Neonatal Teaching: Fetal Growth Disturbances & Prematurity Flashcards
Definition of terms
Prematurity: <37 weeks
Low birth weight (LBW): <2.5 kg
Very low birth weight (VLBW): <1.5 kg
Extreme LBW (ELBW): <1 kg
EELBW: <750 g
Appropriate for date: 10th to 90 percentile
Small for date (for newborn) / gestational age (for fetus): <10th percentile / >2 SD below mean
Large for date (for newborn) / gestational age (for fetus): >90th percentile
Limit of viability: <24 weeks gestation? <500 g?
Fetal growth
- Complex interplay between fetal genetic and intrauterine environmental factors
- Genetic determinant of fetal growth have their greatest impact in early gestation during the period of rapid cell development
- Racial and ethnic backgrounds influence size at birth irrespective of socioeconomic status
- Assessment of fetal growth should be based on fetal growth charts derived from same ethnic groups
***SGA vs Preterm vs IUGR
- Weight (Light-for-date) / Length (Short-for-date)
- <10th percentile for gestational age / >2 SD below mean for gestational age
- SGA infant may be due to ***normal genetic variation instead of pathological growth retardation
SGA vs Preterm
SGA:
- Dry, wrinkled skin and peeling
- Lack of subcutaneous fat
- Meconium staining
- Normal posture
- Alert
- Vigorous activity
- Sucks eagerly
Preterm:
- Shiny transparent skin (Immature skin)
- Edematous
- Lanugo hair (Premature hair)
- Hypotonic posture
- Sleeps mostly
- Few spontaneous movement
- Poor suck + swallow
IUGR:
- Failure of “normal” fetal growth caused by multiple adverse effects on the fetus
- NOT achieve expected in-utero growth ***potential due to genetic / environmental factors and have increased risk for perinatal mortality morbidity (Felix Lai)
Clinical Assessment of Maturity
Scoring system: **New Ballard score, modified from **Dubowitz
Determine preterm normal weight vs term SGA (Phoebe)
External features:
- Skin thickness, lanugo hair
- Creases on sole of foot
- Size of breast tissue
- Recoil / rigidity of ear cartilage
- Testicular descent and scrotal rugae
- Labia majora
Neurological assessment (relative flexor tone of 4 limbs):
- Posture
- Scarf sign, Heel to ear manoeuvre
- Square window, arm recoil, popliteal angle etc.
***IUGR
Asymmetrical IUGR:
- relatively large heads
- moderate reduction in length + greatest reduction in weight
- thin skinfolds + mid-arm circumferences
- diversion of blood flow to more essential organs in utero (brain, heart, adrenals)
- this disturbance of internal organ body proportion may have a ***life-long effect on organ structure and function
Causes (**Reduced growth support (Maternal / Fetal / Placental), **Embryopathy, **Constitutional, **Idiopathic):
1. Maternal factors
- Toxaemia / HT
- Severe maternal illnesses (e.g. SLE)
- Short stature
- Smoking
- Low / High maternal age
- Parity
- Chronic hypoxaemia (e.g. severe anaemia, high altitude)
- Fetal factors
- Multiple pregnancy
- Embryopathy
—> Chromosomal abnormalities (2%)
—> Congenital infection syndrome (TORCH infection) (<1%)
—> Congenital abnormalities (5-10%)
—> Syndromal
—> Endocrine disorders (e.g. fetal thyroxine or insulin deficiency (rare)) - Placental factors
- Uteroplacental vascular insufficiency
- Infarcts
- Premature separation
- Twin-twin transfusion - Constitutional / Genetic
- Defined by virtue of a low birth weight
- Symmetrically small, normal skinfold thickness
- They are not growth retarded but have a low genetic growth potential
- The fetal growth may be limited by uterine restricting factors regulated by the uterine size related to small maternal size - Idiopathic
- Genetic, endocrine or causes yet to be identified
- Some women always produced small babies —> risk for future pregnancies with IUGR increase 5x if first baby is small
Clinical features of SGA
Prenatal:
1. History of risk factors (e.g. maternal disease)
- Serial ultrasound measurements
- Abdominal circumference
- Biparietal diameter
- Femur length - Clinical assessment
- Fundal height
- Fetal size
- Liquor volume
Postnatal:
1. Growth measurement
- Body weight <10% (light for date)
- Body length <10% (short for date)
- Head circumference / Chest circumference ratio ( >1: Asymmetrical SGA)
- Ponderal index (PI)
- PI = weight (g) / length^3 (cm) x 100 - Mid arm circumference / Head circumference
- Assessment of gestational age
***Complications of SGA
- ***Intrapartum asphyxia
- ↑ Fetal death rate (14% of stillbirth are SGA babies) - ↑ ***Congenital malformation incidence
- 5-7% of SGA babies have congenital malformation - ***Birth asphyxia
- Prompt resuscitation
- Paediatrician stand-by delivery - ***Hypoglycaemia
- ↓ Liver stores of glycogen
- Impaired gluconeogenesis
- Relative hyperinsulinaemia
- Deficient catecholamine secretion - ***Hyperglycaemia
- Transient form of diabetes, not associated with ketonaemia sometimes occurs in SGA babies - ***Hypothermia
- Large surface to volume rates
- Large head
- Less subcutaneous fat
- Old exposure may aggravate hypoglycaemia -
**Polycythaemia
- Chronic hypoxia —> ↑ RBC production
- Severe polycythaemia can lead to **Hyperviscosity syndrome —> congestive heart failure + aggravates pulmonary HT - Cardiorespiratory problems
- Cardiac failure
- **Meconium aspiration syndrome
- **Recurrent apnea (when associated with prematurity)
- Pneumonia
- ***Persistent pulmonary HT of newborn
- Pulmonary haemorrhage - Problems related to primary cause
- **Congenital infection syndrome may associated with hepatitis, brain abnormalities, cataract
- **Chromosomal disorders
- ***Congenital malformation
Management of SGA
Prenatal:
1. Early diagnosis of IUGR
2. Proper management of pregnancy
- **Correct treatable causes (e.g. smoking, alcoholism)
- **Monitor antepartum asphyxia: Stress / Non-stress test
3. Decide on optimal time of delivery
Intrapartum:
1. **Intrapartum monitoring of fetal distress
2. **Prompt delivery of fetal distress
Postnatal:
1. Prompt **resuscitation to prevent birth asphyxia and meconium aspiration
2. **Incubator care, observe for **hypothermia, prevention of heat loss
3. Monitor blood glucose, early **feeding, IV glucose infusion
4. Search for ***underlying cause
Future growth + Development of SGA babies
- Catch up growth
- Depends on **timing, **duration, ***severity - Neurodevelopment sequelae
- Major disability in SGA babies: occurs mainly in those with **chromosomal abnormality, **congenital malformation, **1st trimester damage from intrauterine infection / drug
- Minor disability (e.g. clumsiness, learning difficulty, behaviour disturbance): occurs in infants who have had **prolonged slow head growth from early in ***2nd trimester
Long-term implications:
1. ***Baker hypothesis
- During “critical” period of development at fetal / early infancy, an insult will determine life-long effects on organ structure / function
- May be associated with adult disease like HT, cerebrovascular, CAD, non-insulin dependent DM
***LGA
BW >90% for gestation
Causes:
1. **Infants of DM mother
- Macrosomia (Head disproportionately small with increase in body adiposity)
- Facial plethora
- Increase hairiness
- Hypotonic
2. **Syndromal disorder with excessive intrauterine growth (e.g. Beckwith-Wiedemann Syndrome)
3. ***Constitutional / Genetic
Risk factors (SpC Revision):
1. Male sex
2. Advanced gestational age
3. Multiparity
4. Maternal DM
5. Excess weight gain in pregnancy
6. Ethnicity: Hispanic, Caucasian, Native Americans, Samoan
***Complications of DM mother
- Perinatal asphyxia
- Birth injury
- Shoulder dystocia
- Erb’s palsy
- Fracture clavicle - Metabolic disturbances
- Hypoglycaemia
- HypoCa - Increased congenital malformation
- Increased susceptibility to infection
- Respiratory distress syndrome
- Hypertrophic cardiomyopathy
- Transient Tachypnea of Newborn (Wet lung syndrome)
- Polycythaemia - Hyperviscosity syndrome
***Preterm / Prematurity
- <37 weeks gestation
- 5-7% of livebirth
- Very preterm <32 weeks / VLBW <1.5 kg: 0.6-1%
- Extreme prematurity <28 week / ELBW <1 kg): 0.1-0.2%
Causes:
1. Maternal factors
- History of Premature birth
- Cervical insufficiency
- Uterine abnormalities
- Age <16 / >35
- Short interval between pregnancy
- Infection / Acute febrile illness
- Trauma
- Medical disease (e.g. HT, chronic cardiac / pulmonary disorders)
- Smoking, Alcoholism
- Lower socioeconomic class
- Fatigue / Activity
- Fetal factors
- Malformations
- Multiple births
- Premature rupture of membranes - Unknown
- ?Infection-related
***Complications of Preterm / Prematurity
General:
1. Infection
2. Temperature regulation
3. Growth failure
Neurological:
1. **Periventricular / Intraventricular haemorrhage (PVH / IVH)
2. **Post-IVH hydrocephalus
3. Cerebral ischaemia (related to hypoperfusion)
4. ***Periventricular leukomalacia (PVL), periventricular white matter disease (related to intrauterine infection, acute chorioamnionitis)
5. Long-term neurodevelopmental problem
- Cerebral palsy (Diplegic CP)
- Developmental delay
- Speech delay
- Learning difficulty
- Fine motor incoordination
Respiratory:
1. **Respiratory Distress Syndrome (Hyaline membrane disease)
2. **Apnea
3. Birth asphyxia
4. Chronic Lung disease of prematurity
Cardiovascular:
1. PDA
GI:
1. ***Necrotising enterocolitis (NEC)
2. Feeding and nutrition
***Eyes:
1. Retinopathy of prematurity (ROP) (blindness, refractive errors)
Haematological:
1. Anaemia of prematurity
- Immature erythropoiesis + Blood taking
***Metabolic:
1. Hypoglycaemia / Hyperglycaemia
2. HypoCa
3. Hypophosphataemia
4. Poor tolerance to excessive water and dehydration
5. Poor renal concentration of Na
Musculoskeletal:
1. Osteopenia of prematurity / other nutritional insufficiency
Respiratory Distress Syndrome (RDS)
- A disease of ***prematurity mainly
- Lack of surfactant —> widespread atelectasis at end expiration
Surfactant system:
- Phosphotidyocholine, Phosphotidyglycerol
- Surface active substance secreted by Type II alveolar cell —> maintain distension of alveoli
- Generally deficient in premature infants <30-32 weeks
- Many factors may affect the likelihood of RDS in each particular preterm infants
Predisposing factors:
1. **Prematurity
2. M>F
3. **C-section
- Lack of fetal adrenergic surge
- Associated at gestation <32 weeks less clear
4. ***Maternal DM
5. Familial / Ethnic predisposition (?Chinese less RDS)
6. Twins
7. 2nd coming twin has increase RDS
8. Hypothermia
9. Haemolytic disease of newborn
10. Time of cord clamping
- Early cord clamping —> less placental transfusion —> anaemia may predispose to more RDS
Protective factors:
1. **Intrauterine growth retardation (IUGR) (↑ endogenous surfactant production)
2. **Prolonged rupture of membrane
3. **Maternal drugs + smoking
4. **Heroin (~Glucocorticoids can mature surfactant-synthesising system)
Diagnosis:
- Clinical diagnosis
- Acute illness, usually of preterm infants
- Present within 4-6 hours of delivery
- Signs of respiratory distress:
—> Tachypnoea
—> Intercostal, Subcostal, Sternal retraction
- Expiratory grunting (characteristic)
DDx:
1. Pneumonia
2. Transient tachypnoea of newborn (Wet lung syndrome)
3. Pulmonary air leak (e.g. pneumothorax)
4. Pulmonary haemorrhage
5. Metabolic acidosis, hypothermia
6. Congenital malformation (e.g. diaphragmatic hernia)
CXR:
Features of Diffuse atelectasis
1. Decrease lung volume
2. **Reticulogranular pattern (characteristic, **ground glass appearance)
3. ***Air bronchogram
4. Obliteration of cardiac shadow
Prevention:
1. Prenatal steroid therapy
- significantly ↓ incidence of RDS by 50%
2. Prophylactic surfactant
3. Avoid positive pressure ventilation (e.g. use of early CPAP)
Treatment:
1. Oxygen + Ventilator support
- Non-invasive ventilation: Nasal CPAP / Nasal IMV (Intermittent mandatory ventilation)
- Relieve cyanosis
- Surfactant Replacement Therapy
- Major breakthrough in the treatment of RDS
- ↓ Mortality + Morbidity
- Through ETT tube (SpC OG)
Periventricular / Intraventricular haemorrhage (PVH / IVH)
- Onset: 80% occurs within first 72 hours
- Mild (Grade 1-2) —> ***Resolve, no sequelae
- Severe (Grade 3-4) —> High chance of ***long term handicap / death (30-90%)
Risk Factors:
1. Immaturity (esp. <28 weeks)
2. **Birth asphyxia / Perinatal depression
3. **RDS
4. Infection
5. **Acidosis
6. **Hypercarbia, Hypoxia
7. ***Hypotension / Fluctuation of BP
8. Pneumothorax
9. Coagulation defect may worsen grade of haemorrhage
Grading:
- Grade 1: **Germinal matrix haemorrhage
- Grade 2: **Intraventricular haemorrhage (IVH)
- Grade 3: IVH with **Ventricular dilatation
- Grade 4: IVH + **Intracerebral extension
Management:
Prevention > Treatment
1. Skill resuscitation
2. Early treatment of RDS with surfactant
3. Avoid acidosis / hypotension
4. ?Prophylactic Indomethacin
Treatment of post-IVH hydrocephalus:
1. Close monitor + Timely insertion of ***Ventriculo-peritoneal shunt (VP shunt)
