonatal care servicescontribute to the persistent high PNMRs in the develop-ing countries. The PNMRs per 1000 births from differentparts of India ranged from 34.16 in Mumbai (Daftary andMehta, 1994) to 107 in north Bengal (Saha and Saha,2002). PNMRs vary in different parts of India dependingon the socioeconomic strata, literacy, nutritional status,quality of prenatal care, urban or rural setting, and facil-ities available for neonatal care. The common causes ofperinatal mortality (based on the surveys by Rao et al.(2001), Jotwani et al., (2001), and Gaddi and Seetharam(2001)) include prematurity (27%), low birth weight(16%), birth asphyxia (17%), infections (12%), congeni-tal malformations (7%), birth trauma (5%), respiratorydistress syndrome (13%), and the rest (3%).


Preterm delivery and preeclampsia

Preterm delivery and severe preeclampsia are two fre-quent poor pregnancy outcomes. An accurate test for theprediction of women destined to deliver prematurely or todevelop preeclampsia will be extremely valuable even inthe absence of adequate means to treat those conditions.Such a test or tests will permit the selection of a cohort ofpatients that can be systematically analyzed to betterstudy the disease and to develop adequate therapies. Moreinformation about the prediction of preterm delivery andpreeclampsia will be found in the corresponding chaptersof this book. At this time it is sufficient to say that theadvent of cervical length measurements by ultrasound andthe determination of fetal fibronectin in the vaginal secre-tions have been important steps in the prediction ofwomen destined to deliver prematurely. Similarly, thecombination of maternal serum inhibin A, activin A, anduterine artery Doppler at 23 weeks of gestation has a sen-sitivity between 75 and 92% for detecting women thatwill develop preeclampsia, with a false positive rate of 5and 10%, respectively (Spencer et al., 2006). These devel-opments raise hopes of rapid advancements in the upcom-ing years in the identification and treatment of these seri-ous obstetrical complications.

Low-risk pregnancies

One question without answer at this time is if low-riskpregnant women need to be screened for abnormal out-comes. More than 20% of women with negative personaland family history have abnormal outcomes, particularlypreterm labor, FGR, and preeclampsia (Moutquin et al.,1987). The high incidence of abnormal outcomes clearlyjustifies the screening of low-risk women. Although thereare no adequate preventive measures for any of thesethree frequent obstetrical complications, knowledge of ahigh probability of disease will be valuable because fetal,neonatal, and maternal deaths may be prevented by clos-er surveillance and early pregnancy interruption.

ANTEPARTUM FETAL SURVEILLANCE

The timely detection of morbid changes in the fetal statusfollowed by adequate interventions to avoid death or dis-ability is one of the most important objectives of prenatalcare. Unfortunately, despite all the advances of the last 40years this goal remains an unfulfilled promise and some,mostly acute, catastrophic changes in fetal status remainunpredictable and nonpreventable. The largest advanceshave been made in the assessment of the fetus at risk ofdeath and morbidity secondary to placental insufficiency,and there are numerous tests available for that purpose.One of these tests, Doppler studies of the maternalplacental and placentalfetal circulation, has acquired

significant importance in the assessment of placental insuf-ficiency because Doppler abnormalities are detectable daysbefore the onset of more apparent clinical changes. Dopplerevaluation of the fetal middle cerebral artery (MCA) in theassessment of fetal anemia is another example of the valueof this technology for fetal surveillance.

There are limitations to the generalized use of tests offetal well being in obstetrical practice. In the first place,there is no ideal single test that can detect all fetal prob-lems. In the second place, none of the tests for fetal sur-veillance are absolutely specific and interventions due toa false positive test may lead to iatrogenic preterm deliv-ery and increased neonatal morbidity. Finally, on manyoccasions the tests of fetal well-being are unable to time-ly detect the fetal problem and intervention has no ben-eficial effect. Unfortunately, patients are not adequatelyinformed about the limitations of these tests and haveunreasonable expectations that when unfulfilled gener-ate animosity toward the obstetrician and are the sourceof medical legal problems.

The methods used to detect and evaluate the severity ofacute or chronic fetal hypoxia are biophysical in nature.The tests used at present are:

1. Fetal movement count2. The nonstress test (NST)3. The contraction stress test (CST)4. The fetal biophysical profile (BPP)5. The modified biophysical profile (MBPP)6. Umbilical, cerebral, uterine, and venous Doppler7. Percutaneous umbilical blood sampling

Fetal Movement Count

Maternal perception of fetal movements has been a tradi-tional indication of fetal well-being. In contrast, adecrease or cessation of fetal movements has ominousimplications and is associated with fetal compromise anddeath. Maternal assessment of the frequency of the fetalmovements is the simplest and least costly method for theevaluation of fetal well-being in the second half of preg-nancy. Several studies have demonstrated a good correla-tion between fetal movements perceived by the motherbetween 28 and 43 weeks of gestation and fetal move-ments detected by real-time ultrasound. The periods offetal activity last for about 40 minutes and the periods ofrest about 20 minutes. The mother usually perceivesbetween 70 and 80% of these movements. Observationsby ultrasound indicate that the fetus has gross movementsapproximately 10% of the time and as many as 30 move-ments may occur in 1 hour. The peak activity is between9:00 pm and 1:00 am, a time that usually coincides witha period of low maternal plasma glucose levels.

Several factors influence the perception of fetal move-ments including maternal obesity, excessive amount of


amniotic fluid, and ingestion of medications. These fac-tors cause significant subjective variability in the percep-tion of movements. For this reason investigators havedeveloped methods with a more quantitative value. Themethod most commonly used is the count to 10 (Mooreet al., 1989) which is preferred by the patients over othermethods (Christensen et al., 2003). Patients are instructedto begin counting fetal movements until they reach 10movements. If the 10 movements are noticed in 10 hoursor less, the fetus most probably is in good health. If themother notices less than 10 movements in 10 hours, sheshould have further evaluation. Also, the patient shouldhave additional evaluation if there is a doubling in thenumber of hours that are usually required to complete the10 movements. Clinical trials on the usefulness of fetalmovement counting in preventing fetal death have pro-duced contradictory results. A study (Moore et al., 1989)concluded that screening with the count to 10 methodwas effective in reducing fetal mortality. Another study ina large population (Grant et al., 1989) found no decreasein antepartum fetal death rate between no counting androutine counting of fetal movements.

The Nonstress Test

The test most commonly used for antepartum evaluation ofthe fetal status is the NST. The NST is noninvasive, easilyperformed and interpreted, and readily accepted bypatients. The test looks for the presence of temporary accel-erations of the fetal heart rate (FHR) associated with fetalmovement. Heart rate acceleration with movement is areflex that involves the cerebral cortex and is affected byphysiologic or pathologic influences on the fetal brain. Themost common physiologic situation suppressing this reflexis fetal sleep and the most common pathologic condition isfetal hypoxia. For this reason, the absence of accelerationsduring a NST must be considered a consequence of fetalhypoxia unless it can be explained otherwise.

NSTs are categorized as reactive or nonreactive. Areactive or normal NST (Figure 1-5A) is characterized bytwo or more FHR accelerations of at least 15 beats perminute (bpm) and lasting at least 15 seconds from base-line to baseline within a 20-minute period with or with-out association with fetal movements as perceived by thewoman. A nonreactive NST (Figure 1-5B) is character-ized by lack of accelerations, as previously described, fora period of 40 minutes. The NST is performed asdescribed in Box 1-5. Vibroacoustic stimulation (VAS)also elicits acceleration of the FHR and has been addedto the protocol to perform the NST (Zimmer et al.,1993). FHR reactivity, spontaneous or obtained withVAS, is a solid indicator of fetal health and absence ofacidosis. VAS uses stimulation with an artificial larynx(sold in USA by A T & T) over the fetal head during 13seconds. The instrument produces a vibratory acoustic

Figure 1-5. Reactive and non-reactive non-stress tests. A,Reactive NST. Acceleration of the fetal heart of 15 or more bpm,lasting 15 or more seconds following vibroacoustic stimulation. B,Nonreactive NST. There is decreased variability; no accelerationin association with contraction.

stimulus of approximately 80 Hz and 82 db. A healthyfetus will respond with sudden movement (startleresponse) followed by acceleration of the FHR. VAS wasoriginally designed to decrease the time spent in the per-formance of the NST that is frequently prolongedbecause of episodes of fetal sleep, and soon the NST withVAS became the predominant method to perform theNST. The response to VAS is gestational age dependent.Fetuses of less than 24 weeks do not respond to VAS.Between 24 and 27, 2730, and >31 weeks, 30, 86, and96% of the fetuses will respond to the vibroacousticstimulus, respectively. In the majority of cases, the accel-eration of the FHR that follows stimulation lasts for sev-eral minutes. Other normal fetuses respond with a seriesof 25 accelerations lasting 2060 seconds each.Maternal perception of fetal movement following VAS isanother indicator of fetal well-being. However, if themother does not feel the baby moving following VAS but

A

B


there is a clear accelerative response of the FHR, the testis normal. An abnormal response to VAS, found in fetus-es with chronic asphyxia, consists of no acceleration ordeceleration of the FHR. VAS is safe, and no evidence ofhearing impairment or other abnormality has been report-ed in neonates exposed to VAS in utero.

There are several factors that may influence the resultof VAS. Some of them are the thickness of the maternalabdominal wall, the amount of amniotic fluid, the pres-sure exerted by the examiner in holding the artificial lar-ynx against the abdomen, and the intensity of the stimu-lation. The influence of these factors is relatively small,and only 2% of NSTs are nonreactive following VAS. Ofthose NSTs that are nonreactive to VAS, 17% are fol-lowed by positive CSTs or by BPPs equal to or less than 4.Another area of application of VAS is in the managementof intrapartum non-reassuring FHR tracings. In thesecases, a positive response to VAS stimulation indicatesthat the fetus is not acidotic.

The NST is markedly influenced by the gestational ageand approximately 50 and 15% of the NSTs performed inhealthy, noncompromised fetuses 2428 and 2832weeks, respectively, are nonreactive. Less false positiveresults will occur if the definition of reactivity is modifiedfor women between 24 and 32 weeks and the NST isaccepted as reactive if the peak of the accelerations reach-es at least 10 bpm and the accelerations have a durationof at least 10 seconds.

The false negative rate of the test (reactive NST in a fetuswho is actually in distress) is 3.2 per 1000, indicating that

the likelihood of fetal death or serious fetal morbidity fol-lowing a reactive test is very low. The frequency of stillbirthwith reactive NST performed every week is 6.1 per 1000.When the frequency of testing is increased to twice weekly,the frequency of false negatives is substantially less, 1.9 per1000 (Boehm et al., 1986). The false positive rate (nonreac-tive results in normal patients) is very high: 50% for morbidity and 80% for mortality, indicating that the prob-ability of serious fetal problems when the test is nonreactiveis also low. The high number of false positive results makesnecessary to use additional corroborative testing beforeintervening in the majority of nonreactive NST. The largenumber of false positive results and the possibility that thetest cannot recognize early stages of fetal compromise arethe main concerns surrounding the use of the NST.

One of the reasons behind the high frequency of falsepositive results with the NST is that its interpretation relieson only one variable, the presence of accelerations of theFHR associated with fetal movement, and it ignores otherimportant information such as FHR variability and thepresence or absence of decelerations. These observationsare of value in determining the true significance of a non-reactive result. A nonreactive result in the presence ofpoor FHR variability or decelerations strongly suggestsfetal compromise. On the other hand, a nonreactiveresult when the FHR variability is normal and decelerationsare absent most probably is a false positive result. The NSTshould be analyzed taking into consideration all the factorsthat provide information about the fetal well-being. Aninterpretation based solely on reactivity is incompleteand increases the incidence of false positive results. Thevariables that must be evaluated in the NST are:

1. Baseline FHR 2. Variability of the FHR3. Presence or absence of accelerations4. Presence or absence of decelerations

Each of these variables should be analyzed separately. Anormal baseline heart rate frequency is between 110 and160 bpm. Abnormalities in this variable are tachycardia(frequency greater than 160 bpm) and bradycardia (fre-quency less than 110 bpm). Alterations of the baseline fre-quency are most frequently due to maternal medicationsand maternal temperature but tachycardia and bradycardiamay also occur with fetal hypoxia. Variability is of theutmost importance in the evaluation of the NST. Modernfetal heart monitoring equipment allows, under most cir-cumstances, adequate evaluation of variability using indirectrecording of the FHR obtained with Doppler ultrasound.FHR variability depends on the interaction of the fetal sym-pathetic and parasympathetic nervous systems and is influ-enced by gestational age, maternal medications, fetal con-genital anomalies, fetal acidosis, and fetal tachycardia. Anonreactive NST in the presence of adequate variabilitymost probably corresponds to a false positive result. In

BOX 1-5

How to perform a nonstress test

1. Place patient in the semi-Fowlers position. Use pillowsunder one of the hips to displace the weight of the uterusaway from the inferior vena cava. Take the patients bloodpressure every 10 or 15 minutes during the procedurebecause supine hypotension may cause a nonreactive result.

2. Apply the tococardiographic equipment to the maternalabdomen and observe the uterine activity and FHR for 10minutes. Instruct the patient to push the calibration button ofthe uterine contraction tracing every time she feels fetalmovement (FM).

3. A reactive test is present when two or more FHR accelera-tions are clearly recorded during a 20-minute period, each of15 or more bpm and lasting 15 or more seconds, usuallyoccurring simultaneously with episodes of fetal activity.

4. If no spontaneous FM occurs during the initial 20 minutes ofobservation, the test is continued for another 20 minutes, andduring this period FM is provoked by external manipulation.If there is no acceleration with spontaneous or repeatedexternal stimuli during a 40-minute period, the test is consid-ered nonreactive.

5. The test is unsatisfactory (equivocal) if the quality of the mon-itor tracing is inadequate for interpretation.


contradistinction, a nonreactive NST associated withdecreased or absent variability most probably is abnormaland caused by fetal hypoxia. The presence of accelerationsof the FHR associated with fetal movements or in responseto fetal stimulation is a reliable sign of fetal health and, asmentioned before, they occur more frequently as the preg-nancy approaches term. The absence of accelerations in theNST may be a sign of fetal compromise but most common-ly corresponds to periods of fetal sleep. The absence ofdecelerations in the NST is reassuring. The presence ofspontaneous severe variable or late decelerations is worri-some and suggests fetal compromise. Variable decelerationsmay be seen in up to 50% of NSTs and if they are mild andnonrepetitive, do not suggest fetal compromise. However,repetitive variable decelerations are important and suggestfetal compromise even if the FHR pattern is reactive.

One concern about the use of the NST for primaryfetal surveillance is that the test cannot recognize earlystages of fetal compromise. This consideration has notbeen supported by clinical trials and has not impactedthe increasing use of the NST as the primary tool forfetal surveillance in USA. Another problem with thegeneralized use of the NST for primary fetal surveil-lance is the tendency to use the test for all patients withhigh-risk pregnancies without understanding that, insome situations, other tests may be more useful(Kontopoulos and Vintzileos, 2004). One example ofthis situation is the use of the NST to follow patientswith post-term pregnancies, without simultaneous eval-uation of the amniotic fluid volume by ultrasound, orthe use of the NST alone, instead of combining its usewith umbilical artery (UA) Doppler, for the follow-up offetuses with growth restriction.

Purandare (2003) mentioned that of all the variousmethods of antepartum fetal surveillance that are in usetoday, the nonprovocative tests (NST, BPP, and MBPP)are safe and effective for use in an outpatient setting.Whereas the NST is primarily an indicator of fetalhealth, the CST is an indicator of uteroplacental func-tion. The slower the interruption of oxygen delivery tothe fetus, the more likely that there will be an adaptationby the fetus to the hypoxic state, reflecting in loss of beatto beat variability, diminished accelerations, and latedecelerations while the baseline FHR is maintained.Acute hypoxia (placental abruption) leads to markedfetal bradycardia. In patients with postdatism, the NSTshould be interpreted in light of the amniotic fluid index.Whereas in case of suspected IUGR, reduced accelera-tions in spite of fetal movements, FHR decelerationswith uterine contractions, diminished variability withbaseline tachycardia are indicative of poor placentalreserve. Vibroacoustic stimulation during the NST hashigh specificity for negative predictive value and accura-cy for prediction of poor perinatal outcome.

NST has a major role to play in the currently existingantepartum care system. Fetal death rate is lower in pop-ulations undergoing antepartum testing as compared tothe general untested population. Protocols using adjunc-tive tests (BPP, color Doppler) help to further improveobstetric outcomes. Gandhi (2003) emphasizes thatthough the false positivity of NST ranges between 65and 70%, a cumulative review of 50,000 cases (Wareand Devoe, 1994) revealed a perinatal mortality of6.2/1000. The false negative rates remain low, indicatingit to be a good predictor of fetal outcome. Further,Gandhi (2003) states that the diagnostic value of NSTremains as good as CST and is simpler to perform.

The Contraction Stress Test

The CST is one of the best available tests for the primaryfetal surveillance of high-risk pregnancies. The test isbased on experimental evidence showing that the utero-placental blood flow decreases markedly or ceases duringuterine contractions. Therefore, uterine contractionscause a hypoxic stress that a normal, healthy fetus cantolerate without difficulty (Figure 1-6A). In contrast, afetus with chronic or acute problems will not be able totolerate such a decrease in oxygen supply and willdemonstrate this by decelerations of the FHR followingcontractions (Figure 1-6B). The protocol for performinga CST is described in Box 1-6. On many occasions thepatient is having spontaneous contractions and it is notnecessary to administer uterine stimulants. In theabsence of spontaneous contractions, nipple stimulationmay be used to elicit uterine activity but the response isunpredictable, and it is better to use oxytocin for thispurpose.

The end point of the CST is the presence or absenceof late decelerations of the FHR following uterine con-tractions. Late decelerations are one of the earliest indi-cators of fetal compromise and they appear prior to lossof variability, decreased movement, or lack of tone.However, a positive test is falsely positive in 50% of thecases, and an important reason for this is the use of asingle variable to classify the test as negative or positive.A positive CST associated with poor variability and lackof accelerations is more likely to be a true positive thana positive CST in the context of adequate variability andaccelerations.

The CST is used infrequently for primary fetal surveil-lance. This is due to the long duration of the test, therequirement for continuous supervision by trained per-sonnel, and the existence of risks and contraindicationsassociated with its performance (Box 1-7). Presently, theCST is most commonly used to follow a nonreactiveNST. The false negative rate of the CST is 0.4 per 1000,significantly better than that of the NST.


The Biophysical Profile

The BPP is another test for the evaluation of fetal well-being. It combines the NST with the observation by ultra-sound of four variables: fetal breathing movements, fetalbody movements, fetal tone, and amniotic fluid volume(Box 1-8). These variables are dependent on the integrityof the fetal central nervous system and are affected in sit-uations of fetal compromise. The test is time consumingand requires some ultrasound training, but has no con-traindications and no risk for the mother or the fetus.

Each of the five components of the BPP is assigned anumerical value of 2 (if present or normal) or 0 (if absent

BOX 1-8

Biophysical profile

1. Fetal breathing movementThirty seconds of sustained breathing movement during a 30-minute-observation period

2. Fetal movementThree or more gross body movements in a 30-minute-obser-vation period

3. Fetal toneOne or more episodes of limb motion from a position of flex-ion to extension and a rapid return to flexion

4. Fetal heart rate reactivityTwo or more fetal heart rate accelerations associated withfetal movement of at least 15 bpm and lasting at least 15 sec-onds in 10 minutes (reactive NST)

5. Fluid volumePresence of a pocket of amniotic fluid that measures at least2 cm in two perpendicular planes

Figure 1-6. Negative and positive contraction stress test (CST). A,Negative CST: adequate variability. There are no decelerationsassociated with uterine contractions. B, Positive CST: absent vari-ability. Every uterine contraction is followed by a deceleration ofthe fetal heart rate.

A

B

BOX 1-7

Contraindications to the contraction stress test

Placenta previa Prior classical cesarean section Prior extensive uterine surgery Preterm labor High-risk for preterm labor Preterm rupture of membranes

BOX 1-6

How to perform a contraction stress test

1. Place the patient in semi-Fowlers position. Use pillowsunder the patients hip or side to displace the weight of theuterus away from the inferior vena cava. Take the patientsblood pressure every 10 minutes through the test.

2. Apply the tococardiographic equipment to the maternalabdomen and observe the uterine activity and the FHR forapproximately 1520 minutes. Many patients who are receiv-ing the test because of a nonreactive NST show adequatefetal reactivity during this observation period and do notrequire oxytocin stimulation. Other patients show sponta-neous uterine activity of sufficient frequency and durationand do not require oxytocin administration.

3. Start intravenous oxytocin administration at 0.5 mU/minuteusing a pump. Double the rate every 1520 minutes until threecontractions lasting 4060 seconds occur within a 10-minuteperiod. If late decelerations appear before this duration and fre-quency of contractions has been achieved, the administrationof oxytocin must be interrupted. Massage of the nipples with awarm towel by the patient may be all that is necessary to pro-voke uterine contractions and avoid the use of oxytocin.

4. Usually the test requires between 1 and 2 hours. Theamount of oxytocin required to obtain adequate uterine con-tractility is generally below 16 mU/minute.

5. After completing the test, monitoring of FHR and uterine con-tractions should continue until they return to baseline. If uter-ine activity persists, the subcutaneous administration of 250mg of terbutaline is usually sufficient to paralyze the uterus.


or abnormal). A composite value of 8 or 10 indicates thatthe fetal status is reassuring or normal as long as the scoreof 8 does not include an abnormal fluid volume. The pres-ence of oligohydramnios demands further testing, irre-spective of the composite score value. A score of 6 isequivocal and requires further testing to verify fetal well-being. A score of 4 or less is suggestive of fetal compro-mise. The false negative rate of the BPP is 0.7 per 1000, avalue better than that of the NST and similar to that ofthe CST. The false positive rate of the BPP is approximate-ly 30%, better than the NST or the CST. The negative pre-dictive value of the BPP is similar to that of the NST (98%for the NST, 98.5% for the BPP) but the positive predic-tive value of an abnormal BPP (50.8%) is better than thatof a nonreactive NST.

The main problem with the BPP is the structure of thetest because each of the five variables assessed in the test(fetal breathing movements, fetal body movements, fetaltone, amniotic fluid volume, and FHR reactivity) isassigned a score of either

practical guide to high risk pregnancy and delivery

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