Neonatal assessment begins before birth. A structured review of maternal demographics, obstetric history, medical conditions, infections, exposures, fetal surveillance, and the events of labor and delivery allows the team to anticipate complications, assemble the correct resuscitation team and equipment, and target postnatal screening.
Maternal Demographics and Obstetric History
Adolescent mothers (particularly under 17 years) have higher rates of preterm birth, low birth weight, and inadequate prenatal care. Advanced maternal age (35 years or older at delivery) is associated with chromosomal aneuploidy, gestational diabetes, preeclampsia, multiple gestation, and cesarean birth. Poverty, limited education, food insecurity, and lack of social support worsen outcomes by limiting access to prenatal care and nutrition.
Gravidity is the total number of pregnancies regardless of outcome; parity is the number of pregnancies that reached 20 weeks of gestation or more (a multiple birth counts once). A prior spontaneous preterm birth is the strongest historical predictor of another; recurrence risk ranges roughly 15–50% depending on the number and timing of prior preterm births. A history of stillbirth, neonatal death, or an infant with a congenital anomaly or genetic disorder warrants focused evaluation. Multiple gestation increases prematurity, growth restriction, and discordant growth; monochorionic twins share a placenta and are at risk for twin-to-twin transfusion syndrome (donor: anemia, growth restriction, oligohydramnios; recipient: polycythemia, volume overload, polyhydramnios, cardiac dysfunction).
Maternal Medical Conditions
Maternal Conditions and Neonatal Risk| Maternal Condition | Mechanism | Neonatal Implications |
|---|
| Pregestational diabetes (type 1 or 2) | Maternal hyperglycemia → fetal hyperglycemia and hyperinsulinemia; hyperglycemia during organogenesis is teratogenic | Congenital anomalies (cardiac defects including transposition, VSD, and septal hypertrophy; neural tube defects; caudal regression; small left colon), macrosomia, hypoglycemia, hypocalcemia, hypomagnesemia, polycythemia, hyperbilirubinemia, delayed lung maturity (RDS), birth trauma |
| Gestational diabetes | Hyperglycemia develops after organogenesis | Macrosomia, hypoglycemia, polycythemia, birth trauma; anomaly risk is not increased as it is with pregestational diabetes |
| Chronic hypertension, preeclampsia, HELLP syndrome | Uteroplacental insufficiency | Fetal growth restriction, oligohydramnios, iatrogenic preterm birth, abruption; neonatal neutropenia and thrombocytopenia (especially after preeclampsia); effects of maternal magnesium sulfate |
| Maternal ITP (autoimmune thrombocytopenia) | Maternal IgG antiplatelet antibodies cross the placenta | Neonatal thrombocytopenia, usually mild to moderate; platelet nadir typically on days 2–5, so serial counts are needed; intracranial hemorrhage is uncommon |
| Fetal/neonatal alloimmune thrombocytopenia (NAIT) | Maternal sensitization to a paternally inherited fetal platelet antigen (most often HPA-1a); maternal platelet count is normal | Severe thrombocytopenia in an otherwise well infant; risk of intracranial hemorrhage, can occur in the first pregnancy; treated with antigen-negative platelets and IVIG |
| Red cell alloimmunization (anti-D, anti-Kell, others) and ABO incompatibility | Maternal IgG crosses the placenta and destroys fetal red cells (anti-Kell also suppresses erythropoiesis) | Hemolytic disease of the fetus and newborn: anemia, early hyperbilirubinemia, hydrops fetalis; ABO disease is usually milder (mother group O, infant A or B) |
| Chronic renal disease, renal transplant | Hypertension, superimposed preeclampsia, placental insufficiency | Preterm birth and growth restriction; initial neonatal creatinine reflects maternal levels and falls over the first days |
| Hypothyroidism (inadequately treated) | Insufficient maternal thyroxine early in pregnancy, when the fetus depends on maternal supply | Impaired neurodevelopment; newborn screening identifies congenital hypothyroidism |
| Graves disease (current or past, even after ablation) | Thyroid-stimulating immunoglobulins (TRAb) cross the placenta; antithyroid drugs also cross | Fetal tachycardia and goiter; neonatal thyrotoxicosis (tachycardia, irritability, poor weight gain) that may be delayed until maternal antithyroid drug clears; transient hypothyroidism from maternal antithyroid drugs |
| Systemic lupus erythematosus / Sjögren syndrome (anti-Ro/SSA, anti-La/SSB) | Antibodies damage the fetal conduction system and skin | Neonatal lupus: congenital complete heart block (permanent), annular rash, cytopenias, transaminase elevation; preterm birth and growth restriction |
| Antiphospholipid syndrome | Placental thrombosis | Recurrent pregnancy loss, placental insufficiency, growth restriction, preeclampsia |
| Maternal phenylketonuria (poorly controlled) | Elevated maternal phenylalanine is teratogenic | Microcephaly, intellectual disability, congenital heart disease, growth restriction; prevented by strict dietary control before conception and throughout pregnancy |
Maternal Infections as Risk Factors
Maternal infection may reach the fetus transplacentally, by ascending infection, or at delivery. Prenatal records should document syphilis, HIV, hepatitis B (and increasingly hepatitis C) serology, rubella immunity, and group B streptococcus (GBS) status. The table summarizes the neonatal risk; diagnosis and management of neonatal infection are covered in the Infection and Immunology section.
Maternal Infection and Neonatal Risk| Maternal Infection | Neonatal Risk |
|---|
| Cytomegalovirus (CMV) | Most common congenital infection; leading nongenetic cause of sensorineural hearing loss; microcephaly, periventricular calcifications, hepatosplenomegaly, petechiae, growth restriction |
| Toxoplasmosis | Chorioretinitis, diffuse intracranial calcifications, hydrocephalus, developmental delay |
| Rubella (first-trimester infection) | Congenital rubella syndrome: cataracts, congenital heart disease (PDA, peripheral pulmonary stenosis), sensorineural hearing loss, blueberry muffin rash |
| Syphilis | Stillbirth, hydrops, hepatosplenomegaly, rash (including palms and soles), snuffles, osteochondritis and periostitis, neurosyphilis |
| Herpes simplex virus (HSV) | Usually acquired at delivery, highest risk with primary maternal infection near term; skin-eye-mouth, CNS (encephalitis), or disseminated disease |
| Hepatitis B | Perinatal transmission leads to chronic infection in most untreated infants; prevented by birth-dose vaccine plus HBIG within 12 h when mother is HBsAg-positive |
| Hepatitis C | Vertical transmission in a minority of exposed infants; infant testing is required |
| HIV | Transmission minimized by maternal ART with viral suppression and infant ARV prophylaxis; scheduled cesarean reserved for high or unknown maternal viral load near delivery |
| Gonorrhea | Ophthalmia neonatorum (purulent conjunctivitis in the first days), scalp abscess, disseminated infection |
| Chlamydia | Conjunctivitis (typically days 5–14) and afebrile pneumonia at 1–3 months |
| Group B streptococcus colonization | Early-onset sepsis, pneumonia, meningitis; reduced by adequate intrapartum antibiotic prophylaxis |
| Varicella | Congenital varicella syndrome (limb hypoplasia, cicatricial skin scarring, eye and CNS abnormalities) with early-pregnancy infection; severe neonatal varicella when maternal rash begins 5 days before to 2 days after delivery |
| Parvovirus B19 | Fetal anemia from red cell precursor suppression; nonimmune hydrops fetalis |
| Zika virus | Severe microcephaly, brain anomalies, ocular abnormalities, congenital contractures |
Substance Use
Prenatal Substance Exposure| Substance | Fetal and Neonatal Effects |
|---|
| Tobacco / nicotine | Vasoconstriction and reduced oxygen delivery; growth restriction, preterm birth, placental abruption, increased risk of sudden infant death |
| Alcohol | Fetal alcohol spectrum disorders, from neurobehavioral deficits to fetal alcohol syndrome (smooth philtrum, thin upper lip, short palpebral fissures, growth deficiency, CNS abnormalities); no safe amount or timing has been established |
| Opioids (heroin, fentanyl, prescription opioids, methadone, buprenorphine) | Neonatal opioid withdrawal syndrome, NOWS (neonatal abstinence syndrome, NAS); growth restriction and preterm birth with illicit use |
| Cocaine | Vasoconstriction → placental abruption, preterm labor, growth restriction; neurobehavioral effects |
| Methamphetamine | Growth restriction, preterm birth, neurodevelopmental effects |
| Cannabis | Lower birth weight; possible long-term neurodevelopmental effects |
Teratogenic Medications
Teratogenic and Fetotoxic Medications| Medication | Associated Effects |
|---|
| Valproic acid | Neural tube defects (spina bifida), facial dysmorphism, cardiac defects, neurodevelopmental impairment |
| Carbamazepine | Neural tube defects, craniofacial and fingernail anomalies |
| Phenytoin | Fetal hydantoin syndrome: hypoplastic nails and distal phalanges, craniofacial anomalies, growth and developmental delay |
| ACE inhibitors and angiotensin receptor blockers (second and third trimesters) | Fetal renal dysgenesis and anuria → oligohydramnios, pulmonary hypoplasia, skull hypoplasia, neonatal renal failure and hypotension |
| Warfarin | Nasal hypoplasia, stippled epiphyses, CNS abnormalities; fetal hemorrhage |
| Isotretinoin and other retinoids | Craniofacial (ear) anomalies, conotruncal heart defects, CNS malformations, thymic abnormalities |
| Lithium | Ebstein anomaly (low absolute risk); neonatal hypotonia, lethargy, poor feeding, nephrogenic diabetes insipidus, hypothyroidism |
| Methotrexate | Skeletal and craniofacial anomalies, growth restriction |
| Tetracyclines | Tooth discoloration and enamel hypoplasia |
| SSRIs and SNRIs (late pregnancy) | Neonatal adaptation syndrome (jitteriness, irritability, feeding difficulty, tachypnea), usually self-limited; association with persistent pulmonary hypertension of the newborn (PPHN) |
Maternal Intrapartum Medications
Maternal Medications and Neonatal Effects| Medication | Maternal Indication | Neonatal Effects and Nursing Implications |
|---|
| Magnesium sulfate | Seizure prophylaxis in preeclampsia; fetal neuroprotection before anticipated birth at <32 wk | Hypotonia, respiratory depression, apnea, decreased GI motility (feeding intolerance), hypotension; neuroprotective dosing reduces the risk of cerebral palsy in survivors |
| Opioid analgesia (morphine, fentanyl, hydromorphone, butorphanol, nalbuphine) | Labor analgesia | Respiratory depression and decreased tone, especially when given within a few hours of birth; reduced FHR variability; delayed breastfeeding. Support ventilation; naloxone is not part of delivery-room resuscitation |
| Regional anesthesia (epidural, spinal) | Labor analgesia; cesarean anesthesia | Maternal hypotension from sympathetic blockade → decreased uteroplacental perfusion and fetal bradycardia (treated with maternal positioning, fluids, vasopressors); epidural-associated maternal fever may prompt neonatal sepsis evaluation |
| General anesthesia | Emergency cesarean; contraindication to regional | Anesthetic agents cross the placenta → neonatal sedation, hypotonia, apnea; anticipate need for PPV |
| Nifedipine (calcium channel blocker) | Tocolysis; hypertension | Maternal hypotension and reflex tachycardia can reduce uteroplacental perfusion; few direct neonatal effects |
| Indomethacin (prostaglandin synthesis inhibitor) | Tocolysis, usually limited to <32 wk and ≤48 h | Constriction of the fetal ductus arteriosus (risk rises with gestational age and duration), oligohydramnios from decreased fetal urine output; reported associations with NEC and IVH |
| Terbutaline (β-adrenergic agonist) | Short-term tocolysis for uterine tachysystole | Fetal tachycardia; neonatal hypoglycemia from fetal hyperinsulinemia |
| Antenatal corticosteroids (betamethasone 12 mg IM × 2 doses 24 h apart, or dexamethasone) | Anticipated preterm birth within 7 days, typically 24 0/7–33 6/7 wk (may be considered at 22–23 wk and in selected late-preterm pregnancies) | Accelerate lung maturation and surfactant production; reduce RDS, IVH, NEC, and mortality; greatest benefit when birth occurs 24 h to 7 days after the first dose. Late-preterm courses increase neonatal hypoglycemia risk |
Amniotic Fluid and Membranes
Amniotic fluid is produced mainly by fetal urine and lung fluid in the second half of pregnancy and removed by fetal swallowing. Abnormal volume therefore points to problems with fetal kidneys, the gastrointestinal tract, swallowing, or the placenta.
Amniotic Fluid Volume Abnormalities| Finding | Definition | Suggests | Neonatal Implications |
|---|
| Oligohydramnios | AFI ≤5 cm or deepest vertical pocket <2 cm | Renal agenesis, bilateral renal disease, urinary tract obstruction (posterior urethral valves), rupture of membranes, uteroplacental insufficiency, post-term pregnancy, ACE inhibitor or NSAID exposure | Pulmonary hypoplasia, Potter sequence (flattened facies, limb positional deformities, clubfoot), cord compression with variable decelerations |
| Polyhydramnios | AFI ≥24 cm or deepest vertical pocket ≥8 cm | Impaired fetal swallowing or GI obstruction (esophageal atresia with or without TEF, duodenal atresia), CNS or neuromuscular disorders (anencephaly, myotonic dystrophy), trisomies, maternal diabetes, hydrops, twin-to-twin transfusion (recipient) | Pass an orogastric tube to assess esophageal patency; risk of preterm labor, malpresentation, cord prolapse, and abruption |
- Amniotic band sequence: strands of disrupted amnion entangle fetal parts, producing constriction rings, distal lymphedema, digital or limb amputations, syndactyly, and facial clefts. Defects are asymmetric and do not follow embryologic patterns.
- Prelabor rupture of membranes (PROM): rupture before the onset of labor. Preterm PROM (PPROM): rupture before 37 wk; associated with prematurity, infection, cord compression, and (when early and prolonged) pulmonary hypoplasia and limb deformities.
- Prolonged rupture of membranes (≥18 h) before delivery is a recognized risk factor for early-onset sepsis from ascending infection.
- Intraamniotic infection (chorioamnionitis): maternal fever with fetal tachycardia, maternal leukocytosis, or purulent fluid; uterine tenderness and foul-smelling fluid may be present. Managed with maternal antibiotics and expedited delivery (not by itself an indication for cesarean). The newborn requires early-onset sepsis risk evaluation.
Prenatal Screening and Fetal Surveillance
Prenatal Screening and Antenatal Testing| Test | Timing / Method | Interpretation |
|---|
| Maternal serum AFP (MSAFP) | 15–20 wk | Elevated: open neural tube defect, ventral abdominal wall defect (gastroschisis, omphalocele), multiple gestation, fetal demise, underestimated gestational age. Low: trisomy 21, trisomy 18, overestimated gestational age |
| Quad screen (AFP, unconjugated estriol, hCG, inhibin A) | 15–22 wk | Trisomy 21: low AFP, low uE3, high hCG, high inhibin A. Trisomy 18: low AFP, low uE3, low hCG |
| Cell-free DNA (cfDNA) | From 10 wk; analyzes placental DNA fragments in maternal blood | Most sensitive aneuploidy screen for trisomies 21, 18, 13 and sex chromosomes; a screening test only — positive results require diagnostic testing (CVS at 10–13 wk or amniocentesis at ≥15 wk) |
| Ultrasound | First trimester: dating and nuchal translucency; 18–22 wk: anatomy survey; serial: growth, fluid, Doppler | Gestational age, anomalies, placental location, fetal growth, amniotic fluid volume; umbilical artery Doppler (absent or reversed end-diastolic flow indicates severe placental insufficiency) |
| Nonstress test (NST) | External FHR monitoring | Reactive: ≥2 accelerations in 20 min (≥15 bpm for ≥15 s at ≥32 wk; ≥10 bpm for ≥10 s before 32 wk). Nonreactive → further testing (BPP) |
| Biophysical profile (BPP) | NST plus 30-min ultrasound | 5 components, each scored 2 or 0 (total /10): NST, fetal breathing movements, gross body movements, fetal tone, amniotic fluid volume. 8–10 reassuring, 6 equivocal, ≤4 abnormal. Modified BPP = NST + amniotic fluid assessment |
Fetal Heart Rate Monitoring
FHR tracings are interpreted using standardized definitions: baseline rate (mean FHR over 10 min, normal 110–160 bpm), variability, accelerations, decelerations, and trends over time. Moderate variability and the presence of accelerations reliably predict the absence of fetal metabolic acidemia at the time observed.
FHR Patterns| Feature | Definition | Causes / Significance |
|---|
| Tachycardia | Baseline >160 bpm for ≥10 min | Maternal fever or intraamniotic infection, fetal hypoxia, fetal anemia, tachyarrhythmia, maternal hyperthyroidism, β-agonists (terbutaline) |
| Bradycardia | Baseline <110 bpm for ≥10 min | Fetal hypoxia from cord compression or uteroplacental insufficiency, maternal hypotension, congenital heart block, maternal hypothermia or β-blockers |
| Absent variability | Amplitude undetectable | Ominous with recurrent decelerations; fetal acidemia, CNS injury |
| Minimal variability | Amplitude ≤5 bpm | Fetal sleep cycle (usually <40 min), opioids, magnesium sulfate, prematurity, hypoxia |
| Moderate variability | Amplitude 6–25 bpm | Normal; intact autonomic nervous system and adequate oxygenation |
| Marked variability | Amplitude >25 bpm | Significance uncertain; may accompany early hypoxia |
| Accelerations | Abrupt rise ≥15 bpm for ≥15 s (≥10 × 10 before 32 wk) | Reassuring; exclude acidemia |
| Early decelerations | Gradual decrease and return mirroring the contraction | Fetal head compression (vagal); benign |
| Late decelerations | Gradual decrease with nadir after the contraction peak | Uteroplacental insufficiency (hypertension, abruption, tachysystole, maternal hypotension); recurrent lates with minimal or absent variability suggest acidemia |
| Variable decelerations | Abrupt decrease (onset to nadir <30 s) ≥15 bpm lasting ≥15 s; variable timing and shape | Umbilical cord compression (oligohydramnios, nuchal cord, cord prolapse) |
| Prolonged deceleration | Decrease ≥15 bpm lasting ≥2 min but <10 min | Cord prolapse, uterine rupture, abruption, maternal hypotension, tachysystole; requires immediate intervention |
| Sinusoidal pattern | Smooth, sine-wave undulation (3–5 cycles/min) persisting ≥20 min, no variability | Severe fetal anemia (alloimmunization, fetomaternal hemorrhage, ruptured vasa previa) or severe hypoxia; Category III |
Three-Tier FHR Interpretation System| Category | Criteria | Meaning |
|---|
| Category I (normal) | Baseline 110–160; moderate variability; no late or variable decelerations; early decelerations and accelerations may be present or absent | Normal acid–base status at the time observed; routine monitoring |
| Category II (indeterminate) | All tracings not Category I or III (for example, minimal variability, tachycardia, recurrent variables with moderate variability, prolonged deceleration) | Requires evaluation, intrauterine resuscitation, and continued surveillance |
| Category III (abnormal) | Absent variability with recurrent late decelerations, recurrent variable decelerations, or bradycardia; or sinusoidal pattern | Abnormal fetal acid–base status; prompt resuscitative measures and expedited delivery; full neonatal resuscitation team present |
Labor Problems
Labor Complications| Problem | Neonatal Implications |
|---|
| Breech and other malpresentations | Developmental dysplasia of the hip (breech is a major risk factor), torticollis, extended legs in frank breech, head entrapment, cord prolapse, birth trauma |
| Maternal hemorrhage | Fetal hypoxia from reduced uteroplacental perfusion; fetal blood loss when fetal vessels are involved |
| Meconium-stained amniotic fluid | Reflects fetal maturity (more common at ≥41 wk) or fetal hypoxic stress; risk of meconium aspiration syndrome and PPHN. Routine intubation for tracheal suctioning of nonvigorous infants is not recommended; initial steps and ventilation take priority |
| Shoulder dystocia | Associated with macrosomia and maternal diabetes; brachial plexus injury (Erb palsy C5–C6, Klumpke palsy C8–T1), clavicle or humerus fracture, hypoxic-ischemic injury |
| Precipitous delivery | Bruising, facial congestion and petechiae, and other trauma |
| Prolonged labor | Infection risk, molding and caput, operative delivery |
| Cord complications | Nuchal cord occurs in 20–30% of births and is usually benign; true knots can tighten during descent; velamentous insertion predisposes to vasa previa and vessel rupture |
Obstetric Emergencies
Obstetric Emergencies| Emergency | Presentation | Neonatal Implications |
|---|
| Placental abruption | Premature separation of a normally implanted placenta; painful bleeding, uterine tenderness and hypertonus (bleeding may be concealed); risk factors include hypertension, cocaine, smoking, trauma | Acute fetal hypoxia, hypovolemia and anemia, hypoxic-ischemic encephalopathy, stillbirth; prepare for volume replacement |
| Placenta previa | Placenta covers or lies near the internal os; painless bright red bleeding | Preterm birth; neonatal anemia if fetal vessels are disrupted |
| Vasa previa | Unprotected fetal vessels cross the membranes over the cervix; bleeding at membrane rupture with abrupt FHR changes or sinusoidal pattern | Fetal exsanguination — rapid hypovolemic shock; emergency volume expansion (normal saline or O-negative blood 10 mL/kg) |
| Umbilical cord prolapse | Cord precedes the presenting part; sudden bradycardia or variable decelerations | Cord compression → acute asphyxia; maternal knee-chest or Trendelenburg position and manual elevation of the presenting part until emergency delivery |
| Uterine rupture | Most often with a prior uterine scar during labor; sudden fetal bradycardia, loss of station, abdominal pain | Severe hypoxic-ischemic injury, hypovolemia, death |
| Placenta accreta spectrum | Abnormal placental invasion into the myometrium | Primarily maternal hemorrhage; planned preterm cesarean delivery |
Mode of Delivery
Mode of Delivery and Birth Injury| Delivery Mode | Neonatal Risks |
|---|
| Forceps-assisted | Facial nerve palsy (asymmetric cry, eye does not close on affected side), cephalohematoma, skull fracture, facial bruising and abrasions, brachial plexus injury |
| Vacuum-assisted | Subgaleal hemorrhage (most strongly associated), cephalohematoma, chignon and scalp lacerations, retinal hemorrhage |
| Cesarean without labor | Transient tachypnea of the newborn (lack of labor-associated catecholamine surge and lung fluid clearance), respiratory distress; iatrogenic prematurity if scheduled before 39 wk without indication; effects of general or regional anesthesia |
| Vaginal breech or difficult vaginal birth | Brachial plexus injury, clavicle fracture, intracranial hemorrhage, abdominal organ injury |
Apgar Score
Apgar Score| Sign | 0 | 1 | 2 |
|---|
| Heart rate | Absent | <100 bpm | ≥100 bpm |
| Respiratory effort | Absent | Slow, irregular, weak cry | Good, crying |
| Muscle tone | Limp | Some flexion of extremities | Active motion |
| Reflex irritability (response to stimulation) | No response | Grimace | Cry or active withdrawal |
| Color | Blue or pale | Body pink, extremities blue (acrocyanosis) | Completely pink |
The Apgar score is assigned at 1 and 5 minutes; if the 5-minute score is <7, scoring continues every 5 minutes up to 20 minutes. It describes the infant's condition and response to resuscitation but is not used to decide whether to begin resuscitation — that decision is based on the initial assessment of term status, tone, and breathing or crying, followed by heart rate. Elements such as tone and color are influenced by gestational age, maternal medications, and resuscitation, so a low score alone does not establish asphyxia. An expanded form documents concurrent resuscitative interventions.
Exam Focus
- Quad screen for trisomy 21: low AFP, low estriol, high hCG, high inhibin A. Elevated MSAFP: open NTD, abdominal wall defect, multiples, wrong dates.
- Late decelerations = uteroplacental insufficiency; variable = cord compression; early = head compression; sinusoidal = severe fetal anemia.
- Category III: absent variability with recurrent lates, recurrent variables, or bradycardia, or a sinusoidal pattern.
- Polyhydramnios suggests esophageal or duodenal atresia; oligohydramnios suggests renal anomaly or ROM and predicts pulmonary hypoplasia.
- Maternal magnesium → hypotonia and respiratory depression; indomethacin → ductal constriction and oligohydramnios; terbutaline and late-preterm steroids → hypoglycemia.
- Vacuum delivery is the classic setup for subgaleal hemorrhage; vasa previa causes fetal exsanguination.
