CORE CURRICULUM FOR Neonatal Intensive Care Nursing
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CORE CURRICULUM FOR Neonatal Intensive Care Nursing
SIXTH EDITION
EDITED BY
M. TERESE VERKLAN, PhD, RNC, CCNS, FAAN
Professor/Neonatal Clinical Nurse Specialist
Graduate School of Biological Sciences School of Nursing
University of Texas Medical Branch Galveston, TX, United States
MARLENE WALDEN, PhD, APRN, NNP-BC, CCNS, FAAN Nurse Scientist Manager Nursing Research Department Arkansas Children’s Hospital Little Rock, AR, United States
SHARRON FOREST, DNP, APRN, NNP-BC
Associate Professor School of Nursing
The University of Texas Medical Branch Galveston, TX, United States
With the Endorsements of
Elsevier
3251 Riverport Lane
St. Louis, Missouri 63043
CORE CURRICULUM FOR NEONATAL INTENSIVE CARE NURSING
Previous editions copyrighted by Saunders, an imprint of Elsevier, Inc., 2015, 2010, 2004, 1999, 1993
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Notice
Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds or experiments described herein. Because of rapid advances in the medical sciences, in particular, independent verification of diagnoses and drug dosages should be made. To the fullest extent of the law, no responsibility is assumed by Elsevier, authors, editors or contributors for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein.
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To Mom, Cindy, Paul, and Theresa George—thank you for showing me I have no boundaries. And in loving memory of my father.
MTV
In loving memory of my mother, Wanda, and my twin sister, Sharlene, who taught me so much about love and caring for others. Also to my professional colleagues who teach me so much; but most important, to the babies and families who have taught me the art of neonatal nursing.
MW
In loving memory of my mother, Monie—my nursing role model and unwavering champion.
SF
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CONTRIBUTORS
Debra Armentrout, PhD, APRN, NNP-BC
Adjunct Faculty
School of Nursing
University of Texas Medical Branch
Galveston, TX, United States
Teresa B. Bailey, DNP, APRN, NNP-BC
Neonatal Nurse Practitioner
Pediatrix Medical Group
Mednax National Medical Group
Austin, TX, United States
Susan Givens Bell, DNP, MABMH, NNP-BC, RNC-NIC
Neonatal Nurse Practitioner
Neonatal Intensive Care Unit
Asante Rogue Regional Medical Center
Medford, OR, United States
Susan Tucker Blackburn, PhD, RN, FAAN
Professor Emerita
Department of Family and Child Nursing
University of Washington Seattle, WA, United States
Marina Boykova, PhD, RN
Assistant Professor
School of Nursing & Allied Health Professions
Holy Family University
Philadelphia, PA, United States
Non-Executive Director
Council of International Neonatal Nurses
Yardley, PA, United States
Wanda T. Bradshaw, MSN, RN, NNP-BC
Assistant Professor; Lead Faculty NNP Specialty
School of Nursing
Duke University
Durham, NC, United States
Neonatal Nurse Practitioner
Cone Health
Greensboro, NC, United States
Leigh Ann Cates-McGlinn, PhD, APRN, NNP-BC, RRT-NPS, CHSE
Director
McGlinn Institute
Neonatal Nurse Practitioner
Atrium Health
Charlotte, NC, United States
Anita Catlin, DNSc, FNP, CNL, FAAN Manager, Research
Administration
Kaiser Permanente
Vallejo, CA, United States
Lindsey Churchman, MSN, RN, NNP-BC
Assistant Director, Neonatal Nurse Practitioners
Neonatology
Children’s Mercy Hospital
Kansas City, MO, United States
M. Colleen Brand, PhD, APRN, NNP-BC
Neonatal Nurse Practitioner
Neonatology
Texas Children’s Hospital
Houston, TX, United States
Assistant Professor
Neonatology
Baylor College of Medicine
Houston, TX, United States
Karen D’Apolito, PhD, APRN, NNP-BC, FAAN Professor & Program Director NNP Specialty School of Nursing
Vanderbilt University
Nashville, TN, United States
William Diehl-Jones, PhD, MSc, BSc, BScN
Associate Professor
Center for Nursing and Health Research
Athabasca University
Athabasca, AB, Canada
Georgia Ditzenberger, PhD, RNC, NNP-BC
Neonatal Nurse Practitioner
Women and Children’s Department
Salem Health Hospital & Clinics
Salem, OR, United States
Christine D. Domonoske, PharmD
Neonatal Clinical Pharmacy Specialist
Pharmacy
Children’s Memorial Hermann Hospital
Houston, TX, United States
Ann Donze, MSN, APN
Neonatal Intensive Care (retired)
St. Louis Children’s Hospital
St. Louis, MO, United States
Sharron Forest, DNP, APRN, NNP-BC Associate Professor School of Nursing
The University of Texas Medical Branch
Galveston, TX, United States
Debbie Fraser, MN, CNEON(C)
Associate Professor Faculty of Health Disciplines
Athabasca University
Athabasca, AB, Canada
Neonatal Nurse Practitioner
NICU
St Boniface Hospital
Winnigeg, MB, Canada
Editor-in-Chief
Neonatal Network
Springer Publishing New York, New York, United States
Jennifer G. Hensley, EdD, CNM, WHNP, LCCE
Professor, Clinical Nursing Coordinator
D.N.P. Nurse-Midwifery Program School of Nursing
University Louise Herrington Dallas, TX, United States
Certified Nurse-Midwife
Renaissance Women’s Group Austin, TX, United States
Alice S. Hill, PhD, RN, FAAN
Professor, Associate Dean of Graduate Programs, Retired School of Nursing
University of Texas Medical Branch Galveston, TX, United States
Pat Hummel, PhD, APRN, NNP-BC, PPCNP-BC
Neonatal/Pediatric Nurse Practitioner
Neonatology
Loyola University Medical Center Maywood, IL, United States
Helen M. Hurst, DNP, RNC-OB, APRN-CNM
Department Head and Associate to the Dean, Associate Professor Nursing
University of Louisiana at Lafayette Lafayette, LA, United States
CHOC Children’s at Mission Hospital Mission Viejo, California
Carie Linder MSN, APRN, NNP Neonatology
Integris Baptist Medical Center Oklahoma City, Oklahoma
Caitlin O’Brien
Boston Children’s Hospital Stoneham, Massachusetts
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PREFACE
The provision of intensive care to the high-risk neonate challenges every neonatal care provider. Research and refinements in technology have made “high-tech” modalities such as extracorporeal membrane oxygenation (ECMO), nitric oxide, and hypothermia available to many more hospitals. The art and science of neonatal nursing are never stochastic. We learn from scientists; researchers; interprofessional colleagues; and, of course, our infants and their families. At a minimum, we are expected to enhance our application of clinical knowledge by utilizing an evidencebased approach to improve patient outcomes. The role of the nurse is frequently to bring together all the pieces of the puzzle to ensure comprehensive, clinically excellent, and compassionate care to sick newborns and their families.
The sixth edition of Core Curriculum for Neonatal Intensive Care Nursing is intended as a clinical resource and as an aid to prepare the nurse to take the high-risk neonatal nursing certification examination, whether it is the American Association of Critical Care Nurses Certification Examination (CCRN-neo) or the National Certification Corporation (RNC-NIC). The book is divided into sections and designed in an outline format so that it may be used as an easy reference. The first section, Antepartum, Intrapartum, and Transition to Extrauterine Life , addresses clinical issues related to factors that affect the fetus and the neonate’s ability to successfully adapt to postnatal life. Information is also
presented as to how we can assist in the recognition of the high-risk fetus/neonate and plan interventions that support the physiologic demands of the neonate during transition. Cornerstones of Clinical Practice presents concepts common to the delivery of quality care to all high-risk newborns and families. The third section, Pathophysiology: Management and Treatment of Common Disorders , provides a systems approach to the assessment and management of the disease processes high-risk neonates commonly present with. The last section, Professional Practice , focuses on the caregiver to strengthen competency with respect to research use, in addition to providing an overview of universal ethical and legal issues that may be encountered in the practice of neonatal nursing.
This text is the collaborative effort of the three major nursing specialty associations: the Association of Women’s Health, Obstetric and Neonatal Nurses (AWHONN); the American Association of Critical-Care Nurses (AACN); and the National Association of Neonatal Nurses (NANN). The book brings together experts in the care of the highrisk neonate, all having the common goal of providing a comprehensive resource for the management and care of sick newborns. We are honored to be the editors of such an outstanding collaborative effort.
M. Terese Verklan
Marlene Walden
Sharron Forest
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CONTENTS
PART ONE
Antepartum, Intrapartum, and Transition to Extrauterine Life
1. Uncomplicated Antepartum, Intrapartum, and Postpartum Care, 1
Bonita Shviraga and Jennifer G. Hensley Terminology, 1
Normal Maternal Physiologic Changes by Systems, 1
Antepartum Care, 6
Normal Labor and Birth, 13
Puerperium: The “Fourth Trimester”, 16
2. Antepartum–Intrapartum Complications, 20
Helen M. Hurst
Anatomy and Physiology, 20
Conditions Related to the Antepartum Period, 24
Conditions Related to the Intrapartum Period, 28
Obstetric Analgesia and Anesthesia, 34
3. Perinatal Substance Abuse, 38
Karen D’Apolito
Overview, 38
Risk Factors Associated With Substance Use Disorder in Women, 39
Pregnancy Outcomes for Substance Use
Disorder Associated With Common Drugs of Abuse, 39
Fetal and Neonatal Outcomes for Common Drugs of Prenatal Substance Dependence, 41
Childhood Outcomes for Common Drugs of Prenatal Substance Dependence, 42
Breast Milk and Drugs, 43
Preconception Counseling and Screening, 43
Treatment Approaches for Pregnant Women, 44
Barriers to Treatment, 44
Comorbidities Associated With Substance Use Disorders, 44
Screening Methods to Identify Potential Substance Users, 44
Neonatal Abstinence Syndrome, 45
Clinical Signs of Neonatal Abstinence Syndrome, 45
Clinical Signs Associated With Some Drugs, 46
Assessment of Neonatal Abstinence Syndrome, 46
Onset of Signs of Neonatal Abstinence Syndrome, 46
Differential Diagnosis, 46
Nonpharmacologic Treatment of Neonatal Abstinence Syndrome, 46
Pharmacologic Treatment of Neonatal Abstinence Syndrome, 48
Drugs Used to Treat Neonatal Abstinence Syndrome, 48
Standardization of Pharmacologic Management, 48
Environment to Care for Infants with Neonatal Abstinence Syndrome, 50
Discharge and Follow-Up, 50 The Future, 50
4. Adaptation to Extrauterine Life, 54
M. Terese Verklan
Anatomy and Physiology, 54
Routine Care Considerations During Transition, 58
Recognition of the Sick Newborn Infant, 62
Parent Teaching, 66
5. Neonatal Delivery Room Resuscitation, 69
Barbara Elizabeth Pappas and Deanna Lynn Robey Definitions, 69
Anatomy and Physiology, 69
Risk Factors, 70
Anticipation of and Preparation for Resuscitation, 70
Equipment for Neonatal Resuscitation, 74
Apgar Scoring System, 74
Decision-Making Process, 75
Postresuscitation Care, 81
Complications of Resuscitation, 82
The Premature Neonate, 82
Special Situations, 83 Resuscitation Outside the Hospital or Beyond the Immediate Neonatal Period, 84
Ethics, 84
PART TWO
Cornerstones of Clinical Practice
6. Thermoregulation, 86
M. Colleen Brand and Holly A. Shippey Introduction, 86
Physiology of Thermoregulation, 90 Management of the Thermal Environment, 92 Summary, 96
7. Physical Assessment, 99
Ellen Tappero
Perinatal History, 99
Gestational Age Instruments, 101
Classification of Growth and Maturity, 105
Physical Examination, 111
8. Fluid and Electrolyte Management, 131
Susan Givens Bell
Fluid Balance, 131
Disorders of Fluid Balance, 133
Electrolyte Balance and Disorders, 136
Acid–Base Balance and Disorders, 141
9. Glucose Management, 144
Debra Armentrout
Glucose Homeostasis, 144
Hypoglycemia, 145
Infant of Diabetic Mother, 148
Hyperglycemia, 149
Transient or Permanent Neonatal Diabetes, 150
10. Nutritional Management, 152
Leslie A. Parker
Anatomy and Physiology of the Premature Infant’s GI Tract, 152
Nutritional Requirements, 155
Parenteral Nutrition, 158
Enteral Feedings: Human Milk and Commercial Formulas for Term, Special-Needs, and Premature Infants, 161
Enteral Feeding Methods, 164
Nursing Interventions to Facilitate Tolerance of Enteral Feedings, 167
Nutritional Assessment and Standards for Adequate Growth, 167
11. Developmental Support, 172
Carol Turnage Spruill Threats to Development, 172 Early Experience, 173 What is Developmental Care?, 174
Operationalizing Developmental Care, 176
Developmentally Supportive Environment, 182
Developmental Care Practices, 184
Parent Support and Involvement, 187 Teamwork and Continuity of Care, 188
12. Pharmacology, 191
Christine D. Domonoske
Principles of Pharmacology, 191 Pharmacodynamics, 192 Pharmacokinetics, 193
Medication Categories, 200
Nursing Implications for Medication Administration in the Neonate, 206
13. Laboratory Testing in the NICU, 207
Patricia Scheans
Laboratory Testing in the NICU, 207 Laboratory Specimen Collection Best Practices, 209
Laboratory Test Interpretation Principles, 210 Principles of Test Utilization, 211
Laboratory Interpretation—Decision Tree, 212 Laboratory Testing—Iatrogenic Sequelae and Preventive Strategies, 214 Decision Questions to Ask Before Obtaining a Laboratory Test, 216
14. Radiologic Evaluation, 219
Carol Wiltgen Trotter Basic Concepts, 219 Terminology, 219 X-Ray Views Commonly Used in the Newborn Infant, 220
Risks Associated With Radiographic Examination in the Neonate, 221 Approach to Interpreting an X-ray, 221 Respiratory System, 223
Pulmonary Parenchymal Disease, 223 Pulmonary Air Leaks, 226
Parents’ Role in Pain Assessment and Management, 284
17. Families in Crisis, 288
Carole Kenner and Marina Boykova Grief, 288
Interventions for Facilitating Crisis Resolution, 293 Interventions for Facilitating Grief Resolution, 295 Interventions for Parents Experiencing a Perinatal Loss, 296
18. Patient Safety, 301
Joan Renaud Smith and Ann Donze
Domain One—Culture, 302
Structured Effective Methods of Communication, 305 Domain Two—Learning System, 306
Core Value of the Framework: Parent/Family Engagement, 307
19. Discharge Planning and Transition to Home, 329
Pat Hummel and Margaret M. Naber
Introduction, 329
General Principles, 329 Health Care Trends, 329
Individualized Discharge Criteria for the Infant and Family, 330
Parenting in the NICU and After Discharge, 331
Discharge Preparation and Process for All NICU Infants, 333
Additional Considerations for Discharge of Infants With Complex Medical Needs, 337
Family and Infant Care Postdischarge, 340
20. Genetics: From Bench to Bedside, 346
Julieanne Heidi Schiefelbein
Basic Genetics, 346
Chromosomal Defects, 348
Prenatal Diagnosis, 348
Postnatal Testing, 351 Human Genome Project, 352 Genetic Counseling, 352 Newborn Care, 353
21. Intrafacility and Interfacility Neonatal Transport, 359
Webra Price-Douglas and Tammy Rush Historical Aspects, 359 Philosophy of Neonatal Transport, 360 Intrafacility Neonatal Transport, 360 Interfacility Neonatal Transport, 361 Transport Equipment, 365 Neonatal Transport Process, 367 Documentation, 371 Safety, 371 Disaster Preparation, 373 Air Transport Considerations, 373 Legal and Ethical Considerations, 374 Quality Management, 374
22. Care of the Extremely Low Birth Weight Infant, 377
Pathophysiology: Management, and Treatment of Common Disorders
24. Respiratory Distress, 394
Debbie Fraser Lung Development, 394
Physiology of Respiration, 396
Respiratory Disorders, 396
Pulmonary Air Leaks (Pneumomediastinum, Pneumothorax, Pneumopericardium, Pulmonary Interstitial Emphysema), 410
Pulmonary Hypoplasia, 412
Pulmonary Hemorrhage, 412
Other Causes of Respiratory Distress, 412
25. Apnea, 417
Lindsey Churchman
Definitions of Apnea, 417 Types of Apnea, 417 Pathogenesis of Apnea in the Premature Infant, 418
Causes of Apnea, 419 Evaluation for Apnea, 420 Management Techniques, 421 Home Monitoring, 423
26. Assisted Ventilation, 425
Debbie Fraser and William Diehl-Jones
Physiology, 425
Treatment Modalities, 429
Nursing Care of the Patient Requiring Respiratory Support or Conventional Mechanical Ventilation, 432
High-Frequency Ventilation, 434
Nursing Care During Therapy, 438
Medications Used During Ventilation Therapy, 440
Weaning From Conventional Ventilation, 442
Interpretation of Blood Gas Values, 443
27. Extracorporeal Membrane Oxygenation, 446
Leigh Ann Cates-McGlinn
ECMO: A Historical Perspective, 446
Common Neonatal ECMO Pathophysiology, 446
Criteria for Use of ECMO, 447
ECMO Perfusion Techniques, 447
Circuit Components and Additional Devices, 448
Physiology of Extracorporeal Circulation, 452
Care of the Infant Requiring ECMO, 453
Post-ECMO Care, 456
Parental Support, 457
Follow-Up and Outcome, 457
28. Cardiovascular Disorders, 460
Sharyl L. Sadowski and M. Terese Verklan
Cardiovascular Embryology and Anatomy, 461
Congenital Heart Defects, 466
Risk Assessment and Approach to Diagnosis of Cardiac Disease, 468
Defects With Increased Pulmonary Blood Flow, 475
Obstructive Defects With Pulmonary Venous Congestion, 479
Obstructive Defects With Decreased Pulmonary Blood Flow, 481
Mixed Defects, 485
Congestive Heart Failure, 490
Postoperative Cardiac Management, 492
Postoperative Disturbances, 494
29. Gastrointestinal Disorders, 504
Wanda T. Bradshaw
Gastrointestinal Embryonic Development, 504
Functions of the Gastrointestinal Tract, 505
Assessment of the Gastrointestinal System, 505
Abdominal Wall Defects, 508
Obstructions of the Gastrointestinal Tract, 512
Necrotizing Enterocolitis, 522
Short-Bowel Syndrome, 524
Biliary Atresia, 526
Cholestasis, 527
Gastroesophageal Reflux, 528
Multisystem Disorders With Gastrointestinal Involvement, 530
30. Endocrine Disorders, 543
Susan Tucker Blackburn
The Endocrine System, 543
Pituitary Gland Disorders, 545
Thyroid Gland Disorders, 546
Adrenal Gland Disorders, 551
Sexual Development, 556
Disorders of Sexual Development, 556
Pancreas, 564
31. Hematologic Disorders, 568
William Diehl-Jones and Debbie Fraser
Development of Blood Cells, 568
Coagulation, 572
Anemia, 574
Hemorrhagic Disease of the Newborn, 577
Disseminated Intravascular Coagulation, 578
Thrombocytopenia, 580
Polycythemia, 581
Inherited Bleeding Disorders, 582
Transfusion Therapies, 583
Evaluation by Complete Blood Cell Count, 586
32. Infectious Diseases in the Neonate, 588
Kathryn M. Rudd
Transmission of Infectious Organisms in the Neonate, 588
Risk Factors, 589
Diagnosis and Treatment, 589
Neonatal Septicemia, 595
Infection With Specific Pathogens, 600
Infection Control, 611
33. Renal and Genitourinary Disorders, 617
Denise Maguire
Overview, 617
Fetal Development of the Kidney, 617
Development of the Bladder and Urethra, 618
Renal Function, 618
Renal Anatomy, 618
Regulation of Postnatal Renal Hemodynamics, 619
Clinical Evaluation of Renal and Urinary Tract Disease, 621
Laboratory Evaluation of Renal Function, 622
Radiographic Evaluation, 623
Acute Kidney Injury, 623
Renal Tubular Acidosis, 625
Developmental Renal Abnormalities, 625
Disorders of the Genitalia, 627
34. Neurologic Disorders, 629
Georgia Ditzenberger
Anatomy of the Neurologic System, 629
Physiology of the Neurologic System, 631
Neurologic Assessment, 632
Neural Tube Defects (NTDs), 634
Neurologic Disorders, 636
Intracranial Hemorrhages, 644
Seizures, 647
Hypoxic–Ischemic Encephalopathy, 649
Periventricular Leukomalacia, 652
Meningitis, 653
35. Congenital Anomalies, 654
Lisa A. Lubbers
Specific Disorders, 658
Sex Chromosome Abnormalities, 664
Non-Chromosomal Abnormalities, 665
Deformation Abnormalities, 671
Congenital Metabolic Problems, 672
Disorders of Metabolism, 673
36. Neonatal Dermatology, 678
Catherine Witt
Anatomy and Physiology of the Skin, 678
Care of the Newborn Infant’s Skin, 680
Assessment of the Newborn Infant’s Skin, 681
Common Skin Lesions, 681
37. Ophthalmologic and Auditory Disorders, 691
Debbie Fraser and William Diehl-Jones
Anatomy of the Eye, 691
Patient Assessment, 692
Pathologic Conditions and Management, 693
Nasolacrimal Duct Obstruction, 694
Anatomy of the Ear, 701
Innervation, 702
Patient Assessment, 702
PART FOUR
Professional Practice
38. Foundations of Neonatal Research, 705
Alice S. Hill
Research and Generation of Nursing Knowledge, 705
Research Process and Components of a Research Study, 707
Quantitative Research, 708
Qualitative Research, 709
Areas of Exploration in Neonatal Nursing, 709
Nurses as Consumers of Research, 709
Ethics in Research and Nurses as Advocates, 710
39. Ethical Issues, 714
Tanya Sudia and Anita Catlin
Examining Ethical Issues in the NICU, 714
Principles of Biomedical Ethics, 715
Other Approaches to Ethical Issues, 716
Case Analysis Model, 717
The Nurse’s Role in Ethical Issues, 717
Assessing Ethical Advisories From Maternal Child Organizations, 718
Consulting the Hospital Ethics Committee, 718
Summary, 718
40. Legal Issues, 720
M. Terese Verklan
Nursing Process, 720
Standard of Care, 721
Malpractice, 723
Liability, 723
Advanced Practice, 726
Documentation, 727
Informed Consent, 730
Professional Liability Insurance, 731
Appendix A: Newborn Metric Conversion Tables, 734
Index, 737
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PART 1
Antepartum, Intrapartum, and Transition to Extrauterine Life
Uncomplicated Antepartum, Intrapartum, and Postpartum Care
Bonita Shviraga and Jennifer G. Hensley
OBJECTIVES
1. Identify normal physiologic changes of each system in pregnancy.
2. Describe parameters to assess gestational age and establish pregnancy dating.
3. Discuss genetic screening options for pregnancy.
4. Identify medications that may cause congenital malformations.
5. Outline components of prenatal care, including history, physical, laboratory, and diagnostic testing.
Antepartum, intrapartum, and postpartum care are not usually included within the practice parameters of the neonatal nurse. Yet an understanding of the normal processes of pregnancy, birth, and postpartum recovery provides a framework for beginning to understand factors that affect the developing fetus and the high-risk neonate. This chapter discusses uncomplicated antepartum, intrapartum, and postpartum nursing care. In addition, an overview of the normal physiologic changes that can be expected in a healthy mother is included.
Terminology
A. Calculation of gestation: 280 days, 40 postmenstrual weeks, or 10 lunar months counted from the first day of the last menstrual period. (Actual duration of gestation from conception to estimated date of delivery is 38 weeks, assuming a 28-day cycle.)
B. Trimesters: division of gestation into three segments of approximately equal duration.
1. First trimester: 0 to 12 weeks.
2. Second trimester: 13 to 27 weeks.
3. Third trimester: 28 to 40 weeks.
C. Preterm, late preterm, term, and post-term pregnancy: preterm, less than 37 completed weeks; late preterm, 340/7 to 366/7 weeks; term, 37 to 42 weeks; and post-term, greater than 42 weeks.
6. Explain tests of fetal lung maturity.
7. Identify six methods of antepartum fetal surveillance.
8. Discuss the normal stages of labor and delivery.
9. Describe low-risk labor management, including fetal monitoring guidelines.
10. Discuss normal immediate postpartum recovery and related postpartum nursing assessments and management.
Normal Maternal Physiologic Changes by Systems
A. Alimentary tract and perinatal nutrition.
1. During pregnancy, there is an increased caloric need of 300 kcal/day to support the growing fetus and increased maternal metabolic rate (Antony et al., 2017). Pregnant teenagers need an additional 100 to 200 kcal/day. According to the Institute of Medicine (IOM), now known as the National Academy of Medicine, the total recommended weight gain for women with a normal body mass index (BMI) is 25 to 35 pounds, and for underweight women a gain of up to 40 pounds may be recommended (American College of Obstetricians and Gynecologists [ACOG], 2016a). The IOM recommends limiting weight gain to 11 to 20 pounds for obese women; however, some experts feel this target is still too high (ACOG, 2016a; Antony et al., 2017) and that adverse pregnancy outcomes can be further decreased in obese women by further limiting pregnancy weight gain (Antony et al., 2017).
2. An inadequate intake of folic acid has been associated with neural tube defects (NTDs) (U.S. Preventive Services Task Force, 2016). It is likely that the
functional mechanism for folate’s effect on NTDs is its epigenetic role in DNA methylation and histones (Ross and Desai, 2017). Routine supplementation of folic acid 0.4 to 0.8 mg is recommended for women of childbearing age or for those planning a pregnancy to assist in the prevention of NTDs (U.S. Preventive Services Task Force, 2016). Women with a previously affected child should take folic acid 4 mg daily for 1 month prior to conception and throughout the first 3 months of gestation (Agency for Healthcare Research and Quality [AHRQ], 2017; West et al., 2017).
3. Approximately 50% of pregnancies are affected by morning sickness during the first trimester, which is associated with increased levels of human chorionic gonadotropin (hCG) and progesterone (West et al., 2017).
4. The stomach loses tone, has decreased motility, and may have delayed emptying time due to the smooth muscle relaxation effects of progesterone (King et al., 2015). Evidence regarding delayed gastric emptying is inconclusive; however, there is a delay during labor (Antony et al., 2017).
5. Relaxation of the pyloric sphincter and upward displacement of the diaphragm, in combination with increased intra-abdominal pressure from the enlarging uterus, can result in gastroesophageal reflux and heartburn (West et al., 2017).
6. The small bowel has reduced motility and hypertrophy of the duodenal villi to increase absorption of nutrients. Constipation is a problem because of mechanical obstruction from the uterus, reduced motility, and increased water absorption (King et al., 2015; West et al., 2017).
7. The gallbladder has decreased muscle tone and motility after 14 weeks as a result of the effects of progesterone. High levels of estrogen may decrease water absorption by the gallbladder’s mucosa, leading to dilute bile, with resulting inability to sequester cholesterol. This increase in cholesterol may lead to gallstone formation during the second and third trimesters of pregnancy (Antony et al., 2017). Decreased gallbladder tone may also lead to increased retention of bile salts, resulting in pruritus and cholestasis gravidarum. Cholestasis gravidarum has been associated with increased risk of stillbirth and preterm deliveries (Cappell, 2017).
8. The liver is displaced upward by the enlarging uterus. Estrogen may cause altered production of plasma proteins, bilirubin, serum enzymes, and serum lipids. Alterations in laboratory values such as reduced serum albumin, elevated alkaline phosphatase, and elevated serum cholesterol may mimic liver disease. Serum levels of bilirubin, aspartate aminotransferase (AST), and alanine aminotransferase (ALT) are unchanged in normal pregnancy and may be used as an indicator of hepatic
compromise during pregnancy. During labor, alkaline phosphatase levels may increase further, and AST, ALT, and lactate dehydrogenase levels may increase as a result of the stress of labor (Cappell, 2017).
9. The gut microbiome changes in pregnancy, with an altered bacterial load and composition. These changes resemble the gut microbiome found in proinflammatory and prodiabetogenic states and may promote energy storage and fetal growth (Antony et al., 2017).
B. Respiratory system.
1. The increased vascularity and vascular congestion of the upper respiratory tract, resulting from increased levels of estrogen, causes hypersecretion of mucus from the nasopharynx, which may lead to nasal stuffiness, sinus congestion, and epistaxis (nosebleed) during pregnancy (Antony et al., 2017).
2. Maternal oxygen requirements increase during 20% during pregnancy (Cunningham et al., 2014).
3. The chest wall profile changes. Increased levels of estrogen and relaxin cause relaxation of intercostal ligaments with resulting increased chest expansion and chest circumference and an increase in the subcostal margin angle (Cunningham et al., 2014). The diaphragm is elevated by 4 cm in the third trimester (King et al., 2015).
4. Respiratory changes during pregnancy include a 30% to 40% increase in tidal volume, a 15% to 20% decrease in expiratory reserve volume, a 20% to 25% decrease in residual volume, and a 20% decrease in functional residual capacity ( Antony et al., 2017). Forced expiratory volume does not change in pregnancy and is a reliable indicator of respiratory illness, including asthma, in pregnant women (Antony et al., 2017). Increasing progesterone levels lead to chronic hyperventilation by 8 weeks, as reflected in the increase in tidal volume. Maternal Paco2 levels decrease to 32 mm Hg and oxygen levels rise to 106 mm Hg early in pregnancy to allow fetal–placental exchange ( Antony et al., 2017). As a result of these cumulative respiratory changes, pregnant women may experience physiologic dyspnea. To prevent the maternal acidosis due to the carbon dioxide levels from the fetus, mild hyperventilation occurs, which may cause a respiratory alkalosis. According to Cunningham et al. (2014), progesterone lowers the threshold and increases chemosensitivity to carbon dioxide; in response to the respiratory alkalosis, plasma bicarbonate levels decrease from 26 to 22 mmol/L, creating a slight increase in blood pH that shifts the oxygen dissociation curve to the left. Although pulmonary function is not impaired, respiratory diseases may be more serious during pregnancy ( Cunningham et al., 2014).
C. Sleep.
1. Pregnancy may increase sleep disorders and change sleep profiles, which may extend into the postpartum period. The majority of pregnant women (66% to 94%) report sleep alterations, which may begin as early as the first trimester and worsen as pregnancy progresses (Antony et al., 2017).
2. There is a decrease in rapid eye movement (REM) sleep, which is important for cognition, and a decrease in stage 3 and 4 non-REM sleep, which is important for rest. By the third month postpartum, stage 3 and 4 alterations resolve; however, sleep disruption may occur due to nocturnal infant awakenings (Antony et al., 2017).
3. Restless leg syndrome (RLS) onset or its worsening in pregnancy may also contribute to sleep disturbances and should be assessed (Antony et al., 2017).
D. Skin.
1. Because of elevated levels of estrogen, spider angiomas are frequently seen on the neck, face, throat, and arms. Palmar erythema is common in two thirds of white women and one third of African American women (Antony et al., 2017; Cunningham et al., 2014).
2. Striae gravidarum occurs in some women due to the thinning of the elastin fibers in the connective tissue under the skin (King et al., 2015).
3. Increased pigmentation is due to increased levels of estrogen and melanocyte-stimulating hormone and occurs in approximately 90% of women. This is most marked on the nipples, areolas, perineum, and midline of the lower portion of the abdomen (commonly called the linea nigra) (Antony et al., 2017).
4. Hyperpigmentation of the face, known as chloasma or melasma and also referred to as the mask of pregnancy, is caused by melanin deposits in the epidermis and macrophages. The resulting dark, blotchy appearance of the face, forehead, and upper lip occurs in up to 70% of women and is exacerbated by ultraviolet light (Wang and Kroumpouzos, 2017).
5. During gestation, a greater percentage of the hair remains in the anagen (growth) phase, which decreases normal hair loss. Hair loss commonly occurs between 2 and 4 months after delivery due to an increase in the telogen (resting) phase of hair growth. The hair returns to a normal growth phase within 1 to 5 months (Wang and Kroumpouzos, 2017).
6. Changes in secretory glands occur during pregnancy. Sebaceous gland activity alterations are variable, and the resulting changes in acne development are unpredictable (Wang and Kroumpouzos, 2017). Eccrine sweat gland activity increases as a result of increased thyroid activity, body weight,
and metabolic activity and may result in miliaria and dyshidrotic eczema.
7. Changes in the nails are uncommon but may occur beginning in the first trimester. Changes include brittleness, distal separation of the nail bed, subungual hyperkeratosis, whitish discoloration (leukonychia), and transverse grooving (Wang and Kroumpouzos, 2017). The cause is unknown.
8. There is a change in the vaginal microbiome, with decreased diversity and decreased number of species present and a predominance of Lactobacillus species. One of the predominant neonatal gastrointestinal (GI) species, L. johnsonii, is increased in the vaginal microbiome and may be important in the establishment of the neonatal GI microbiome (Antony et al., 2017).
E. Urinary system.
1. Structural renal changes begin during the first trimester and are a result of progesterone, pressure from the enlarging uterus, and increase in blood volume. The kidneys enlarge, the ureters dilate, hyperplasia of the smooth muscle walls of the ureters occurs, and the ureters elongate. Hydronephrosis occurs in 80% of pregnant women (Antony et al., 2017; Columbo, 2017).
2. An increase in asymptomatic bacteriuria (ASB) may lead to cystitis and pyelonephritis in pregnancy. The most common pathogen for ASB is Escherichia coli (Columbo, 2017).
3. The renal plasma flow increases by 75%, with a 25% decrease in the third trimester (Antony et al., 2017). The increased renal plasma flow is accompanied by an increase in the glomerular filtration rate of 50%, which leads to an increase in creatinine clearance and a decrease in nitrogen levels, as reflected by decreased blood urea nitrogen (BUN) and serum creatinine levels (Antony et al., 2017).
4. Due to the expansion of plasma volume and water retention in pregnancy, even though sodium retention is increased by 900 mEq, serum levels of sodium decrease by 3 to 4 mmol/L (Antony et al., 2017).
5. The reduced threshold for glucose reabsorption may result in glycosuria in pregnancy. Glycosuria can be detected in up to 90% of pregnant women with normal blood glucose. However, repetitive glycosuria warrants evaluation (Antony et al., 2017). Glucose measurements in the management of diabetes mellitus may be affected.
6. A small amount of proteinuria may occur in pregnancy due to decreased protein reabsorption (King et al., 2015). Urinary protein excretion increases in pregnancy, with an upper limit of 300 mg in a 24-hour period (Antony et al., 2017). Greater than trace proteinuria may not indicate pathology, but warrants evaluation for urinary tract infection and preeclampsia.
F. Cardiovascular system.
1. There is an increase in maternal blood volume by 40% to 50% from the end of the first trimester, peaking at 32 weeks (King et al., 2015). If the plasma volume increases faster than red blood cell (RBC) production, a physiologic anemia may result (King et al., 2015).
2. There is an increase in maternal heart rate, which increases by 17% above the nonpregnant state by the third trimester. Stroke volume increases by 8 weeks’ gestation until 20 weeks at 20% to 30% above prepregnancy levels. There is an increase in cardiac output beginning in the first trimester and peaking at 30% to 50% above prepregnancy levels, with most of the increase in cardiac output to the uterus, placenta, and breast (Antony et al., 2017).
3. Because the heart is displaced leftward and upward by the enlarging uterus, the cardiac silhouette increases on x-ray films. It is important to confirm cardiomegaly with an echocardiogram and not rely solely on x-ray (Antony et al., 2017).
4. Altered cardiac sounds in pregnancy include splitting of the first heart sound, an audible S3 heart sound, systolic ejection murmurs (96% of pregnant women), and transient diastolic murmurs (up to 18% of pregnant women). Diastolic murmurs should be evaluated (Antony et al., 2017).
5. Blood pressure (BP) remains at the prepregnancy level in the first trimester and drops during the second trimester at approximately 24 weeks of gestation by a mean arterial pressure (MAP) of 5 to 10 mm Hg. It returns to normal prepregnancy levels at the end of pregnancy. It is recommended in the ambulatory setting that BP be taken in the sitting position and that the fifth Korotkoff sound be used for diastolic BP measurement (Antony et al., 2017).
6. Between 20 and 24 weeks of gestation, pressure on and resulting obstruction of the inferior vena cava may occur in the supine position. The resulting 10% to 30% fall in cardiac output, due to the decrease in stroke volume as a result of decreased blood in the heart, results in supine hypotension. Positioning the mother in a lateral position or with lateral displacement of the uterus with placement of a wedge under her hip assists in the prevention of supine hypotension (Antony et al., 2017).
7. Blood stagnates in the lower extremities because of compression of the pelvic veins and the inferior vena cava, contributing to dependent edema and the development of varicosities (King et al., 2015). G. Breasts.
1. Early changes in the breasts during the first trimester include tenderness and paresthesia (Cunningham et al., 2014). The symptoms usually subside at the end of the first trimester.
2. The areolas enlarge and darken. Sebaceous glands on the areolae increase activity in preparation for lactation and therefore become more prominent (Cunningham et al., 2014).
3. Estrogen, progesterone, human placental lactogen (hPL), hCG, prolactin, and luteal and placental hormones cause hyperplasia of the breast tissue and development of lactiferous ducts and lobular alveolar tissue during the second and third trimesters (King et al., 2015). Physical examination may reveal palpable milk ducts and excretion of colostrum from the nipples.
4. Colostrum, which is a high-protein precursor of breast milk, may be expressed toward the end of pregnancy (King et al., 2015).
5. The breast begins lactogenesis with alveolar cells changing to a secretory epithelium toward the middle of pregnancy. After delivery, the second stage of lactogenesis, milk production, begins (King et al., 2015).
H. Skeletal changes.
1. Compensating for the anteriorly positioned growing uterus, the lower portion of the back curves. This lordosis shifts the center of gravity backward over the lower extremities and causes low back pain, a common complaint in pregnancy (Antony et al., 2017; King et al., 2015).
2. The sacroiliac and pubic symphysis joints loosen during pregnancy due to effects of the hormone relaxin and may result in pain localized to the symphysis pubis and radiating down the inner thigh (Antony et al., 2017).
3. Alteration in the center of gravity, loosening of the joints, and an unsteady gait increase the risk of falls in pregnancy.
4. Although serum calcium levels decrease during pregnancy, serum ionized calcium levels are unchanged. Maternal serum calcium levels are maintained, and fetal calcium needs are met through increased maternal intestinal absorption of calcium (Antony et al., 2017).
5. Bone turnover is low in the first trimester and later increases in the third trimester when peak fetal calcium transfer occurs; however, osteoporosis is not associated with pregnancy bone turnover (Antony et al., 2017).
I. Hematologic changes.
1. Plasma volume increases 15% by the end of the first trimester, undergoes a rapid expansion during the second trimester, peaks at 32 to 34 weeks, and then plateaus near term (Cunningham et al., 2014). Plasma volume at or near term is 50% above prepregnancy levels (Antony et al., 2017).
2. The white blood cell (WBC) count rises progressively during pregnancy and labor. Prepregnancy levels range from 5000 to 12,000 cells/microliter