Causes and risk factors
The etiology of IUGR is multifaceted. The baseline mechanism is most often placental insufficiency. All triggers of the pathology are grouped into several broad categories:
- Environmental and nutritional. Maternal bad habits, toxic working conditions, low standard of living, as well as nutritional deficiencies (lack of protein, vitamins) and poor weight gain during pregnancy.
- Extragenital pathology. Maternal diseases provoking chronic fetal hypoxia: arterial hypertension, diabetes mellitus, severe anemia, congenital heart defects, autoimmune processes, and kidney diseases.
- Intrauterine infections. Fetal development is hindered by viruses (cytomegalovirus, rubella), bacteria (syphilis, listeriosis), and protozoa (toxoplasmosis).
- Obstetric and fetal factors. Multiple pregnancy, post-term pregnancy, gestosis, placental anomalies. Statistical fact: congenital malformations or dysmorphogenesis stigmata are detected in 10% of children with IUGR.
Clinical variants of IUGR
The diagnosis is valid for children of any gestational age (both premature and full-term). Appearance and proportions depend on the timing of the adverse exposure:
- Hypoplastic (symmetric) variant. Forms during early damage (I–II trimester). The child lags evenly: weight, height, and head circumference all suffer. The baby looks miniature but proportional. Soft, pliable cranial sutures and fontanelles, and the absence of an ossification center in the femoral head are characteristic. There is a high risk of birth asphyxia and respiratory distress syndrome.
- Hypotrophic (asymmetric) variant. The most frequent form (80%), occurring when problems arise in the final months of pregnancy. Body length and head circumference are normal, but weight is critically reduced. The child is disproportional: long, thin, with a visually large head. Subcutaneous fat is depleted, tissue turgor is reduced. Neurologically, central nervous system depression is noted (lethargy, hypotonia, weak suck reflex).
- Dysplastic variant. Characterized by a combination of weight deficiency with body build anomalies, malformations, and pronounced stigmatization. Accompanied by severe nervous system lesions.
Severity degrees of pathology
Gradation depends on how severely the child's weight and height lag behind the expected norms, as well as on the severity of trophic disorders:
- Grade I (mild). Weight deficit of 10–20%. Subcutaneous adipose tissue is moderately depleted, turgor and muscle tone are slightly reduced.
- Grade II (moderate). Weight deficit up to 30%, height lag of 1–1.5 cm. The tissue is sharply depleted, the skin becomes pale, dry, with pronounced desquamation.
- Grade III (severe). Weight deficit exceeds 30%, height lags by 2–4 cm. Subcutaneous fat is completely absent. Skin is flabby, gathers into deep folds; fissures form on the soles and in the groin.
Adaptation features and management of the newborn
In the early neonatal period, infants with IUGR face a cascade of transitional states. They exhibit a large initial weight loss and slow recovery, prolonged jaundice, absence of the hormonal crisis, and slow healing of the umbilical wound. Laboratory findings reveal energy deficiency syndrome (decreased glucose, calcium, and magnesium levels).
Principles of therapy in the maternity hospital:
- Thermoregulation: placement under a radiant warmer immediately after birth due to an extremely high tendency to hypothermia.
- Bleeding prophylaxis: intramuscular administration of vitamin K (menadione sodium bisulfite) in the first hours of life is mandatory for all forms of IUGR.
- Feeding: early initiation of enteral feeding (no later than 2 hours after birth). Expressed breast milk is used; transition to the breast depends on the child's condition and body weight.
Developmental prognosis
Children with Grade I IUGR recover quickly, catching up with peers in physical development by 6–12 months. With Grade II, recovery is delayed up to 1–2 years; in older age, neuropathies, iron deficiency anemia, and rickets may manifest.
The prognosis for Grade III and the dysplastic variant is extremely unfavorable. Developmental lag persists at least until age three. Severe organic brain lesions develop in 10–15% of such patients: cerebral palsy (CP), hydrocephalus, epilepsy, and mental retardation. Infectious morbidity manifests immediately after birth in these infants.
To remember the phenotypes, focus on timing: EARLY exposure stunts all parameters (SYMMETRIC variant), LATE exposure manages to affect weight only (ASYMMETRIC variant).
Class and exam questions
Can IUGR be diagnosed before birth?
Yes, at the prenatal stage, the main method is ultrasound diagnostics. The physician performs ultrasound fetometry, comparing fetal dimensions with norms for the given gestational age.
Why do newborns with IUGR need an early start of enteral feeding?
Due to the depletion of glycogen stores and poor development of subcutaneous fat, they rapidly develop energy deficiency syndrome (hypoglycemia). Feeding compensates for these physiological deficits.
Which form of IUGR has the worst prognosis?
The dysplastic variant. It is combined with severe metabolic imbalance, malformations, and a high risk of severe organic CNS lesions.
What else to study on this topic
- Pathogenetic prenatal therapy for placental dysfunction.
- Correction of cardiorespiratory disorders in newborns with IUGR.
- Neurosonography (NSG): differential diagnosis of hypoxic lesions.
- Meconium aspiration syndrome as a frequent intranasal complication of IUGR.
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