MODULE 5FETUS/NEWBORN AT RISK

• ASSESSMENT OF FETAL WELL BEING

• NEWBORN AT RISK

–CONDITIONS PRESENT AT BIRTH

–BIRTH RELATED STRESSORS

• THE POSTPARTUM FAMILY AT RISK

MODULE 5 PART 1ASSESSMENT OF FETAL WELL

BEING

ASSESSMENT OF FETAL WELL BEING

• ANTEPARTUM RISK FACTORS– MATERNAL AGE <16, >35– Rh ISOIMMUNIZATION– HISTORY OF UNEXPLAINED STILLBIRTH– SUSPECTED IUGR– POSTDATES GESTATION– PIH, DIABETES MELLITUS, CARDIAC

DISEASE– DOMESTIC VIOLENCE

ULTRASOUND

• ULTRASOUND—USE OF HIGH FREQUENCY SOUND WAVES TO VISUALIZE STRUCTURES OF VARYING DENSITIES – NEW RESEARCH– NONINVASIVE, PAINLESS– SEVERAL TESTS MAY BE COMPLETED

FOR COMPARISON

ULTRASOUND

• TRANSABDOMINAL

• ENDOVAGINAL

• CLINICAL (DIAGNOSITIC) APPLICATIONS– FHR, FBM, FETAL TONE– EARLY DETECTION OF PREGNANCY– MEASURMENT OF BPD

ULTRASOUND

– MULTIPLE GESTATION– ESTIMATIONS OF FETAL BIRTH WEIGHT– DETECTION OF ANOMALIES– AMNIOTIC FLUID INDEX (AFI)– PLACENTA LOCATION, GRADING– DETECTION OF IUFD– FETAL POSITION, PRESENTATION– USED IN AMNIOCENTESIS, PBS, BPP,

DOPPLER BLOOD FLOW STUDIES

DOPPLER BLOOD FLOW VELOCITY

• ASSESSES PLACENTAL PERFUSION

• ULTRASOUND BEAM DIRECTED AT UMBILICAL ARTERY

• SIGNAL REFLECTED OFF CIRCULATING RBCS—CREATES WAVELIKE PATTERN– S/D RATIO

NONSTRESS TEST (NST)

• ACCELERATIONS IN FHR WITH FETAL MOVEMENT INDICATES ADEQUATE OXYGENATION AND INTACT CNS

• REACTIVE TEST

• NONREACTIVE TEST

Figure 14–5 Example of a reactive nonstress test (NST). Accelerations of 15 bpm lasting 15 seconds with each fetal movement (FM). Top of strip shows FHR; bottom of strip shows uterine activity tracing. Note that FHR increases (above the baseline) at least 15 beats and remains at that rate for at least 15 seconds before returning to the former baseline.

Figure 14–6 Example of a nonreactive NST. There are no accelerations of FHR with FM. Baseline FHR is 130 bpm. The tracing of uterine activity is on the bottom of the strip.

Figure 14–7 NST management scheme. Source: Devoe, L. D. (1989). Nonstress and contraction stress testing. In R. Depp, D. A. Eschenbach, & J. J. Sciarri (Eds.), Gynecology and obstetrics (Vol. 3, p. 9, Figure 5). Philadelphia: Lippincott.

BIOPHYSICAL PROFILE

• FIVE COMPONENTS

– NST

– FETAL BREATHING MOVEMENTS

– FETAL TONE

– FETAL MOVEMENTS

– AMNIOTIC FLUID INDEX (AFI)

AMNIOCENTESIS

• NEEDLE IS INSERTED THROUGH ABDOMINAL WALL INTO UTERUS DURING ULTRASOUND TO OBTAIN AMNIOTIC FLUID SAMPLE FOR ANALYSIS

• DIAGNOSTIC CRITERIA– MATERNAL AGE 35 OR OLDER– GENETIC DEFECTS– METABOLIC DEFECTS– FETAL LUNG MATURITY L/S RATIO

AMNIOCENTESIS

– NEURAL TUBE DEFECTS– FETAL SEX– ADVANTAGES, RISK

• CHORIONIC VILLI SAMPLING– SMALL SAMPLE OF CHORIONIC VILLI

FROM PLACENTA OBTAINED FOR TESTING

– ADVANTAGES, RISKS

Figure 14–9 Amniocentesis. The woman is scanned by ultrasound to determine the placental site and to locate a pocket of amniotic fluid. Then the needle is inserted into the uterine cavity to withdraw amniotic fluid.

OTHER ANTEPARTUM TESTING

• PERCUTANEOUS UMBILICAL BLOOD SAMPLING (PUBS)

– BLOOD SAMPLE TAKEN FROM UMBILICAL CORD IN UTERO UNDER ULTRASOUND WITH NEEDLE THROUGH MATERNAL ABDOMEN AND UTERUS

NEWBORN AT RISK

• NEWBORN RISK FACTORS– LOW SOCIO-ECONOMIC LEVEL OF MOTHER– PRE-EXISTING MATERNAL CONDITIONS– EXPOSURE TO ENVIRONMENTAL HAZARDS– MATERNAL AGE AND PARITY– PREGNANCY COMPLICATIONS– MEDICAL CONDITIONS RELATED TO

PREGNANCY

NEWBORN WEIGHT & GESTATIONAL AGE

– LARGE FOR GESTATIONAL AGE (LGA)

– AVERAGE FOR GESTATIONAL AGE (AGA)

– SMALL FOR GESTATIONAL AGE (SGA)

• SGA INFANT—MAY BE– PRETERM– TERM– POSTTERM

NEWBORN WEIGHT AND GESTATIONAL AGE

• BIRTH WEIGHT AND GESTATIONAL AGE ARE USED TOGETHER TO ASSESS NEONATAL MATURITY & MORTALITY RISK

• INTRAUTERINE GROWTH RESTRICTION– SYMMETRIC– ASYMMETRIC

IUGR/SGA

• RISK FACTORS RELATING TO IUGR• COMPLICATIONS RELATED TO SGA

NEWBORN• CLINICAL MANAGEMENT

– WEIGHT GAIN—TAKES FEEDING WITHOUT FATIGUE

– STABLE RESPIRATORY STATUS– STABLE TEMPERATURE & GLUCOSE

LEVELS

LGA

• LARGE FOR GESTATIONAL AGE– FACTORS ASSOCIATED WITH LGA

• MULTIPARITY• GENETIC PREDISPOSITION• MALE INFANTS• VARIOUS SYNDROMES• DIABETES

– COMPLICATIONS ASSOCIATED WITH LGA

INFANT OF DIABETIC MOTHER

• PATHOPHYSIOLOGY

• COMPLICATIONS OF THE IDM

• CLINICAL MANAGEMENT

• POSTMATURITY SYNDROME– COMMON COMPLICATIONS– CLINICAL MANAGMENT

POSTTERM INFANT

• BORN AFTER 42 WEEKS GESTATION

• INACCURATE EDC

• POSTMATURITY SYNDROME

• COMPLICATIONS

• CHARACTERISITICS

PRETERM INFANT• PRETERM INFANT

– PRETERM AND SGA INFANTS HAVE HIGHEST MORTALITY RISK

• IMMATURITY OF ALL SYSTEMS– RESPIRATORY/CARDIOVASCULAR– THERMOREGULATION– RENAL– REACTIVITY/ BEHAVIORAL STATES– NUTRITION & FLUID REQUIREMENTS– IMMUNE COMPROMISED

PRETERM INFANT

• COMPLICATIONS– RDS (RESPIRATORY DISTRESS

SYNDROME)

– IVH (INTRAVENTRICULAR HEMMORHAGE)

– PDA (PATENT DUCTUS ARTERIOSIS)

– NEC (NECROTIZING ENTEROCOLITIS)

PRETERM INFANT

– APNEA

– ANEMIA

– ROP (RETINOPATHY OF PREMATURITY)

– BPD (BRONCO-PULMONARY DISPLASIA)

– SEPSIS, COLD STRESS, HYPOGLYCEMIA

PRETERM INFANT

• LONG TERM NEEDS AND OUTCOME

– NEUROLOGIC DEFECTS– AUDITORY DEFECTS– SPEECH DEFECTS

NEWBORN OF SUBSTANCE ABUSING MOTHER

– FETAL ALCOHOL SYNDROME (FAS)– COMPLICATIONS– CHARACTERISTICS– CLINICAL MANAGEMENT

– DRUG DEPENDENCY• CHARACTERISTICS, RISKS• COMPLICATIONS• CLINICAL MANAGEMENT• NEW RESEARCH FINDINGS

– NEWBORN WITHDRAWAL

NEWBORN WITH CONGENTIAL ANOMALY

– CHOANAL ATRESIA– HYDOCEPHALUS– CLEFT LIP, PALATE– TRACHOESOPHAGEAL FISTULA– DIAPHRAGMATIC HERNIA– MYELOMENINGOCELE, IMPERFORATE

ANUS– OMPHALOCELE, GASTROCHISIS– CONGENITAL DISLOCATED HIP

NEWBORN WITH CONGENITAL HEART DEFECT

• ACYANOTIC– PDA– ASD– VSD– COARCTATION OF THE AORTA– HYPOPLASTIC LEFT HEART SYNDROME

• CYANOTIC– TETRALOGY OF FALLOT– TRANSPOSITIONS OF THE GREAT VESSELS

NEWBORN WITH INBORN ERROR OF METABOLISM

• PKU

• MAPLE SYRUP URINE DISEASE

• GALACTOSEMIA

• CONGENITAL HYPOTHYROIDISM

• TESTING TESTS DIFFER AMONG STATES

THE NEWBORN WITH ASPHYXIA

• PATHOPHYSIOLOGY

• RISK FACTORS

• CLINICAL THERAPY

• RESPIRATORY DISTRESS– PREMATURITY– SURFACTANT DEFICIENCY

• TRANSIENT TACHYPNEA

Figure 26–3 Cycle of events of RDS leading to eventual respiratory failure. Source: Modified from Gluck, L., & Kulovich, M. V. (1973). Fetal lung development. Pediatric Clinics of North America, 20, 375.

Figure 26–6 Evaluation of respiratory status using the Silverman-Andersen index. The baby’s respiratory status is assessed. A grade of 0, 1, or 2 is determined for each area, and a total score is charted in the baby’s record or on a copy of this tool and placed in the chart. Source: Ross Laboratories, Nursing Aid No. 2. Columbus, OH; Silverman, W. A., & Andersen, D. H. (1956). Pediatrics, 17, 1–10. Copyright 1956, American Academy of Pediatrics.

MECONIUM ASPIRATION SYNDROME

• PATHOPHYSIOLOGY– ALVEOLI OVERDISTEND DUE TO AIR

ALLOWED IN BUT OBSTRUCTION OF AIR OUTFLOW DURING EXPIRATION—LEADS TO AIR TRAPPING AND AIR LEAK (PNEUMOTHORAX AND PNEUMOMEDIASTINUM) (20-30%)

– BILE SALTS AND PANCREATIC ENZYMES IN MECONIUM CAUSE A CHEMICAL PNEUMONITIS

MECONIUM ASPIRATION SYNDROME

• CLINICAL MANIFESTATIONS– PROLONGED LABOR– POSTTERM– FETAL HYPOXIA– DECREASED FETAL MOVEMENTS– SLOWING OF FHR, WEAK, IRREGULAR– DECREASE IN SHORT TERM VARIABILITY– MECONIUM STAINED FLUID– LOW APGAR SCORES

MECONIUM ASPIRATION SYNDROME

• CLINICAL MANAGEMENT– INITIAL RESUSCITATION– MECHANICAL VENTILATION– CHEST X-RAY– ABGs– SURFACTANT REPLACEMENT THERAPY– ECHMO

NEWBORN WITH COLD STRESS

• ABILITY OF INFANT TO RESPOND TO COLD STRESS IMPAIRED BY:– HYPOXEMIA– INTRACRANIAL HEMORRHAGE– HYPOGLYCEMIA

• CLINICAL MANAGEMENT

Figure 26–8 Cold stress chain of events. The hypothermic, or cold-stressed, newborn attempts to compensate by conserving heat and increasing heat production. These physiologic compensatory mechanisms initiate a series of metabolic events that result in hypoxemia and altered surfactant production, metabolic acidosis, hypoglycemia, and hyperbilirubinemia.

NEWBORN WITH HYPOGLYCEMIA

• PATHOPHYSIOLOGY– WHY ARE INFANTS OF GESTATIONAL AND

IDDM MOTHERS HYPOGLYCEMIC AFTER BIRTH?

• MOST COMMON METABOLIC DISORDER OCCURING IN:– AGA PRETEM INFANT– INFANT OF A DIABETIC MOTHER– SGA INFANT

NEWBORN WITH HYPOGLYCEMIA

• CLINICAL PRESENTATION

• CLINICAL MANAGEMENT

• BLOOD GLUCOSE SAMPLING

NEWBORN WITH JAUNDICE

• CONSIDERED PATHOLOGIC IF:– JAUNDICE EVIDENT IN 1ST 24 HOURS OR

AFTER 4 DAYS OF LIFE– SERUM BILIRUBIN > 5mg/dL/DAY– TOTAL SERUM BILIRUBIN

CONCENTRATIONS EXCEED 12.9 mg/dL in TERM INFANTS; 15mg/dL IN PRETERM

– CLINICAL JAUNDICE PERSISTS BEYOND 7 DAYS IN TERM, 14 DAYS PRETERM

NEWBORN WITH JAUNDICE

• PATHOPHYSIOLOGY• CAUSES

– HEMOLYTIC DISEASE• ERYTHROBLASTOSIS FETALIS• HYDROPS FETALIS

– POLYTHYCEMIA– BILIARY ATRESIA OR OBSTRUCTION– SEPSIS– METABOLIC PROBLEMS

NEWBORN WITH JAUNDICE

• CLINICAL MANAGEMENT– PHOTOTHERAPY– EXCHANGE TRANSFUSION– ALBUMIN INFUSION—WHY?

NEWBORN WITH INFECTION

• SEPSIS NEONATORUM

– PREDISPOSING FACTORS/RISKS

– MATERNALLY TRANSMITTED NEWBORN DISEASES

– NOSOCOMIAL INFECTION

• CLINICAL MANAGEMENT

DIFFERENTIAL DIAGNOSES

• HOW DO WE DIFFERENTIATE THE DIAGNOSES OF COLD STRESS, HYPOGLYCEMIA, DRUG WITHDRAWAL, AND SEPSIS?

– WHAT SYMPTOMS DO THEY SHARE?– WHAT SYMPTOMS ARE UNIQUE TO SPECIFIC TO

EACH CONDITION?– WHAT WE DO FIRST?

POSTPARTUM FAMILY AT RISK

• EARLY POSTPARTAL HEMORRHAGE– FIRST 24 HOURS AFTER BIRTH– UTERINE ATONY

• OVERDISTENTION OF UTERUS• OXYTOCIN• GRAND MULTIPARITY• PIH• RAPID OR PROLONGED LABOR

POSTPARTUM FAMILY AT RISK

• INTRA AMNIOTIC INFECTION• USE OF DRUGS/ANESTHESIA THAT CAUSE

UTERUS TO RELAX• ASIAN OR HISPANIC HERITAGE

– RETAINED PLACENTAL FRAGMENTS– VULVAR, VAGINAL, PELVIC HEMATOMAS– LACERATIONS OF REPRODUCTIVE TRACT

• CLINICAL MANAGEMENT

POSTPARTUM FAMILY AT RISK

• PUERPERAL INFECTION (REPRODUCTIVE TRACT INFECTION)– ENDOMETRITIS– PELVIC CELLULITIS– PERINEAL WOUND INFECTIONS– CESAREAN WOUND INFECTION

• URINARY TRACT INFECTION

POSTPARTUM FAMILY AT RISK

• LATE POSTPARTAL HEMORRHAGE– 24 HOURS TO 6 WEEKS AFTER BIRTH– DUE TO SUBINVOLUTION OF PLACENTAL

SITE DUE TO RETAINED PLACENTAL FRAGMENTS

• CLINICAL MANAGEMENT

POSTPARTUM FAMILY AT RISK

– OVERDISTENTION OF BLADDER– INABILITY TO VOID– CYSTITIS

• MASTITIS

• THROMBOEMBOLIC DISEASE– CONTRIBUTING FACTORS– SUPERFICIAL VEIN THROMBOPHLETITIS– DEEP VEIN THROMBOSIS

POSTPARTUM FAMILY AT RISK

– SEPTIC PELVIC THROMBOPHLEBITIS

• CLINICAL MANAGEMENT

• POSTPARTUM PSYCHIATRIC DISORDER