OU MFM board AI content

Fetal shunts and oxygenated blood delivery

Fetal shunts facilitate oxygenated placental blood reaching the fetal systemic circulation: ductus venosus, foramen ovale, and ductus arteriosus. They preferentially direct the most oxygenated blood to the myocardium and brain. (ExamPro MFM Course Manual, Schamroth 3e, slide p.4)

Venous return and O2 saturation in the fetus

Umbilical venous blood is the most highly saturated blood in the fetal circulation. Ductus venosus carries it by extension. Liver blood supply: umbilical vein 75-80%, portal vein remainder, hepatic artery ~5%. (ExamPro MFM Course Manual, Schamroth 3e, slide p.4)

Preferential streaming of fetal venous return

Ductus venosus flow crosses the foramen ovale to the left atrium, delivering oxygenated blood to myocardium/brain. IVC/SVC flow directs deoxygenated blood to RA/RV and back to the placenta for re-oxygenation. (ExamPro MFM Course Manual, Schamroth 3e, slide p.5)

Fetal cardiac output

The ventricles work in parallel producing a 'combined' ventricular output with intracardiac shunting. Stroke volumes differ: RV > LV (approximately 65% vs 35% of combined output). (ExamPro MFM Course Manual, Schamroth 3e, slide p.5)

Intracardiac and vascular pressures in the fetus

Right-sided pressures are higher than left due to preferential streaming (greater volume of flow) and mild flow resistance in the ductus arteriosus. (ExamPro MFM Course Manual, Schamroth 3e, slide p.6)

Determinants of fetal cardiac output (myocardial function)

Determinants: preload (ventricular filling pressure; Frank-Starling mechanism of fiber stretch and muscular force), afterload (impedance to ventricular ejection), contractility (intrinsic inotropic capacity), and heart rate. (ExamPro MFM Course Manual, Schamroth 3e, slide p.6)

Autoregulation and baroreflex control of fetal CV system

Autoregulation: blood flow redistribution during hypoxia to brain, heart and adrenals at the expense of other visceral organs. Baroreflex: changes in arterial blood pressure detected by carotid/aortic baroreceptors produce vagally mediated FHR responses. (ExamPro MFM Course Manual, Schamroth 3e, slide p.7)

Chemoreflex and autonomic control of fetal CV system

Chemoreflex: changes in O2/CO2 content detected by aortic chemoreceptors produce hypertension. Autonomic nervous system: sympathetic effect on FHR (beta receptors) and vascular tone (alpha receptors) predates parasympathetic development. Gradual slowing of baseline FHR across gestation; interplay of both produces FHR variability. (ExamPro MFM Course Manual, Schamroth 3e, slide p.7)

Fetal myocardial function limits

The fetal heart operates at the limits of the cardiac function curve due to immaturity of structure, function and sympathetic innervation. Stroke volume response is impaired (smaller myocardial cell diameter, altered ratio of non-contractile to contractile elements). Cardiac output is exquisitely sensitive to changes in FHR. (ExamPro MFM Course Manual, Schamroth 3e, slide p.8)

Hormonal regulation of the fetal cardiovascular system

Renin-angiotensin system responds to hypovolemia; vasopressin (ADH) is a stress response; atrial natriuretic factor modulates right ventricular overload; prostaglandins have diverse effects on vascular tone (e.g. DA patency); nitric oxide and endothelin have potent effects on vascular tone. (ExamPro MFM Course Manual, Schamroth 3e, slide p.8)

Placental respiratory gas exchange steps

Steps: transport of atmospheric oxygen to the gravid uterus; oxygen uptake by the uterus; transport of oxygen to fetal tissue; oxygen therapy; and placental CO2 transfer. (ExamPro MFM Course Manual, Schamroth 3e, slide p.10)

Source of data on fetal physiology

Human fetal physiology data are scant; the majority of data come from sheep with chronically implanted vascular catheters in the maternal and fetal circulations. Oxygen transport chain: atmosphere - diffusion across alveolar membrane - diffusion across the placenta - diffusion into total tissues. (ExamPro MFM Course Manual, Schamroth 3e, slide p.11)

Fick principle for O2 uptake by uterus and fetus

The Fick principle estimates O2 uptake by uterus and fetus using uterine and umbilical blood flow and the O2 content of maternal artery, uterine vein, umbilical vein and umbilical artery. Oxygen uptake = quantity of oxygen lost per mL of blood x blood flow. (ExamPro MFM Course Manual, Schamroth 3e, slide p.11)

Venous equilibration system of placental O2 uptake

The placenta approximates a venous equilibration system (ideal but not achievable in biologic systems). The venous pO2 of the umbilical circulation cannot be higher than the venous pO2 of the uterine circulation. (ExamPro MFM Course Manual, Schamroth 3e, slide p.12)

Factors that determine uterine venous pO2

Determinants include hemoglobin structure, temperature, red cell pH, 2,3-DPG, the oxyhemoglobin dissociation curve of maternal blood, arterial O2 saturation, uteroplacental blood flow, O2 capacity, placental and fetal O2 consumption, and O2 saturation in uterine venous blood. (ExamPro MFM Course Manual, Schamroth 3e, slide p.12)

Inefficiencies in fetal oxygen uptake

Placental O2 uptake inefficiencies arise from shunting (anatomic and diffusional through myo/endometrium), uneven perfusion among placental cotyledons, and impaired oxygen-diffusing capacity (permeability vs resistance, e.g. IUGR/placental vascular lesions). (ExamPro MFM Course Manual, Schamroth 3e, slide p.13)

Transport of oxygen to fetal tissues

Despite low pO2 (relative hypoxia), the fetus transports large amounts of oxygen to its tissues via high O2 affinity of fetal hemoglobin, high fetal cardiac output relative to body size and metabolic rate, distribution of cardiac output (somatic and umbilical), and the ability to redistribute blood flow during pathologic hypoxia. (ExamPro MFM Course Manual, Schamroth 3e, slide p.14)

Maternal O2 therapy effect on the fetus

Maternal O2 therapy produces only a small increase in fetal pO2 but a significant effect on fetal O2 content (in both acute and chronic fetal hypoxemia), explained by the venous equilibration model and the fetal oxyhemoglobin dissociation curve. (ExamPro MFM Course Manual, Schamroth 3e, slide p.14)

Placental CO2 transfer

Diffusional transfer of fetal CO2 to the mother requires fetal PCO2 to be higher than maternal. CO2 is highly diffusible across the human hemochorial placenta, so maternal and fetal acid-base disturbances readily affect each other. (ExamPro MFM Course Manual, Schamroth 3e, slide p.15)

Contributors to improved perinatal outcome

Neonatal intensive care; regionalized referrals; safety of cesarean delivery; avoidance of birth trauma; improved care of diabetes and pre-eclampsia; high-resolution ultrasound/prenatal diagnosis/fetal therapy; prevention/therapy of Rh disease; improved detection of IUGR (10x RR of IUFD); and antepartum fetal surveillance (APFS). (ExamPro MFM Course Manual, Schamroth 3e, slide p.17)

Etiologies of antepartum fetal death

Antepartum deaths outnumber intrapartum (80% vs 20%). Etiologies: chronic asphyxia (30-50% of cases), IUGR, post-term gestation, congenital malformations, superimposed pregnancy complications (placental abruption, fetal infection, Rh disease), unexplained causes, and fetomaternal hemorrhage. (ExamPro MFM Course Manual, Schamroth 3e, slide p.17)

Avoidable fetal death - interventions

Intervene for abnormal FHR tracings, intervene for abnormal fetal growth, evaluate significant maternal weight loss, and respond to decreased fetal movement. (ExamPro MFM Course Manual, Schamroth 3e, slide p.18)

Findings of early APFS cohort studies (1980s)

Non-randomized cohort studies: perinatal mortality in the high-risk tested population was half that of the non-tested low-risk population; fetal mortality (false-negative) rate was less than half (11.2 vs 2.2 per 1000). Two-thirds of antepartum fetal deaths are due to chronic placental failure amenable to detection by surveillance techniques. (ExamPro MFM Course Manual, Schamroth 3e, slide p.18)

Goal and definition of APFS

Goal of APFS: reduce the risk of fetal death or harm. Fetal death accounts for 48% of all perinatal mortality. US fetal death rate is

Collaborative Perinatal Project - fetal death etiologies

In high-risk pregnancies the fetal mortality rate was 40-50/1000. Etiologies: cord and placenta 30%, maternal and fetal infection 17%, prematurity 10%, congenital anomalies 8%, Rh disease 4%. (ExamPro MFM Course Manual, Schamroth 3e, slide p.19)

APFS potential interventions

Preterm/term delivery; backup tests (BPP, Doppler); maternal O2 therapy; correction of maternal disorders (e.g. DKA); antenatal corticosteroids; bed rest/observation for maturity; and fetal therapy: IUT for fetal anemia (Rh, FMH, parvovirus), fetal surgery (thoracentesis, vesicocentesis), diagnostic procedures (amniocentesis, cordocentesis), and direct fetal therapy (e.g. antiarrhythmics for fetal SVT). (ExamPro MFM Course Manual, Schamroth 3e, slide p.20)

APFS and test validity - definitions

Sensitivity = TP/(TP+FN); Specificity = TN/(TN+FP); PPV = TP/(FP+TP); NPV = TN/(TN+FN). For APFS purposes, high sensitivity is desired to minimize false negatives (missed compromise). (ExamPro MFM Course Manual, Schamroth 3e, slide p.20)

Fetal neurobehavioral states (Nijhuis)

State 1F (quiet sleep): brief gross body movements, non-REM/few FBM, stable FHR with few/no accelerations and diminished variability. State 2F (active sleep): frequent gross body movements, REM/FBM, frequent accelerations and more variability. State 3F (quiet awake): no gross body movements, REM, stable FHR with few accelerations but more variability than 1F. State 4F (active awake): vigorous continual activity, REM, frequent accelerations coalescing to tachycardia with exaggerated variability. (ExamPro MFM Course Manual, Schamroth 3e, slide p.21)

Fetal movement - normative ultrasound data

In the 3rd trimester the fetus is moving ~10% of the time (30 movements/hour, peaks 2100-0100 hours). Active states average 40 minutes; inactive states average 20 minutes (75-minute threshold). Movement increases with maternal hypoglycemia; maternal glucose does not increase activity; fetal movement decreases in proportion to hypoxemia. Gravidas appreciate 70-80% of fetal movements. (ExamPro MFM Course Manual, Schamroth 3e, slide p.22)

Factors obscuring maternal perception of fetal movement

Maternal activity, amniotic fluid volume, placental location, obesity, fetal anomaly, and drugs (narcotics, barbiturates). (ExamPro MFM Course Manual, Schamroth 3e, slide p.23)

Decreased fetal movement - implications

About 5% of gravidas complain of decreased fetal movement. It is associated with a 10x relative risk of depressed Apgar scores and increased risk of IUGR. Fetal movement does not decrease before delivery. (ExamPro MFM Course Manual, Schamroth 3e, slide p.23)

Fetal movement counting - Count-to-Ten method

Normative FMC data obtained in a cohort of all pregnancies with counting encouraged in the evening; median time to 10 movements ~21 minutes with 90% compliance. Perinatal mortality declined; there was a 13% increase in patients tested for decreased fetal movement. Concerning threshold: fewer counts / more than 2 SD below median. (ExamPro MFM Course Manual, Schamroth 3e, slide p.24)

Fetal movement counting - advantages

Inexpensive, simple, effective, and universally applicable. Should be employed in all gravidas beginning at 28 weeks. (ExamPro MFM Course Manual, Schamroth 3e, slide p.24)

Fetal breathing movements (FBM)

Begin as early as 10 weeks and increase across gestation; episodic and separated by periods of apnea (apnea >=6 seconds). Present ~30% of the time in the last 10 weeks. A maturational process reflected in the rate of FBM and breath-to-breath interval. (ExamPro MFM Course Manual, Schamroth 3e, slide p.25)

Factors influencing fetal breathing movements

Influenced by neurobehavioral state, gestational age, maternal CO2, maternal blood glucose (increases FBM), incipient/true labor (PGE2 mediated), advanced preterm labor, chorioamnionitis (inflammatory cytokines), and fetal hypoxemia (decreases FBM). (ExamPro MFM Course Manual, Schamroth 3e, slide p.25)

The Contraction Stress Test (CST)

First test of antenatal fetal well-being; an antenatal extension of intrapartum FHR monitoring, now rarely used. Tests the fetal FHR response to stress from contractions (spontaneous, nipple stimulation, or IV oxytocin). Advantage: low false-negative rate (~1/100). Disadvantages: relative contraindications (PTL/PPROM, previa, abruption, incompetent cervix), frequent equivocal/false-positive tests, difficult reproducibility, excessive uterine activity, and time/support requirements. (ExamPro MFM Course Manual, Schamroth 3e, slide p.26)

CST interpretation categories

Negative (~80%): absence of late decelerations in a 10-minute window. Positive (3-5%): repetitive late decelerations with >50% of contractions. Suspicious/equivocal (5%): inconsistent late decelerations. Hyperstimulation (5%): FHR decelerations with excessive uterine activity (

Non-reactive NST with positive CST - outcomes

Associated with perinatal mortality 7.3-10%, IUGR 29.3%, fetal anomaly 17.1%, high labor induction and cesarean rate (C/S 58.5%; C/S for late decelerations 33.3%). (ExamPro MFM Course Manual, Schamroth 3e, slide p.27)

The Non-Stress Test (NST)

Observation of FHR characteristics reflecting fetal condition: fetal movement accompanied by a reflex increase in FHR in normally oxygenated fetuses; hypoxemia impairs the FHR response to movement. A normal fetus may lack accelerations for up to 80 minutes (state 1F). Advantages: easily and rapidly performed, no contraindications, easy interpretation, low false-negative rate (1-5/1000). Disadvantage: requires twice-weekly testing for optimal outcome. (ExamPro MFM Course Manual, Schamroth 3e, slide p.28)

Reactive NST - criteria

Two FHR accelerations of >=15 bpm lasting >=15 seconds within a 10- (or 20-) minute window. Fetal acoustic stimulation and maternal glucose have no effect. Initial test: 85% reactive, 15% non-reactive. Non-reactive rates increase with prematurity: 15% at 28-32 weeks and 50% at 24-28 weeks. (ExamPro MFM Course Manual, Schamroth 3e, slide p.28)

Non-reactive NST - management and significance

Must differentiate quiet sleep from hypoxemia; requires backup BPP or CST. High false-positive rate. Associated with oligohydramnios, fetal acidosis, meconium-stained fluid, placental infarction, IUGR, ~25% positive CST, and C/S for non-reassuring fetal status. Perinatal mortality 30-40/1000, but as high as 50% when persistently non-reactive at 80 minutes. (ExamPro MFM Course Manual, Schamroth 3e, slide p.29)

Fetal acoustic stimulation (FAS)

Sound with frequency and harmonics; vibroacoustic stimulation. Comparable reliability to a spontaneously reactive NST, reliable at 28 weeks gestation, and associated with normal auditory acuity at 4 years of life. Useful to shorten testing time by rousing the fetus from quiet sleep. (ExamPro MFM Course Manual, Schamroth 3e, slide p.29)

Variable FHR decelerations on NST - etiology and associations

Etiologies: abnormal cord position, oligohydramnios, Rh disease, placental compression, or unknown. Even with a reactive NST they are associated with intrapartum variable decelerations and other non-reassuring patterns, oligohydramnios, IUGR, fetal acidemia, and perinatal mortality in postdate pregnancy. (ExamPro MFM Course Manual, Schamroth 3e, slide p.30)

Prolonged decelerations on NST

Associated with >50% C/S for fetal distress, oligohydramnios/IUGR/vulnerable cord position, and congenital malformations. Carry fetal mortality risk; when associated with a non-reactive NST there is 50% fetal mortality. (ExamPro MFM Course Manual, Schamroth 3e, slide p.31)

Amniotic fluid volume as an index of fetal condition

Oligohydramnios is associated with IUGR, congenital malformations, abnormal antepartum FHR patterns, perinatal morbidity/mortality, placental insufficiency, and cord compression. Semi-quantitative techniques: subjective impression, largest vertical pocket, and the AFI (4-quadrant assessment). (ExamPro MFM Course Manual, Schamroth 3e, slide p.31)

Amniotic fluid index (AFI)

The AFI is the sum of the largest vertical pockets of fluid from each of the 5 (four) quadrants of the uterus. (ExamPro MFM Course Manual, Schamroth 3e, slide p.32)

Biophysical profile (BPP) - overview

An evaluation of fetal biophysical activities and amniotic fluid volume as acute and chronic indicators of fetal condition. Advantages: normal test is reassuring, no contraindications, low false-positive rate and improved predictive value make it a good backup test. Disadvantages: time, equipment and personnel requirements. (ExamPro MFM Course Manual, Schamroth 3e, slide p.33)

Fetal Biophysical Profile - components and scoring

Five components, each scored 2 if normal: NST (reactive), fetal breathing (duration >30 sec), fetal movement (>=3 movements), fetal tone (flexion/extension of limb or trunk, open/close hand), and amniotic fluid volume (AFI >5.0 cm or largest pocket). (ExamPro MFM Course Manual, Schamroth 3e, slide p.33)

BPP - fetal CNS centers and graded hypoxia (Vintzileos)

Biophysical variables appear in a developmental order and are lost in reverse with graded hypoxia: fetal tone (7.5-8.5 weeks), fetal movements (9 weeks), fetal breathing (20-21 weeks), and FHR reactivity (24-28 weeks). The last to develop are the first to be lost with hypoxia. (ExamPro MFM Course Manual, Schamroth 3e, slide p.34)

Modified BPP

The modified BPP is NST + AFI performed once or twice weekly. Advantages: assesses acute (NST) and chronic (AFI) condition with a very low false-negative rate (<=1/1000). (ExamPro MFM Course Manual, Schamroth 3e, slide p.35)

Modified BPP - Clark study results

In 5973 tests on 2628 high-risk pregnancies (NST with FAS after 5 min plus AFI, weekly/semi-weekly): mean testing time 10 minutes, non-reactive NST 2%, intervention rate 3%, no unexpected fetal deaths, and false-negative rate 0/1000. (ExamPro MFM Course Manual, Schamroth 3e, slide p.36)

Delivery considerations from fetal testing

Consider delivery for: AFI <5% for EGA; NST with prolonged FHR deceleration; BPP <=4; postdate pregnancy with variable FHR decelerations; and FHR decelerations associated with IUGR or oligohydramnios in a non-postdate pregnancy. (ExamPro MFM Course Manual, Schamroth 3e, slide p.36)

APFS - test choice and false-negative rates

False-negative rates per 1000: CST weekly ~1; NST weekly 5-10; NST semiweekly (2x) 2-5; BPP weekly ~1; NST/AFI (modified BPP) semiweekly ~1. (ExamPro MFM Course Manual, Schamroth 3e, slide p.37)

Indications for APFS and gestational age to start

Start APFS at: diabetes A1 ~40 wk; diabetes A2-R 32 wk; medical disorders 32 wk; prior IUFD 32 wk (or 1 week before the prior IUFD); postdate 41 wk; Rh disease 32 wk; multiple gestation depends on plurality; decreased fetal movement, abnormal FHR, and suspected IUGR at diagnosis. (ExamPro MFM Course Manual, Schamroth 3e, slide p.38)

Doppler ultrasound - vessels assessed

Arterial circulation: umbilical artery, uterine arteries, middle cerebral artery, descending aorta. Venous circulation: ductus venosus, umbilical vein, inferior vena cava. Also intracardiac Doppler and color/power/high-definition flow imaging. (ExamPro MFM Course Manual, Schamroth 3e, slide p.39)

Doppler ultrasound - principles

Allows non-invasive evaluation of fetal and maternal blood flow; simultaneous real-time ultrasound, color flow and pulsed Doppler target a specific vessel. The measure of blood flow resistance is a surrogate for volume of flow (true volume requires vessel diameter, and significant errors occur). Indices: systolic/diastolic ratio, resistance index, and pulsatility index. (ExamPro MFM Course Manual, Schamroth 3e, slide p.41)

Umbilical artery Doppler - significance

Assesses downstream placental vascular resistance in the fetoplacental circulation; obtained mid-cord during fetal apnea with normal FHR. Placental vascular resistance declines across gestation. Abnormal umbilical artery Doppler reflects vascular obliteration in tertiary stem villi with atheromatous changes and is associated with IUGR, pre-eclampsia and preterm birth. (ExamPro MFM Course Manual, Schamroth 3e, slide p.42)

Umbilical artery Doppler - meta-analysis benefits

Meta-analyses (including Cochrane reviews) show umbilical artery Doppler reduces perinatal mortality, reduces antenatal admissions, reduces inductions of labor, and reduces cesarean for fetal distress. (ExamPro MFM Course Manual, Schamroth 3e, slide p.43)

Middle cerebral artery Doppler - brain sparing

The cerebral circulation is normally high-resistance. Hypoxemia/acidemia redistributes blood flow to high-priority organs (brain, heart, adrenals). MCA Doppler shows augmented diastolic flow with decreased S/D ratio and PI ('brain sparing'). The cerebroplacental ratio is used in IUGR. (ExamPro MFM Course Manual, Schamroth 3e, slide p.43)

Fetal venous Doppler

Assesses the ductus venosus, IVC and umbilical vein as indicators of fetal cardiac function. With acidemia there is abnormal venous flow. May be a better indicator of delivery timing than standard modes of fetal surveillance. (ExamPro MFM Course Manual, Schamroth 3e, slide p.44)

Uterine artery Doppler and trophoblastic invasion

The secondary wave of trophoblastic invasion at 16-20 weeks converts low-flow, high-resistance circuits into high-flow, low-resistance circuits by 20-22 weeks, with a 10x increase in blood flow. Failure of conversion occurs in ~10% and is associated with IUGR, pre-eclampsia, PTD, abruption and IUFD. (ExamPro MFM Course Manual, Schamroth 3e, slide p.45)

APFS summary principles

Fetal movement counting in all pregnancies at 28 weeks; no test is perfect; use the test you are most comfortable with; select testing schemes addressing the specific indication; intervene when indicated; be consistent in interpretation; clinical judgment is probably more important than test choice; and Doppler of the fetoplacental, fetal venous and uteroplacental circulations are important adjuncts in high-risk management. (ExamPro MFM Course Manual, Schamroth 3e, slide p.45)

Regionalized neonatal care - general principles

Regionalized neonatal care is cost-effective with lower neonatal mortality in Level III centers with greater volumes (>15 patients average daily census), a strong argument for centralizing high-risk deliveries. (ExamPro MFM Course Manual, Schamroth 3e, slide p.48)

Birth trauma / birth injuries

Occur in 2-7/1000 live births. Antepartum causes: amniocentesis, PUBS, IUT, fetal surgery. Intrapartum (most common): macrosomia, prematurity, malpresentation, prolonged labor, dystocia, CPD, instrumentation (C/S not completely protective). Postnatal: resuscitation. (ExamPro MFM Course Manual, Schamroth 3e, slide p.48)

Cephalohematoma

Subperiosteal, parieto-occipital collection associated with hairline fractures. Can result in anemia and jaundice but rarely requires transfusion. Does not cross suture lines. DDx: caput succedaneum. (ExamPro MFM Course Manual, Schamroth 3e, slide p.49)

Subgaleal hemorrhage

Rare (4/10,000 deliveries), more frequent with instrumental delivery, and serious (mortality up to 26%). Blood collects in the space between the galea aponeurotica and the periosteum of the skull, crossing suture lines. Can cause hypovolemia, hypotension, shock, DIC and seizures. Treatment: blood and blood products. (ExamPro MFM Course Manual, Schamroth 3e, slide p.49)

Brachial plexus injury

Traction or avulsion of cervical nerve roots. Horner's syndrome occurs if T1 sympathetic roots involved. Associated with prolonged labor/traction/dystocia/breech and can occur in utero. Treatment is expectant: 88% resolve by 4 months and 93% by 2 years. (ExamPro MFM Course Manual, Schamroth 3e, slide p.51)

Respiratory distress syndrome (RDS) - risk factors and pathophysiology

Risk factors: prematurity, maternal diabetes, hydrops, perinatal asphyxia. Severity varies with gestational age. Pathophysiology: impaired or delayed surfactant synthesis superimposed on a structurally immature lung. (ExamPro MFM Course Manual, Schamroth 3e, slide p.52)

RDS - clinical presentation and X-ray

Presentation: tachypnea, subcostal and intercostal retractions, nasal flaring, and expiratory grunting. Onset 1-2 hours postnatally with peak severity at 2-3 days (shortened by surfactant, prolonged by PDA, air leak, chronic lung disease). X-ray: reticulogranular pattern, similar to GBS pneumonia. (ExamPro MFM Course Manual, Schamroth 3e, slide p.53)

RDS - treatment

Exclude other causes. Provide nutrition, thermal regulation, acid/base balance, fluid/electrolytes, correction of anemia. Use pulse oximetry, +/- umbilical arterial catheter, surfactant, and assisted ventilation. (ExamPro MFM Course Manual, Schamroth 3e, slide p.53)

Surfactant therapy in RDS

Natural preparations are better than synthetic and cost-effective. Benefits: decreased neonatal mortality in preterm infants, increased survival without BPD, improved O2 saturation/decreased air leaks, and reduced mortality with prophylactic vs rescue therapy at early gestational ages. Unresolved issues: pulmonary hemorrhage (6%) and the role of high-frequency ventilation. (ExamPro MFM Course Manual, Schamroth 3e, slide p.54)

Neonatal assisted ventilation

Modes: CPAP (non-invasive), conventional mechanical ventilation, and high-frequency ventilation (rapid rate, small volumes; jet or oscillator). Goal: reduce ventilator-induced lung injury. No data yet show improved survival or decreased chronic lung disease (BPD). (ExamPro MFM Course Manual, Schamroth 3e, slide p.54)

Transient tachypnea of the newborn (TTN)

Respiratory distress in term or near-term infants with a modest O2 requirement. X-ray differs from RDS but is difficult to differentiate from pneumonia or meconium aspiration. Resolution within 48 hours. (ExamPro MFM Course Manual, Schamroth 3e, slide p.55)

Meconium aspiration syndrome (MAS)

Occurs in IUGR or post-date infants, chronic asphyxia, and infection. No single intrapartum FHR pattern is predictive; may occur before onset of labor. Oropharyngeal suctioning and prophylactic amnioinfusion for thick meconium do not reduce the risk of MAS. Therapy: ventilation, antibiotics, surfactant, ECMO/nitric oxide. (ExamPro MFM Course Manual, Schamroth 3e, slide p.55)

Persistent pulmonary hypertension / persistent fetal circulation

Causes include pulmonary hypoplasia, meconium aspiration, perinatal asphyxia, bacterial pneumonia, and sepsis; high morbidity/mortality. Treatment: conventional or high-frequency ventilation, nitric oxide, correction of acidosis, prostacyclin, cardiovascular support (dopamine), sedation, and ECMO. (ExamPro MFM Course Manual, Schamroth 3e, slide p.56)

Hyperbilirubinemia and kernicterus

Most commonly encountered in the term neonate. Kernicterus is yellow staining of the basal ganglia and hippocampus leading to CNS damage and death from excess bilirubin; generally does not occur at <25 mg% but rare reports at ~10 mg%. Resurgence in term infants due to early discharge, poorly supervised breast-feeding, and inadequate follow-up. (ExamPro MFM Course Manual, Schamroth 3e, slide p.57)

Physiologic vs pathologic hyperbilirubinemia

Physiologic causes: increased production (high HCT, short RBC life), decreased clearance (functional UGT deficiency), and increased enterohepatic reabsorption; TSB peaks at 48-96 hours and resolves by ~1 week. Pathologic features: TSB >95th percentile for age in hours, rate of rise >0.2 mg/dL/hr, jaundice in first 24 hours, and conjugated bilirubin elevation suggesting cholestasis. UGT = uridine glucuronyl transferase. (ExamPro MFM Course Manual, Schamroth 3e, slide p.57)

Treatment of neonatal jaundice

Perform a thorough workup and ensure adequate hydration. Phototherapy isomerizes bilirubin so it can be excreted. Exchange transfusion in general if phototherapy fails or TSB >20-30 mg/dL. (ExamPro MFM Course Manual, Schamroth 3e, slide p.58)

Cerebral palsy - definition

A chronic disability of the CNS with aberrant control of movement and posture, appearing early in life and non-progressive. Features: abnormal tone and reflexes, abnormal consciousness, abnormal feeding, abnormal respirations, and seizures. (ExamPro MFM Course Manual, Schamroth 3e, slide p.59)

Neonatal encephalopathy - causes

Causes include hypoxic-ischemic encephalopathy (HIE) from intrapartum hypoxemia, CVA, infection, cerebral malformation, genetic disorders, and other etiologies. (ExamPro MFM Course Manual, Schamroth 3e, slide p.59)

Why FHR monitoring does not reduce cerebral palsy

Asphyxial damage may be present before labor; sudden acute total/near-total asphyxia (cord prolapse, uterine rupture, vasa previa, abruption) may not allow time for intervention; a higher proportion of CP is now attributable to increased survival; some antenatally-associated CP was previously unappreciated; and the threshold for asphyxia-related neurologic damage is very close to that for asphyxia-related fetal death. (ExamPro MFM Course Manual, Schamroth 3e, slide p.60)

What is damaging asphyxia

Damaging asphyxia is defined by profound umbilical artery metabolic or mixed acidemia (pH <7.0), Apgar 0-3 for longer than 5 minutes, neonatal neurologic sequelae (encephalopathy, seizures, coma, hypotonia), and multiorgan system dysfunction (cardiovascular, GI, hematologic, pulmonary, renal). (ExamPro MFM Course Manual, Schamroth 3e, slide p.61)

Independent predictors of cerebral palsy (ACOG/AAP)

Independent predictors: fetal growth restriction, intrauterine infection, coagulation disorders, maternal or fetal thyroid disease, multiple pregnancy, antepartum hemorrhage, abnormal presentations, aneuploidy, and congenital anomalies. Only a minority are attributable to intrapartum hypoxia. (ExamPro MFM Course Manual, Schamroth 3e, slide p.61)

ACOG criteria for intrapartum (HIE) etiology of cerebral palsy

Essential criteria (all 4 needed): metabolic acidemia (pH

Intracranial hemorrhage in the neonate - risk factors

Associated with prematurity (<32 weeks), intra-amniotic infection, capillary fragility, abnormal cerebral blood flow regulation, coagulation/blood gas derangements, and hypo/hypertension. Bleeding begins in the subependymal germinal matrix and may extend to the lateral ventricles and parenchyma. Antenatal corticosteroids reduce the incidence of severe intracranial hemorrhage. (ExamPro MFM Course Manual, Schamroth 3e, slide p.62)

Intracranial hemorrhage - grading

Grade I: subependymal germinal matrix. Grade II: extension into lateral ventricles. Grade III: ventricular dilatation. Grade IV: intraparenchymal extension (worst prognosis for neurologic outcome). (ExamPro MFM Course Manual, Schamroth 3e, slide p.63)

Neonatal infection - immunity and routes

Incidence of neonatal septicemia is inversely related to gestational age (stable incidence, reduced mortality). Impaired immunity: abnormal chemotaxis/phagocytosis/bactericidal activity, abnormal opsonic activity, complement pathway defects, and impaired humoral immunity (IgM and IgG). Amniotic fluid is normally sterile and bacteriostatic; infection occurs by hematogenous or ascending (preterm PTL/PPROM; term prolonged ROM) routes. (ExamPro MFM Course Manual, Schamroth 3e, slide p.64)

Congenital CMV infection

CMV is the most common congenital viral infection. Maternal seroconversion 2-2.5%; affects 0.5-2.5% of live births with variable fetal/neonatal sequelae (5-20% symptomatic). (ExamPro MFM Course Manual, Schamroth 3e, slide p.65)

Group B Streptococcus (GBS) - epidemiology

Maternal colonization rates ~50%; neonatal attack rate 1-2/1000, higher in prematurity. Universal screening at 35-37 weeks with intrapartum antibiotic prophylaxis (IAP) reduces early-onset disease. (ExamPro MFM Course Manual, Schamroth 3e, slide p.65)

Perinatal HIV transmission

Vertical transmission accounts for 90% of infected children, with a transmission rate of ~25% without therapy, 8% with antenatal/intrapartum AZT, and 1-2% with HAART plus cesarean delivery for viral RNA load >1000 copies/mL. (ExamPro MFM Course Manual, Schamroth 3e, slide p.65)

Necrotizing enterocolitis (NEC)

Etiology unknown; ~25% associated with bacteremia/sepsis, and prematurity is the major risk factor. Variable presentation: abdominal distention, intestinal perforation, peritonitis, shock, DIC. X-ray: pneumatosis intestinalis or portal venous gas. Treatment: bowel rest, IV fluids, broad-spectrum antibiotics, and surgical resection. (ExamPro MFM Course Manual, Schamroth 3e, slide p.65)

Physiologic uterine changes in pregnancy - size and growth

The uterus increases capacity 500-1000x (non-pregnant ~80 g and 10 cc to term ~1100 g and ~5 L). Muscular hyperplasia and hypertrophy occur under hormonal (estrogen) stimulation, with growth more pronounced at the fundus/placental site. It rises out of the pelvis by 12 weeks (8 weeks = orange, 12 weeks = grapefruit). (ExamPro MFM Course Manual, Schamroth 3e, slide p.67)

Physiologic uterine changes - rotation and activity

The uterus is dextrorotated due to the rectosigmoid. First-trimester uterine activity is 'contracture' - segmental, localized, with few gap junctions. Third-trimester activity is 'false labor'/Braxton-Hicks - coordinated contractions from cell-to-cell communication via gap junctions. (ExamPro MFM Course Manual, Schamroth 3e, slide p.68)

Uterine blood flow in pregnancy

Uterine blood flow is maximal at term (~2% of cardiac output in the non-pregnant state). Regulation: estrogen/progesterone and VEGF (stimulatory), catecholamines/angiotensin II (inhibitory), nitric oxide (vasodilator), and prostacyclin (PGI2). Contractions inhibit blood flow in a duration- and intensity-dependent manner (risk with hyperstimulation or pre-existing fetal compromise). (ExamPro MFM Course Manual, Schamroth 3e, slide p.68)

Physiologic changes - cervix and ovary

Cervix softens (Goodell sign) and becomes cyanotic by ~4 weeks; endocervical glands proliferate forming the tenacious mucus plug. Ovary: ovulation and follicular maturation cease; corpus luteum produces 17-OH progesterone; the luteo-placental shift occurs at 6-7 weeks from LMP (4-5 weeks post-ovulation). (ExamPro MFM Course Manual, Schamroth 3e, slide p.69)

Physiologic changes - vagina

Increased vascularity with violet discoloration (Chadwick's sign) and increased mucosal thickness. Leukorrhea of pregnancy is due to estrogen stimulation and sloughing of vaginal squamous epithelium producing copious thick white milky discharge (a diagnosis of exclusion). A change in discharge in the second trimester requires investigation. (ExamPro MFM Course Manual, Schamroth 3e, slide p.69)

Myometrium - structural aspects

Composed of smooth muscle cells in a matrix of collagen and glycosaminoglycans; contraction differs from skeletal muscle; grows by hyperplasia and hypertrophy with increased fibrous/connective tissue; growth induced by estrogen, progesterone and uterine distention; cellular contact in late pregnancy via gap junctions facilitates synchronized contractions. (ExamPro MFM Course Manual, Schamroth 3e, slide p.70)

Decidua - structure and cell types

An endometrial change stimulated by estrogen, progesterone and relaxin, with stromal cell enlargement and gland/blood vessel growth. Layers: decidua basalis, decidua capsularis, and decidua vera (parietalis). Cell types: epithelial cells, stromal cells, mast cells, leukocytes, and endothelium/blood vessels. (ExamPro MFM Course Manual, Schamroth 3e, slide p.71)

Decidual function

Serves as an immunological barrier; has endocrine function (hormone metabolism and secretion); performs prostaglandin synthesis and cytokine production; and has cell membrane receptors for cytokines, immunoglobulins, peptide hormones and steroids. (ExamPro MFM Course Manual, Schamroth 3e, slide p.73)

Cervical ripening

Involves proteolytic collagen dissolution (MMPs, elastases, enhanced by cytokines), increased water content of ground substance, alteration of GAG (dermatan to hyaluronic acid), hormonal control (estrogen stimulatory, ?relaxin), and prostaglandin mediation (PGE2 > PGF2). (ExamPro MFM Course Manual, Schamroth 3e, slide p.74)