Fetal Growth Abnormalies Flashcards
(20 cards)
intrauterine Fetal growth restriction
- Estimated fetal weight < 10
th percentile for gestational age
At term, the cut off birth weight for IUGR is 2,500 g (5lb, 8 oz)
IUGR (<10th percentile) refers to a small group of fetuses or neonates whose growth potential has been limited
by pathologic processes in utero, with resultant increased perinatal morbidity and mortality
Small for gestational age
- Infant birth weight <2,500 g at term or < 10th percentile for gestational age
Large for gestational age
- Infant birth weight >90th percentile for gestational age
Macrosomia
A fetal weight of more than 4g (other authorities 4.5 kg) at term or fetal birth weight > 90 percentile for the
gestational age
also known as big baby syndrome, is sometimes used synonymously with LGA,
Risk factors / causes of macrosomia
- Maternal factors
a) Genetic/constitutional
b) Prior history of macrosomia
c) Obese women- tend to give birth to macrosomic babies
d) Excessive maternal weight gain during pregnancy
e) Multiparity - first baby is about 100 gm smaller than the next
f) Post-date (post maturity) – GA > 40 weeks
g) Advanced maternal age
h) Ethnicity
i) Poorly controlled maternal diabetes and gestational diabetes
j) Dyslipidemia - Fetal factors
a) Genetic syndromes including Beckwith-Wiedemann syndrome (large bodies, large tongues, midline
abdominal wall defect, neonatal hypoglycemia), Sotos syndrome
b) Male fetus than female
c) Hydrops foetalis
Macrosomia and diabetes
A ¼ of insulin dependent mothers have Macrosomic infants
Excess growth happens in 3rd trimester
GDM mothers have slight increase in incidence of macrosomic infants as other diabetics
Fetal macrosomia:
a) Maternal hyperglycemia → hypertrophy and hyperplasia of the fetal islets of Langerhans → increased
secretion of fetal insulin → stimulates carbohydrate utilization and accumulation of fat.
Insulin like growth factors (IGF-I and II) are also involved in fetal growth and adiposity.
b) Elevation of maternal free fatty acid (FFA) in diabetes leads to its increased transfer to the fetus →
acceleration of triglyceride synthesis → adiposity
Diagnosis of macrosomia
Macrosomia is suspected if there is:
a) Disproportionate increase in uterine size/ HOF
b) Clinically the fetus is felt big by Leopold maneuvers.
c) Ultrasonographic measurements of fetal Biometry: BPD, HC, FL and AC help predict estimated fetal wgt
Complications of macrosomia
Fetal
a) Dystocia due to cephalopelvic disproportion,
b) Shoulder dystocia- lead to brachial plexus injury; Erb-Duchenne palsy (C5, C6), Klumpke paralysis: injury to C8, T1
c) Asphyxia
d) Meconium aspiration syndrome.
Maternal
a) Prolonged pregnancy
b) Obstructed labour due to cephalopelvic disproportion
c) Trauma (vagina, perineum),
d) PPH
e) Puerperal sepsis.
f) Maternal morbidity is high.
Management of macrosomia
Rule out maternal diabetes; if diabetes is diagnosed, optimal diabetic management of pregnancy is necessary
Early induction or early delivery not indicated for suspected macrosomia
a) Early induction of labor does not decrease maternal or neonatal morbidity
* Early induction does increase rate of Cesarean delivery
Proper antenatal care: to prevent Macrosomia (glycaemic control in DM and GDM) and diagnose it before
labour commences
Prophylactic induction of labor (preterm) to reduce the risk of shoulder dystocia
Caesarean section: is the safest for both mother and fetus
types of IUGR
Divided into:
a) Constutitionally small and healthy, BWT is < 10th percentile for GA, but has normal ponderal index, normal
subcutaneous fat
b) Growth is restricted by pathological process (true IUGR)
Depend on relative size of head, abdomen and femur of fetuses. Its subdivided into:
(i) Symmetrical or Type I
(ii) Asymmetrical or Typ
Symmetrical growth restriction
20 % of IUGR Infants-proportional decrease in all organs
HC/AC ratio is normal. Growth of both the head and the body is inadequate.
Pathological process is intrinsic to the fetus and involves all the organs including the head.
Occurs in early pregnancy: Cellular hyperplasia
Increased risk for long term neurodevelopment dysfunction
Affected by noxious effect very early in the phase of cellular hyperplasia.
Often caused by structural or chromosomal abnormalities or congenital intrauterine infection (TORCH)
Asymmetrical growth restriction
80% of IUGR Infants
Increase HC/AC ratio : decrease in abdominal size
Head size is proportionally larger than the abdominal size due to brain
sparing effects
Occurs in late pregnancy: cellular hypertrophy
Insufficient nutrition to fetus, caused by either poor maternal nutrition or maternal diseases reducing
uteroplacental blood flow, restricting O2 and nutrient transfer or by reducing the placental size.
Number of cell are reduced
Fetal phenotype (small size) is known as thrifty phenotype
Have increased risk of developing obesity, diabetes, and cardiovascular disease in later life, if nutrition
improves soon after birth
Risk for perinatal hypoxia, neonatal hypoglycemia
Has a good prognosis
Etiology of fetal growth restriction
a) Maternal factors:
1) Constitutional- Small women, maternal genetic and racial background.
2) Maternal undernutrition before and during pregnancy
3) Poor maternal weight gain
4) Maternal diseases:
* Long-standing diabetes,
* CVS- Anemia, sickle cell disease, HTN, Thrombotic diseases (hereditary thrombophilias), cyanotic
heart disease, collagen vascular disease
* Renal- CKD,
* Resp- pulmonary insufficiency leading to Chronic hypoxemia
* Viral infections (rubella, varicella, cytomegalovirus, parvovirus B19).
5) Toxins-Alcohol, smoking, cocaine, heroin, drugs (anticonvulsants, warfarin, folic acid antagonists),
teratogen exposure
6) Antiphospholipid antibodies syndrome
b) Placental factors:
Causes include prolonged poor uterine blood flow to placental site, leading to chronic placental
insufficiency with inadequate substrate transfer
1) Primary placental disease
2) Placental abnormalities: chronic abruption, mosaicism, Placenta previa , circumvallate placenta
3) Uterine anomalies affecting placental implacentation e.g. uterine septum or fibroids
4) Uteroplacental insufficiency- by microinfarctions and Mosaicism, PIH and chronic HTN
5) Obesity (associated with leptin resistance which leads to placental dysfunction)
6) Chorioangioma
c) Fetal factors:
1) Constitutional
2) Genetic disorders / chromosomal abnormality: triploidy and aneuploidy-Trisomies (13, 18, 21) and
Turner’s syndrome, Single gene defects, e.g. Seckel’s syndrome.
3) Structural anomalies either congenital heart diseases, renal (renal agenesis), anencephaly or others
4) Multiple gestation - mechanical hindrance to growth and excessive fetal demand
5) Syphilis, Tuberculosis, Malaria, Intrauterine infection (listeriosis and TORCHS)
6) Reduced fetoplacental perfusion, e.g. in single umbilical artery, twin–twin transfusion syndrome
7) Marginal or velamentous insertion of umbilical cord
d) Unknown: cause remains unknown in about 40%
Ponderal Index
Ultrasound criteria for diagnosis of fetal malnutrition;
Gestation age independent;
Way of characterizing the relationship of height to mass for an individual.
PI = 1000 x sq mass (kg)/height (cms)
Typical values are 20 to 25.
PI is normal in symmetric IUGR.
PI is low in asymmetric IUGR.
Mass should be in (kgs) and height in (cms
clinical Diagnosis of IUGR
1) Fundal Height (in cms)- closely correlates with GA after 24wks & lag of 4 cm or more suggestive
2) Stationary or at times falling maternal weight gain during 2nd half
of pregnancy.
3) Stationary or falling measurement of the abdominal girth showing
Biophysical Diagnosis of IUGR
Biophysical:
* USG confirm the clinical estimation of GA, diagnose IUGR and
identify symmetrical or asymmetrical fetus
Initial U/S at 16 to 20wks to establish GA, identify anomalies and repeated at 32 to 34 weeks to
evaluate fetal growth
* HC/AC ratio
a) HC/AC is elevated in asymmetric IUGR but reduced in symmetric
* Femur length (FL) is not affected in asymmetric IUGR.
FL/AC ratio is 22 at all GA from 21 weeks to term.
FL/AC ratio greater than 23.5 suggests IUGR
* Amniotic fluid volume- often reduced in asymmetrical IUGR
A vertical pocket of amniotic fluid < 1 cm suggests IUGR
Mild IUGR – Normal amniotic fluid
AFI < 5 indicates Oligohydramnios (severe IUGR). Normal when between 5 and 25 cm
* Anatomical survey: To exclude fetal anomalies by sonography (Aneuploidy, structural defects)
* Doppler assessments- elevations of umbilical artery and uterine artery resistance as early as midpregnancy have been associated with a greater risk of IUGR
a) Doppler velocimetry
Normal velocimetry pattern with an S/D ratio of <30. (Peak systolic frequenct shift (S), End diastolic
frequency shift value (D))
The diastolic velocity approaching zero reflects increased placental vascular resistance.
During diastole, arterial flow is reversed (negative S/D ratio), which is an ominous sign that may
precede fetal demise characterized by absent or reversed enddiastolic flow
Associated with fetal growth restriction
Biochemical markers: Elevated levels of MSAFP (maternal serum α-fetal protein), hCG, and unconjugated
estriol [UE3]) level in 2nd trimester are the markers of abnormal placentation and risks of IUGR
Physical features at birth Diagnostic of IUGR
a) Birth weight deficit of about 600g below minimum in percentile standard using birth weight-GA chart
b) Unaffected length
c) In asymmetric IUGR- HC > AC
d) Other features
* Show dry and wrinkled skin because of less subcutaneous fat
* Pinna of ear has cartilaginous ridges
* Scaphoid abdomen
* Thin meconium stained vernix caseosa
* Thin umbilical cord
* Well defined plantar creases
* Baby has an “old man look”
* Normal reflexes including Moro- reflex
* Alert, active baby and having normal cry
Complications of IUGR
a) Asphyxia, bronchopulmonary dysplasia and RDS
b) Hypothermia-decreased subcutaneous fat, increased surface/volume ratio decreased heat production
c) Hypoglycemia-due to decreased glycogen stores/ glycogenolysis/ gluconeogenesis & increased metabolic rate
d) Hypocalcemia deficient catecholamine release associated with perinatal stress, asphyxia, prematurity
e) Meconium aspiration syndrome
f) Microcoagulation leading to DIC
g) Polycythemia, anemia, thrombocytopenia
h) Hyperviscosity thrombosis
i) Necrotizing enterocolitis due to reduced intestinal blood flow
j) Intraventricular hemorrhage (IVH)
k) Pulmonary hemorrhage
l) Electrolyte abnormalities- hyper phosphatemia, hypokalemia due to impaired renal function (12)
m) Multiorgan failure
n) Increased perinatal morbidity and mortality
o) Increased risk of metabolic syndrome in adult life: obesity, hypertension, diabetes and coronary heart disease
p) LBW infants have an altered orexigenic mechanism that causes increased appetite and reduced satiety.
q) Reduced number of nephrons—causes renal vascular hypertension
Management of IUFGR
Prepregnancy: to prevent it by identifying risk factors and treat as necessary (e.g. improve nutrition intake, stop
smoking or alcohol, ASA in APA syndrome, and Heparin in thrombophilias)
Antepartum: identify risk factors that can be changed
Fetal surveillance by ultrasound (BPP) and twice-weekly fetal heart monitoring (Non-Stress Test).
Comprehensive diagnostic workup
Constitutionally small babies require no intervention
For symmetric IUGR, investigate to exclude fetal anomalies, infections and genetic syndromes.
Growth restriction near term (GA > 37 weeks): Delivery should be done.
Prompt delivery
Recommend delivery at 34 weeks or beyond if there is clinically significant Oligohydramnios
Objective of clinical management is to expedite delivery before occurrence of fetal compromise, but after
fetal lung maturation has been achieved.
Balance decision for early delivery with risk of neonatal deaths due to complications and increased
risk of IUFD due to delay in delivery
Growth restriction remote from term
No specific treatment if diagnosis is prior to GA 34wks, adequate liquor & fetal surveillance are normal
Observation is recommended
Fetal well-being is assessed by Kick count, NST, biophysical profile, amniotic fluid volume and
cordocentesis for blood gases
Lung maturation is assessed by presence of phosphatidyl glycerol & L: S ratio of > 2 from amniocentesis
If ultrasonic findings are equivocal for IUGR; recommend, bed rest, improve malnutrition, treat associated
complicating factors, fetal surveillance, avoidance of smoking, drugs, tobacco and alcohol; maternal
hyperoxygenation at the rate of 2.5 L/min by nasal prong, Low dose aspirin (50 mg daily) in selected cases with
H/O thrombotic disease, hypertension, pre-eclampsia, serial ultrasonic measurements at 3-wkly intervals and
attempt to avoid preterm delivery
Treat the specific causes of IUGR and supportive care
If severe IUGR or bad obstetric conditions e.g., SPE, termination of pregnancy should be consider by C/S
WHAT FACTORS SHOULD BE CONSIDERED WHEN TIMING THE DELIVERY FOR IUFGR?
Consider the following factors for timing of delivery::
a) Presence of fetal abnormality
b) Duration of pregnancy
c) Degree of growth restriction
d) Associated complicating factor
e) Degree of fetal compromise
f) Previous obstetric history; and
g) Availability of NICU
