Obstetric Clinical Algorithms E-Book

Errol R. Norwitz

• Herausgeber: John Wiley & Sons
• Kategorie: Fachliteratur
• Sprache: Englisch

Seitenzahl: 393

Veröffentlichungsjahr: 2016

Beschreibung

Clinical management algorithms for common and unusual obstetric problems have been developed to help guide practitioners to the best treatment options for patients. In this quick-reference guide, clear diagrams and concise notes show treatment options and evidence for over 80 high-risk obstetric complications, presented in two-page full color spreads to promote quick decision making in time-pressed situations.  

This new edition includes sections on obesity, late-preterm and early term delivery, and pregnancy termination.  As a clinical manual, the book provides guidance to many common and less common obstetric situations in which either the mother or her fetus is at risk. An algorithm for each situation provides obstetric care providers with a step-by-step guide of necessary actions for any given clinical case.

Written by internationally renowned experts, Clinical Obstetric Algorithms enables all obstetrics care providers to ensure delivery of a healthy mother and a healthy baby.

Leseprobe

Table of Contents

Cover

Title Page

Preface

List of Abbreviations

SECTION 1: Preventative Health

1 Abnormal Pap Smear in Pregnancy

2 Immunization

3 Preconception Care

4 Prenatal Care

SECTION 2: Maternal Disorders

5 Antiphospholipid Antibody Syndrome

6 Asthma

7 Cholestasis of Pregnancy

8 Chronic Hypertension

9 Deep Vein Thrombosis

10 Gestational Diabetes Mellitus

11 Gestational Hypertension

12 Preeclampsia

13 Pregestational Diabetes Mellitus

14 Pulmonary Edema

15 Pulmonary Embolism

16 Renal Disease

17 Seizure Disorder

18 Systemic Lupus Erythematosus

19 Thrombocytopenia

20 Thyroid Dysfunction

SECTION 3: Infectious Complications

21 Asymptomatic Bacteriuria

22 Urinary Tract Infection/Pyelonephritis

23 Lower Genital Tract Infection

24 Group B

β

‐Hemolytic Streptococcus

25 Hepatitis B

26 Herpes Simplex Virus

27 Human Immunodeficiency Virus

28 Parvovirus B19

29 Syphilis

30 Tuberculosis

31 Chorioamnionitis (Intraamniotic Infection)

SECTION 4: Antenatal Complications

32 Advanced Maternal Age

33 Antepartum Fetal Testing

34 Breast Lesions

35 Cervical Insufficiency

36 First‐trimester Vaginal Bleeding

37 Higher‐Order Multifetal Pregnancy

38 Hyperemesis Gravidarum

39 Intrauterine Fetal Demise

40 Fetal Growth Restriction

41 Isoimmunization

42 Macrosomia

43 Medically‐Indicated Late Preterm and Early Term Delivery

44 Obesity

45 Oligohydramnios

46 Recurrent Pregnancy Loss

47 Placenta Accreta

48 Placenta Previa

49 Placental Abruption

50 Polyhydramnios

51 Post‐term Pregnancy

52 Pregnancy Termination

53 Prenatal Diagnosis

54 Preterm Labor

55 Screening for Preterm Birth

56 Preterm Premature Rupture of the Membranes

57 Vaginal Birth after Cesarean (VBAC)

58 Teratology

59 Term Premature Rupture of the Membranes

60 Twin Pregnancy

SECTION 5: Intrapartum/Postpartum Complications

61 Breech Presentation

62 Intrapartum Fetal Testing

63 Cesarean Delivery

64 Operative Vaginal Delivery

65 Severe Perineal Lacerations

66 Intrapartum Management of Twin Pregnancy

67 Postpartum Hemorrhage

68 Retained Placenta

69 Postpartum Endomyometritis

70 Mastitis

71 Vasa Previa

72 Postpartum Psychiatric Disorders

73 Sterilization

SECTION 6: Obstetric Emergencies

74 Acute Abdomen in Pregnancy

75 Acute Asthma Exacerbation

76 Acute Shortness of Breath

77 Cord Prolapse

78 Cardiopulmonary Resuscitation

79 Diabetic Ketoacidosis

80 Eclampsia

81 Shoulder Dystocia

82 Thyroid Storm

Recommended Reading

Index

End User License Agreement

List of Tables

Chapter 58

The Food and Drug Administration (FDA) in the United States Classification of Drugs in Pregnancy

Guide

Cover

Table of Contents

Begin Reading

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Obstetric Clinical Algorithms

Second Edition

Errol R. Norwitz, M.D., Ph.D., M.B.A.

Louis E. Phaneuf Professor of Obstetrics & GynecologyTufts University School of MedicineChairman., Department of Obstetrics & GynecologyTufts Medical CenterBoston, USA

George R. Saade, M.D.

University of Texas Medical BranchGalveston, TX, USA

Hugh Miller, M.D.

Department of Obstetrics and GynecologyUniversity of ArizonaTuscon, AZ, USA

Christina M. Davidson, M.D.

Baylor College of MedicineBen Taub HospitalHouston, TX, USA

This edition first published 2017 © 2010, 2017 by John Wiley & Sons, Ltd.

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Library of Congress Cataloging‐in‐Publication Data

Names: Norwitz, Errol R., author. | Saade, George R., 1960– author. | Miller, Hugh S. (Hugh Stephen), author. | Davidson, Christina (Christina Marie) author.Title: Obstetric clinical algorithms / Errol R. Norwitz, George R. Saade, Hugh Miller, Christina M. Davidson.Description: 2nd edition. | Chichester, West Sussex, UK ; Hoboken, NJ : John Wiley & Sons, Inc., 2017. | Preceded by: Obstetric clinical algorithms : management and evidence / Errol R. Norwitz ... [et al.]. 2010. | Includes bibliographical references and index.Identifiers: LCCN 2016024815 (print) | LCCN 2016026085 (ebook) | ISBN 9781118849903 (pbk.) | ISBN 9781118849873 (pdf) | ISBN 9781118849880 (epub)Subjects: | MESH: Pregnancy Complications–diagnosis | Pregnancy Complications–therapy | Algorithms | Decision Support TechniquesClassification: LCC RG571 (print) | LCC RG571 (ebook) | NLM WQ 240 | DDC 618.3–dc23LC record available at https://lccn.loc.gov/2016024815

A catalogue record for this book is available from the British Library.

Wiley also publishes its books in a variety of electronic formats. Some content that appears in print may not be available in electronic books.

Cover image: Jasmina/Gettyimages

Preface

Recent advances in obstetrical practice and research have resulted in significant improvements in maternal and perinatal outcome. Such improvements carry with them added responsibility for the obstetric care provider. The decision to embark on a particular course of management simply because “that’s the way we did it when I was in training” or because “it worked the last time I tried it” is no longer acceptable. Clinical decisions should, wherever possible, be evidence‐based. Evidence‐based medicine can be defined as “the conscientious, explicit, and judicious use of current best evidence in making decisions about the care of individual patients” [1]. In practice, evidence‐based medicine requires expertise in retrieving, interpreting, and applying the results of scientific studies and in effectively communicating the risks and benefits of different courses of action to patients. This daunting task is compounded by the fact that the volume of medical literature is doubling every 10–15 years. Even within the relatively narrow field of Obstetrics & Gynecology, there are more than five major publications each month containing an excess of 100 original articles and 35 editorials. How then does a busy practitioner maintain a solid foundation of up‐to‐date knowledge and synthesize these data into individual management plans? New information can be gleaned from a variety of sources: the advice of colleagues and consultants, textbooks, lectures and continuing medical education courses, original research and review articles, and from published clinical guidelines and consensus statements. The internet has created an additional virtual dimension by allowing instant access to the medical literature to both providers and patients. It is with this background in mind that we have written Obstetric Clinical Algorithms: Management and Evidence, 2nd edition.

Standardization of management reduces medical errors and improves patient safety and obstetrical outcomes [2,3]. In this text, we have developed a series of obstetric algorithms based on best practice to mimic the decision‐making processes that go on in our brains when faced with a vexing clinical problem. To further facilitate decision‐making, we have superimposed “levels of evidence” as defined by the report of the US Preventive Services Task Force (USPSTF) of the Agency for Healthcare Research Quality, an independent panel of experts appointed and funded by the US government to systematically review evidence of effectiveness and develop recommendations for clinical preventive services [4]. The table below summarizes the ‘levels of evidence’ used in this text.

‘Levels of Evidence’ used in Obstetric Clinical Algorithms: Management and Evidence, 2nd edition:

Color key

Levels of evidence available on which to base recommendations

*

Recommendation/suggestions for practice

Red bold

Level I/II‐1

Definitely offer or provide this service

Red regular

Level II‐1/II‐2

Consider offering or providing this service

Red italics

Level II‐2/II‐3/III

Discuss this service, but insufficient evidence to strongly recommend it

Black regular

Level II‐3/III

Insufficient evidence to recommend this service, but may be a reasonable option

* Levels of evidence are based on the ‘hierarchy of research design’ used in the report of the 2nd US Preventive Services Task Force:

Level I: Evidence obtained from at least one properly powered and conducted randomized controlled trial (RCT); also includes well‐conducted systematic review or meta‐analysis of homogeneous RCTs.

Level II‐1: Evidence obtained from well‐designed controlled trials without randomization.

Level II‐2: Evidence obtained from well‐designed cohort or case‐control analytic studies, preferably from more than one center or research group.

Level II‐3: Evidence obtained from multiple time series with or without the intervention; dramatic results from uncontrolled trials might also be regarded as this type of evidence.

Level III: Opinions of respected authorities, based on clinical experience; descriptive studies or case reports; or reports of expert committees.

Obstetric care providers can be broadly divided into two philosophical camps: those who believe that everything possible should be offered in a given clinical setting in the hope that something may help (also called the “we don’t have all the information we need” or “might as well give it, it won’t do any harm” group) and those who hold out until there is consistent and compelling scientific evidence that an individual course of action is beneficial and has a favorable risk‐to‐benefit ratio (sometimes referred to as “therapeutic nihilists”). As protagonists of the latter camp, we argue that substantial harm can be done—both to individual patients and to society as a whole—by implementing management plans that have not been the subject of rigorous scientific investigation followed by thoughtful introduction into clinical practice. In Obstetric Clinical Algorithms: Management and Evidence, 2nd edition, we provide evidence‐based management recommendations for common obstetrical conditions. It is the sincere hope of the authors that the reader will find this book both practical and informative. However, individual clinical decisions should not be based on medical algorithms alone, but should be guided also by provider experience and judgment.

Errol R. NorwitzGeorge R. SaadeHugh MillerChristina M. Davidson

1. Sackett DL, Rosenberg WM, Gray JA

et al

. Evidence based medicine: what it is and what it isn’t.

BMJ

1996;

312

:71–72.

2. Pettker CM, Thung SF, Norwitz ER

et al

. Impact of a comprehensive patient safety strategy on obstetric adverse events.

Am J Obstet Gynecol

2009;

200

:492 (e1‐8).

3. Clark SL, Belfort MA, Byrum SL

et al

. Improved outcomes, fewer cesarean deliveries, and reduced litigation: results of a new paradigm in patient safety.

Am J Obstet Gynecol

2008;

199

:105 (e1‐7).

4. Report of the US Preventive Services Task Force (USPSTF). Available at

http://www.ahrq.gov/clinic/uspstfix.htm

(last accessed on 19 February 2016).

List of Abbreviations

ABG

arterial blood gas

AC

abdominal circumference

ACA

anticardiolipin antibody

ACE

angiotensin‐converting enzyme

ACIP

Advisory Committee on Immunization Practices

ACOG

American College of Obstetricians and Gynecologists

AED

antiepileptic drug

AED

automated external defibrillator

AFE

amniotic fluid embolism

AFI

Amniotic Fluid Index

AGA

appropriate for gestational age

AGC

atypical glandular cells

AHA

American Heart Association

AIDS

acquired immune deficiency syndrome

AIS

adenocarcinoma in situ

AMA

advanced maternal age

ANA

antinuclear antibodies

APLAS

antiphospholipid antibody syndrome

ARB

angiotensin receptor blockers

ARDS

acute respiratory distress syndrome

ART

assisted reproductive technology

ART

antiretroviral therapy

ARV

antiretroviral

ASCUS

atypical squamous cells of undetermined significance

ATP

alloimmune thrombocytopenia

AZT

azidothymidine

BCG

Bacillus Calmette‐Guérin

BMI

body mass index

BP

blood pressure

BPD

biparietal diameter

BPP

biophysical profile

BUN

blood urea nitrogen

BV

bacterial vaginosis

CAOS

chronic abruption‐oligohydramnios sequence

CBC

complete blood count

CDC

Centers for Disease Control and Prevention in the U.S.

CFU

colony‐forming units

CI

cervical insufficiency

CL

cervical length

CMV

cytomegalovirus

CO

cardiac output

CPD

cephalopelvic disproportion

CST

contraction stress test

CT

computed tomography

CTG

cardiotocography

CVS

chorionic villous sampling

CXR

chest radiograph

DCIS

ductal carcinoma in situ

DES

diethylstilbestrol

DIC

disseminated intravascular coagulopathy

DKA

diabetic ketoacidosis

DVT

deep vein thrombosis

ECC

endocervical curettage

ECG

electrocardiography

ECT

electroconvulsant therapy

ECV

external cephalic version

EDD

estimated date of delivery

EFM

electronic fetal monitoring

EFW

estimated fetal weight

ELISA

enzyme‐linked immunosorbant assay

EMB

endometrial biopsy

FEV1

forced expiratory volume in one second

fFN

fetal fibronectin

FFP

fresh frozen plasma

FL

femur length

FSE

fetal scalp electrode

FTA‐ABS

fluorescent treponemal antibody absorption

FVC

forced vital capacity

GBS

Group B β‐hemolytic streptococcus

GCT

glucose challenge test

GDM

gestational diabetes mellitus

GFR

glomerular filtration rate

GLT

glucose load test

GTT

glucose tolerance test

HBsAb

anti‐hepatitis B surface antibodies

HBsAg

hepatitis B surface antigen

HBIg

hepatitis B immunoglobulin

HBV

hepatitis B virus

HC

head circumference

hCG

human chorionic gonadotropin

HEG

hyperemesis gravidarum

HELLP

hemolysis, elevated liver enzymes, low platelets

HGSIL

high‐grade squamous intraepithelial lesions

HIE

hypoxic ischemic encephalopathy

HIV

human immunodeficiency virus

HPV

human papilloma virus

HSV

herpes simplex virus

IAI

intraamniotic infection

ICP

intrahepatic cholestasis of pregnancy

ICU

intensive care unit

IgA

immunoglobulin A

IgG

immunoglobulin G

IGRA

interferon gamma release assay

INH

isoniazid

IOL

induction of labor

IOM

Institute of Medicine

ITP

immune thrombocytopenic purpura

IUFD

intrauterine fetal demise

IUGR

intrauterine growth restriction

IUPC

intrauterine pressure catheter

IV

intravenous

IVIG

intravenous immune globulin

LAC

lupus anticoagulant

LEEP

loop electrosurgical excision procedure

LFT

liver function test

LGA

large‐for‐gestational age

LGSIL

low‐grade squamous intraepithelial lesions

LMP

last menstrual period

LMWH

low molecular weight heparin

LTL

laparoscopic tubal ligation

MCA

middle cerebral artery

MDI

metered dose inhaler

MFM

maternal‐fetal medicine

MFPR

multifetal pregnancy reduction

MHA‐TP

microhemagglutination assay for antibodies to

T. pallidum

MoM

multiples of the median

MRCP MR

cholangiopancreatography

MRI

magnetic resonance imaging

MS‐AFP

maternal serum α‐fetoprotein

MTX

methotrexate

NIDDM

non‐insulin‐dependent diabetes mellitus

NIPT

noninvasive prenatal testing

NR‐NST

non‐reactive NST

NSAIDs

non‐steroidal anti‐inflammatory drugs

NST

non‐stress testing

NT

nuchal translucency

NTD

neural tube defect

NVP

nausea and vomiting in pregnancy

OCT

oxytocin challenge test

OST

oxytocin stimulation test

PCOS

polycystic ovarian syndrome

PCP

pneumocystis carinii

pneumonia

PCR

polymerase chain reaction

PE

pulmonary embolism

P

EFR

peak expiratory flow rate

PKU

phenylketonuria

po

per os (orally)

POC

products of conception

PPD

purified protein derivative

PPH

postpartum hemorrhage

pPROM

preterm PROM

PRBC

packed red blood cell

PROM

premature rupture of membranes

PTT

partial thromboplastin time

PTU

propylthiouracil

PUBS

percutaneous umbilical blood sampling

q

every

QFT‐GIT

QuantiFERON

®

‐TB Gold In‐Tube test

RhoGAM

anti‐Rh[D]‐immunoglobulin

R‐NST

reactive NST

RPL

recurrent pregnancy loss

RPR

rapid plasma reagin

SC

subcuticular

SGA

small for gestational age

SIADH

syndrome of inappropriate ADH secretion

SLE

systemic lupus erythematosus

SMA

spinal muscular atrophy

SSI

surgical site infection

STI

sexually transmitted infection

TB

tuberculosis

TBG

thyroxine‐binding globulin

TFT

thyroid function test

TORCH

toxoplasmosis, rubella, cytomegalovirus, herpes

TPPA

T. pallidum

particle agglutination assay

TRAP

twin reverse arterial perfusion

TST

tuberculin skin testing

TTP/HUS

thrombotic thrombocytopenic purpura/hemolytic uremic syndrome

TTTS

twin‐to‐twin transfusion syndrome

UA C&S

urine culture and sensitivity

UDCA

ursodeoxycholic acid

UFH

unfractionated heparin

UTI

urinary tract infection

VAS

vibroacoustic stimulation

VBAC

vaginal birth after cesarean

VDRL

Venereal Disease Research Laboratory

VL

viral load

V/Q

ventilation‐perfusion

VTE

venous thromboembolism

ZDV

zidovudine

SECTION 1Preventative Health

1Abnormal Pap Smear in Pregnancy

Recommendations for screening and management of abnormal cervical cytology in pregnancy follow from the general guidelines for screening onset and frequency that were updated in 2012 to reflect the recommendations of the American Cancer Society ACOG, and U.S. Preventive Services Task Force for detection of cervical cancer. Routine pap screening should

not

be collected until age 21 regardless of first vaginal intercourse. The risk of severe dysplasia or cancer is very low among adolescents, but they should be encouraged to receive human papilloma virus (HPV) vaccination and counseled about safe sex practices to limit exposure to sexually transmitted infections. Women between the age of 21–29 years should be screened with cervical cytology alone. Women >30 years of age should be screened with cytology and HPV testing every 5 years (or with cytology alone every 3 years). Women with a history of cervical cancer, HIV or other risk factors (such as immunocompromise) should continue annual screening. These guidelines and the associated algorithm are based on a large database of patients including adolescents who were managed using former criteria in the Kaiser Healthcare system. The American Society of Colposcopy and Cervical Pathology (ASCCP) has developed an updated free App that can assist with the current recommendations.

Women who have risk factors for cervical/vaginal cancer (such as a history of

in utero

diethylstilbestrol (DES) exposure, HIV, women who are immunocompromised, or those on chronic steroids) should be screened annually.

Women aged 21–29 with normal cytology but absent or insufficient endocervical–transformation zone elements can continue regular screening, which should not include HPV testing. In women

>

30 years with a similar cytology result, HPV testing is recommended. Positive HPV results should prompt repeat co‐testing in one year, unless the HPV genotype is known to be 16 or 18, in which case, immediate colposcopy is recommended. A negative HPV result in a woman

>

30 years means that she can go back to routine screening.

Unsatisfactory cytology is less common in current practice with the use of liquid‐based media for cervical screening. Insufficient squamous cells to detect epithelial abnormalities generally arise from blood or inflammation that obscures the result. Repeat cytology is recommended in 2–4 months. Colposcopy can be considered in women >30 years with positive HPV, and is recommended in those women who have had two consecutive unsatisfactory cytology test results.

Women should always be informed of an abnormal Pap result by her physician or another healthcare professional who can answer basic questions and allay anxiety. Verbal notification should be followed with written information and clear recommendations for follow‐up. Additionally, if there is evidence of infection along with cellular abnormalities, the infection should be treated.

The 2012 criteria substantially clarify the management of ASCUS, which is guided by HPV test results whether obtained reflexively or as a co‐test. The management in pregnancy differs only in that colposcopy and endocervical curettage (ECC) should be deferred until 6 weeks postpartum unless a CIN 2+ lesion is suspected. Women

>

25 years old with a negative HPV test should be returned to a regular three‐year follow‐up cycle. Following pregnancy colposcopy is recommended in women who are HPV+ with annual co‐test follow‐up. Similarly, an endocervical curettage (ECC) should be obtained whenever possible and excisional procedures should be avoided to prevent over‐treatment. In women 21–24 years old, cytology should be repeated in one year. A positive HPV result does not change the recommended follow‐up, but a negative result should return the woman to a three‐year follow‐up cycle.

Atypical squamous cells cannot exclude high‐grade squamous intraepithelial lesions (HSIL) (ASC‐H), which is associated with a higher risk of CIN 3+ regardless of patient age and a five‐year invasive cancer risk of 2% regardless of HPV status. That said, HPV is highly correlated with ASC‐H, but the cancer risk demands that all women receive immediate colposcopy, including those 21–24 years of age. Colposcopy with directed biopsies of any area that might be concerning for micro invasion should be done by a highly trained clinician. Treatment should be dictated by histologic evaluation of the biopsied lesions.

Atypical glandular cells (AGC) or adenocarcinoma in situ (AIS) warrant aggressive investigation and close follow‐up. Although the risk of cancer is lower in younger age groups, women

>

30 years have a 9% risk of CIN3+ and 2% risk of invasive cancer. All such women of all ages should have antenatal colposcopy with 6‐weeks postpartum follow‐up to include colposcopy, ECC and endometrial biopsy (EMB). Subsequent treatment and follow‐up are dictated by the biopsy results, maternal age, and the histologic evaluation of the glandular elements.

Approximately 60% of low‐grade squamous intraepithelial lesions (LGSIL) will regress spontaneously without treatment depending on the age of the patient, HPV status, and HPV genotype. For women

>

25 years old in whom HPV testing is negative, repeat co‐testing in ome year is preferred but colposcopy is acceptable. However, if the HPV is positive, then colposcopy is preferred. If colposcopy is not part of the initial evaluation, subsequent co‐testing needs to be entirely normal to allow patients to return to three‐year follow‐up. Any abnormality at the one‐year follow‐up visit should result in colposcopy. In women 21–24 years old, annual repeat cytology without HPV testing is preferred and colposcopy should be avoided unless the results recur for two consecutive years or if one of the following lesions is detected: ASC‐H, AGC, or HSIL. Pregnant women

>

25 years old with low‐grade squamous intraepithelial lesions should undergo immediate colposcopy without ECC, while those 21–24 years old should be evaluated postpartum.

High‐grade squamous intraepithelial lesions (HGSIL) are associated with a 60% risk of CIN2+ and a 2% risk of invasive cervical cancer. Immediate colposcopy with directed biopsies of any area that might be concerning for micro invasion is recommended, regardless of maternal age. The antepartum diagnosed of HGSIL should prompt a 6‐weeks postpartum follow‐up colposcopy with ECC and treatment as dictated by the biopsy results. If diagnosed early in pregnancy, colposcopy can be repeated every 12 weeks. Treatment during pregnancy should be reserved for invasive carcinoma and should be managed in concert with a gynecologic oncologist.

2Immunization

Immunization can be active (vaccines, toxoid) or passive (immunoglobulin, antiserum/antitoxin). In

active immunity

, the immune response is induced by wild infection or vaccination, which is generally robust and long‐lasting. As such, subsequent exposure to the vaccine‐preventable infection will result in the release of antibodies and the prevention of illness. In

passive immunity

, antibodies are acquired passively through maternal transfer across the placenta or breast milk or through the receipt of exogenous immunoglobulins. Protection is temporary and fades within a few weeks to months. The immune system of the recipient is therefore not programmed, and subsequent exposure to vaccine‐preventable infections can lead to active infection.

Vaccination

works by inducing antibodies in recipients that protects them against infection after future exposure to specific disease‐causing microbes. The level of protection varies according to the strength and durability of the immune response induced by the vaccine as well as the virulence, prevalence, and ease of transmission of the infection itself. Vaccination programs may have different goals: (i) to protect at‐risk individuals (e.g., meningococcal disease); (ii) to establish control by minimizing the overall prevalence of the infection (e.g., measles, varicella); or (iii) to attain global elimination of an infection (e.g., neonatal tetanus, polio).

Vaccination in pregnancy is of benefit and at times poses concern relative to the increased vulnerability of the mother and fetus. Inactivated vaccines are approved for use in pregnancy. The inactivated influenza vaccine should be given to

all pregnant women

during the influenza season (October through May in the northern hemisphere), regardless of gestational age. It is clear that there are significant maternal benefits including fewer cases of fever and respiratory illness and substantial neonatal protection through the transplacental passage of antibodies that provide months of protection at a time when the infant is vulnerable and could not be directly vaccinated. However, live‐attenuated vaccines (including rubella, MMR, varicella) are not recommended for pregnant women despite the fact that no cases of congenital anomalies have been documented. Exceptions include yellow fever and polio, which can be given to pregnant women when traveling to high prevalence areas. In addition, women should be advised not to get pregnant within 1 month of receiving a live‐attenuated vaccine. The live‐attenuated influenza vaccine is available as an intranasal spray, which is considered safe in the postpartum period. Vaccines considered safe in pregnancy include tetanus, diphtheria, hepatitis B, and influenza. Tetanus immunization during pregnancy is a common strategy used in the developing world to combat neonatal tetanus

Risk factors for specific vaccine‐preventable illnesses include:

illicit drug users (hepatitis A and B, tetanus)

men who have sex with men (hepatitis A) or >1 sexual partner in the past 6 months (hepatitis A, human papilloma virus)

travel to or immigration from areas where infection is endemic (hepatitis A and B, measles, meningococcus, rubella, tetanus, varicella)

healthcare workers (hepatitis B, influenza, varicella)

nursing home residents (meningococcus, pneumococcus, varicella) or ≥50 years of age (influenza)

chronic medical diseases: diabetes, asthma, HIV, liver disease and/or renal disease (hepatitis A, influenza, pneumococcus)

adults who have had their spleens removed (meningococcus, pneumococcus)

accidental or intentional puncture wounds (tetanus)

One of the ongoing controversies about vaccination in pregnancy is whether vaccines containing thimerosal pose a risk to the fetus. Thimerosal is a mercury‐containing preservative that has been used in multidose vaccines since the 1930s. Although there has been concern about the cumulative levels of mercury, the current scientific evidence does not consider thimerosal to be associated with adverse outcomes in children exposed in utero. The Centers for Disease Control and Prevention’s Advisory Committee on Immunization Practices (ACIP) does not recommend avoiding thimerosal containing vaccines. Although the ACIP does not recommend any specific formulation, there are newer trivalent and quadrivalent influenza vaccines (containing two A and two B influenza strains) that are available for use. The following adult vaccines are thimerosal‐free: Tdap (but not Td), Recombivax hepatitis B vaccine (but not Engerix‐B), and some influenza vaccines (Fluzone with no thimerosal).

Tetanus toxoid, reduced diphtheria toxoid and acellular pertussis vaccine (Tdap) may be given at any time of pregnancy or the postpartum period but ideally is administered between 27–36 weeks to confer the best passive immunity through the transfer of antibodies to the fetus. This recommendation has developed to address the significant impact of pertussis disease in the newborn.

3Preconception Care

Fetal organogenesis occurs before most women are aware that they are pregnant. As such, the ideal time for addressing primary prevention of reproductive health risks is in the preconception period. Since approximately half of all pregnancies in the United States are unplanned, all women of reproductive age should be considered candidates for discussion of these issues.

Discuss social, financial, and psychological issues in preparation for pregnancy.

Maternal alcohol use is the leading known cause of congenital mental retardation and is the leading preventable cause of birth defects in the Western world. An accurate drinking history is best elicited using a tool that employs standardized screening questions (such as the CAGE questionnaire). The adverse effects of alcohol may be compounded with abuse of other drugs. Cigarette smoking, cocaine, and other drug use should be included in the history. Patients at risk should be provided education, contraceptive counselling, and referral for treatment as necessary.

Screen for domestic violence. Be aware of available state and local resources and state laws regarding mandatory reporting. Risk increases with pregnancy. Domestic violence is not isolated to any particular risk group in pregnancy; it cuts across socio‐economic and ethnic lines.

Take an occupational history that will allow assessment of workplace risks to the pregnancy. Elicit information about any exposures to hazardous materials or biologic hazards (HIV, cytomegalovirus (CMV), toxoplasmosis) and review the use of safety equipment. Talk to patients about the appropriate and correct use of seat belts while in a moving vehicle.

Counsel patients with a history of preeclampsia, placental abruption, unexplained fetal death, or severe intrauterine growth restriction (IUGR) about the risks of recurrence. Low‐dose aspirin starting at the end of the first trimester is recommended to prevent recurrent preeclampsia. The use of low‐dose aspirin, calcium supplementation, and/or anticoagulation for women with documented inherited thrombophilias to prevent adverse pregnancy outcome is controversial, and cannot be routinely recommended.

Personal and family histories should be examined for evidence of genetic diseases. Genetic testing is available to determine a patient’s carrier status for some autosomal recessive conditions such as Tay–Sachs, Canavan disease, sickle cell disease, and the thalassemias. Consider referral for further genetic counselling if patients are at high risk. ACOG currently recommends that all couples be offered prenatal testing for cystic fibrosis. ACMG (but not ACOG) recommends that all couples also be offered genetic testing for spinal muscular atrophy (SMA).

Emphasize the importance of nutrition. Assess appropriateness of patient’s weight for height, special diets and nutrition patterns such as vegetarianism, fasting, pica, bulimia, and vitamin supplementation. Recommend folic acid supplementation as necessary: 0.4 mg per day for all pregnant women or women considering pregnancy, 4.0 mg per day if the woman has a personal/family history of a child with a neural tube defect or is on anticonvulsant medications (especially valproic acid). Counsel to avoid oversupplementation (such as vitamin A). Review the recommendations on dietary fish ingestion (<12 ounces per week of cooked fish) to minimize mercury intake, and steps for prevention of listeriosis (avoiding raw or undercooked meat/fish, unpasteurized milk and soft cheeses, unwashed fruit and vegetables) and toxoplasmosis (exposure to cat feces).

A thorough immunization history should be obtained that addresses vaccination. Women should be tested for immunity to rubella and vaccinated prior to pregnancy if not immune. Women without a history of chickenpox (varicella) should be tested and offered vaccination prior to pregnancy. Hepatitis B vaccination should be offered to all women at high risk, and screening for other sexually transmitted infections should be offered as needed. The U.S. Centers for Disease Control and Prevention (CDC) recommends that pregnancy be delayed for at least 1 month after receiving a live‐attenuated vaccine (such as MMR, varicella, live‐attenuated influenza, BCG).

Discuss birth spacing and the options available for postpartum contraception.

Effects of the pregnancy on any medical conditions for both mother and fetus should be discussed. Pregnancy outcomes can be improved by optimizing control of chronic medical conditions prior to pregnancy (such as glycemic control in patients with diabetes and blood pressure control in patients with hypertension). Medications should be reviewed, and patients counselled regarding alternatives that may be safer in pregnancy. Close communication with the patient’s primary care and subspecialty physicians should always be maintained.

4Prenatal Care1

The goal of prenatal care is to promote the health and well‐being of the pregnant woman, fetus, infant, and family up to 1 year after birth. To achieve these aims, prenatal care must be available and accessible. The three major components are: (i) early and continuing risk assessment, including preconception assessment (see

Chapter 3

, Preconception Care); (ii) continued health promotion; and (iii) both medical and psychosocial assessment and intervention.

Routine prenatal tests that should be completed for all pregnant women include complete blood count (CBC), blood group type and screen (Rh status), rubella serology, HIV, hepatitis B, syphilis serology (VDRL/RPR), Pap smear, cystic fibrosis (CF) carrier status, chlamydia/gonorrhea cultures, and urine culture and sensitivity (UA C&S).

Approximately 20% (1 in 5) of pregnancies are considered high risk. Risk factors for adverse pregnancy outcome may exist prior to pregnancy or develop during pregnancy or even during labor (examples are listed below, although this list should not be regarded as comprehensive).

The frequency and timing of prenatal visits will vary depending on the risk status of the pregnant woman and her fetus. In low‐risk women, prenatal visits are typically recommended q 4 weeks to 28 weeks, q 2 weeks to 36 weeks, and then weekly until delivery.

See

Chapter 12

(Preeclampsia).

See

Chapter 53

(Prenatal diagnosis).

See

Chapter 10

(Gestational diabetes mellitus)

See

Chapter 24

(GBS)

See

Chapter 55

(Screening for preterm birth)

High‐Risk Pregnancies

Maternal factors

Pre‐existing medical conditions (diabetes, chronic hypertension, cardiac disease, renal disease, pulmonary disease)

Preeclampsia

Gestational diabetes

Morbid obesity

Extremes of maternal age

Active venous thromboembolic disease

Poor obstetric history (prior preterm birth, preterm PROM, stillbirth, IUGR, placental abruption, preeclampsia, recurrent miscarriage)

Fetal factors

Fetal structural or chromosomal anomaly

History of a prior baby with a structural or chromosomal anomaly

Family or personal history of a genetic syndrome

Toxic exposure (to environmental toxins, medications, illicit drugs)

IUGR

Fetal macrosomia

Multiple pregnancy (esp. if monochorionic)

Isoimmunization

Intra‐amniotic infection (chorioamnionitis)

Nonreassuring fetal testing

Uteroplacental factors

Preterm premature rupture of membranes

Unexplained oligohydramnios

Large uterine fibroids (esp. if submucosal)

Prior cervical insufficiency

Prior uterine surgery (especially prior “classic” hysterotomy)

Placental abruption

Placenta previa

Uterine anomaly (didelphys, septate)

Abnormal placentation (placenta accreta, increta or percreta)

Vasa previa

SECTION 2Maternal Disorders

5Antiphospholipid Antibody Syndrome

Antiphospholipid antibody syndrome (APLAS) is an autoimmune disease characterized by the presence in the maternal circulation of one or more autoantibodies against membrane phospholipid as well as one or more specific clinical syndromes. It is an acquired rather than an inherited condition. As such, it cannot explain a family history of venous thromboembolism (VTE). A significant family history of VTE should prompt testing to exclude inherited thrombophilias, including factor V Leiden mutation, prothrombin gene mutation, and protein S, protein C, and antithrombin deficiency.

The diagnosis of APLAS requires two distinct elements: (i) the correct clinical setting; and (ii) confirmatory serologic testing. Approximately 2–4% of healthy pregnant women will have circulating antiphospholipid antibodies in the absence of any clinical symptoms. As such, routine screening for these antibodies in all pregnant women is strongly discouraged.

Clinical manifestations of APLAS include: (i) recurrent pregnancy loss (defined as  ≥ 3 unexplained first‐trimester pregnancy losses or  ≥ 1 unexplained second‐trimester pregnancy loss); (ii) unexplained thrombosis (venous, arterial, cerebrovascular accident or myocardial infarction); and/or (iii) autoimmune thrombocytopenia (platelets <100,000/mm

3

). Recent consensus opinions suggest that such clinical conditions as unexplained intrauterine growth restriction (IUGR), massive placental abruption, and recurrent early‐onset severe pre‐eclampsia be included.

At least one of three serologic tests confirming the presence of circulating antiphospholipid antibodies (below) is required to make the diagnosis of APLAS. Moreover, the diagnosis requires the persistence of such antibodies as confirmed by two or more positive tests at least 12 weeks apart.

Lupus anticoagulant

(LAC) is an unidentified antiphospholipid antibody (or antibodies) that causes prolongation of phospholipid‐dependent coagulation tests

in vitro

by binding to the prothrombin–activator complex. Examples of tests that can confirm the presence of LAC include the activated PTT test, dilute Russel viper venom test, kaolin clotting time, and recalcification time.

In vivo

, however, LAC causes thrombosis. LAC results are reported as present or absent (no titers are given). The term LAC is a misnomer: it is not specific to lupus (SLE) and it acts

in vivo

as a procoagulant and not an anticoagulant.

Antibodies against specific phospholipids as measured by enzyme‐linked immunosorbant assay (ELISA). These high‐avidity IgG antibodies have anticoagulant activity

in vitro

, but procoagulant activity

in vivo

. The most commonly used ELISA test is the

anticardiolipin antibody

(ACA). Cardiolipin is a negatively charged phospholipid isolated from ox heart. ACA ELISA is at best semi‐quantitative. Results have traditionally been reported as low, medium or high titers. More recently, standardization of the phospholipid extract has allowed for standard units to be developed (GPL units for IgG, MPL units for IgM). ACA IgM alone, IgA alone, and/or low‐positive IgG may be a nonspecific (incidental) finding since they are present in 2–4% of asymptomatic pregnant women. As such, moderate‐to‐high levels of ACA IgG (>40 GPL units) are required to make the diagnosis of APLAS.

The presence of anti‐β2‐glycoprotein I antibodies.

A number of additional antiphospholipid antibodies are described, including antiphosphatidylserine, antiphosphatidylethanolamine, antiphosphatidylcholine, anti‐Ro, and anti‐La, but these are not sufficient to make the diagnosis. A false‐positive test for syphilis (defined as a positive rapid plasma reagin (RPR) or Venereal Disease Research Laboratory (VDRL) test, but negative definitive test for syphilis) is another common finding in women with APLAS, but is nonspecific and is not sufficient to confirm the diagnosis. Antinuclear antibodies (ANA) are not antiphospholipid antibodies, and may suggest the diagnosis of SLE but not APLAS.

Treatment for APLAS depends on the clinical features:

For women with

thrombosis

(such as stroke or pulmonary embolism),

therapeutic

anticoagulation is indicated with either unfractionated heparin (UFH) or low molecular weight heparin (LMWH) during pregnancy followed by oral anticoagulation (coumadin) postpartum because of a 5–15% risk of recurrence. In pregnancy, regular blood tests are required 4 hours after administration of the drug to ensure that anticoagulation is therapeutic: the PTT should be 1.5‐ to 2.5‐fold normal and anti‐Xa activity levels should be 0.6–1.0 U/mL. Side‐effects include hemorrhage, thrombocytopenia, and osteopenia and fractures. Such women may need lifelong treatment.

For women with

recurrent pregnancy loss

, treatment should include

prophylactic

UFH (5000–10,000 units sc bid) or LMWH (enoxaparin (Lovenox) 30–40 mg sc daily or dalteparin (Fragmin) 2500–5000 U sc daily) starting in the first trimester of pregnancy. Although prophylactic dosing does not change PTT, it will increase anti‐Xa activity to 0.1–0.2 U/mL. However, it is not necessary to follow serial anti‐Xa activity in such patients. The goal of this treatment is to prevent pregnancy loss and to prevent VTE, which is possible in women with APLAS in pregnancy even if they have not had a VTE in the past. Therefore, anticoagulation should be administered throughout pregnancy and typically for 6–12 weeks after delivery.

For women with

autoimmune thrombocytopenia or a history of severe pre‐eclampsia, IUGR or placental abruption

, the optimal treatment is unknown. Consider treating as for recurrent pregnancy loss. Postpartum anticoagulation is probably not necessary.

6Asthma

Asthma is a chronic inflammatory disorder of the airways characterized by intermittent episodes of reversible bronchospasm. The “classic” signs and symptoms of asthma are intermittent dyspnea, cough, and wheezing. Pulmonary function tests that are most helpful in diagnosing asthma are peak expiratory flow rate (PEFR), spirometry (which includes measurement of forced expiratory volume in one second [FEV1] and forced vital capacity [FVC]), and bronchoprovocation testing (such as with a metacholine or exercise challenge). PEFR, which correlates well with FEV1, can be measured using a hand‐held peak flow meter and is a useful measure in the clinic or home setting. PEFR is determined for each patient (personal best) or by using charts adjusted for age, height, gender, and race. PEFR results are categorized into green (80–100% of normal or personal best), yellow (50–80%), and red (less than 50%). Usually, the green zone means that the asthma is well controlled, yellow means that adjustments to medications and/or environment are needed, and red is a medical alert that needs immediate attention. Findings consistent with asthma include a variability of >20% in PEFR, a reduction in FEV1 and FEV1/FVC ratio on spirometry, an increase in FEV1 of more than 15% from the baseline following administration of 2–4 puffs of a bronchodilator, and heightened sensitivity to bronchoprovocation. Asthma complicates 1–4% of all pregnancies. Pregnancy has a variable effect on asthma (25% improve, 25% worsen, 50% are unchanged). In general, women with mild, well‐controlled asthma tolerate pregnancy well. Women with severe asthma are at risk of symptomatic deterioration.

Respiratory adaptations during pregnancy are designed to optimize maternal and fetal oxygenation, and to facilitate transfer of CO

2

waste from the fetus to the mother. The mechanics of respiration change with pregnancy. The ribs flare outward and the level of the diaphragm rises 4 cm. During pregnancy, tidal volume increases by 200 mL (40%) resulting in a 100–200 mL (5%) increase in vital capacity and a 200 mL (20%) decrease in the residual volume, thereby leaving less air in the lungs at the end of expiration. The respiratory rate remains unchanged or increases slightly. The end result is an increase in minute ventilation and a drop in arterial

P

CO

2

. Arterial

P

O

2

is essentially unchanged. A compensatory decrease in bicarbonate enables the pH to remain unchanged. Pregnancy thus represents a state of

compensated respiratory alkalosis

.

pH

P

O

2

(mmHg)

P

CO

2

(mmHg)

Non‐pregnant

7.40

93–100

35–40

Pregnant

7.40

100–105

28–30

The differential diagnosis of asthma includes pneumonia, pulmonary embolism, pneumothorax, congestive cardiac failure, pericarditis, pulmonary edema, and rib fracture.

Characteristic triggers for asthma include exercise, cold air, and exposure to allergens. Exercise‐triggered symptoms typically develop 10–15 minutes after exertion and are more intense when the inhaled air is cold. Allergens that typically trigger asthma symptoms include dust, molds, furred animals, cockroaches, pollens, and other irritant‐type exposures (cigarette smoke, strong fumes, airborne chemicals). Viral infections can also trigger asthma symptoms. Influenza vaccination is recommended (see

Chapter 2

on Immunization).

The principal goals of treatment are to minimize symptoms, normalize pulmonary function, prevent exacerbations, and improve health‐related quality of life. Initial treatment for relief of symptoms should be an inhaled short‐acting beta‐agonist used on an as‐needed basis rather than at regularly scheduled intervals. The most commonly used agent is an albuterol inhaler at a dose of 2–4 puffs as needed every 4–6 hours. If this is not adequate to control symptoms, inhaled glucocorticoids (such as beclomethasone dipropionate) should be given by metered dose inhaler (MDI) and should be taken at regular intervals two to three times daily.

Pregnancy‐related complications of severe asthma include intrauterine growth restriction (IUGR), stillbirth, and maternal mortality.

A number of alternative therapies are available on an outpatient basis. These include a short course of oral glucocorticoids. A typical regimen is prednisone 0.5 mg per kg body weight given orally each day and tapered over a period of one to two weeks. This can be given alone or in combination with a leukotriene modifying agent––such as the leukotriene D4 receptor antagonists zafirlukast (Accolate) and montelukast (Singulair) or the 5‐lipoxygenase inhibitor zileuton (Zyflo)––or a slow‐release theophylline.

See

Chapter 75

(Acute Asthma Exacerbation).

7Cholestasis of Pregnancy

Cholestasis of pregnancy (also referred to as intrahepatic cholestasis of pregnancy (ICP)) represents a clinical syndrome that results from a complex interplay between reproductive hormones, biliary transport proteins, and genetic factors that contribute to an inability to adequately metabolize and excrete bile acids during pregnancy. Risk factors for cholestasis