Respiratory and circulatory systems
The leading problem in premature infants is respiratory distress syndrome (RDS), also known as hyaline membrane disease. It is primarily caused by primary surfactant deficiency. Without it, alveoli progressively collapse, atelectasis forms, and gas exchange is impaired.
RDS treatment is strictly algorithmic:
- Prevention: antenatal administration of glucocorticoids to the mother.
- Replacement therapy: endotracheal administration of exogenous surfactant in the first hours of life.
- Respiratory support: oxygen therapy in an incubator, continuous positive airway pressure (CPAP), or mechanical ventilation.
- Supportive therapy: strict temperature control. With hypothermia (below 35 °C), the synthesis of own surfactant stops completely.
Cardiovascular issues include arterial hypotension (requiring infusions to restore circulating blood volume and administration of glucocorticoids) and patent ductus arteriosus (PDA). PDA is closed medically (cyclooxygenase inhibitors: ibuprofen, indomethacin). If ineffective, surgical ligation of the duct is performed. Risk factors for PDA include pathological pregnancy, birth asphyxia, prematurity itself, and concomitant RDS.
Gastrointestinal and ocular pathologies
The most formidable gastrointestinal complication is necrotizing enterocolitis (NEC). It manifests against the background of intestinal wall ischemia and subsequent bacterial invasion. Often the triggering mechanism is excessive enteral load, especially with cow's milk formulas. NEC therapy boils down to functional bowel rest (switching to total parenteral nutrition), massive systemic antibiotic therapy, and respiratory support. When complications develop (perforations, peritonitis), surgical intervention is indicated. Natural feeding is resumed strictly after stabilization.
Transient dyspepsia is also common — frequent, loose stools with mucus and lumps. Causes: late initiation of breastfeeding, immaturity of the local immunity of the gastrointestinal mucosa, and sanitation and hygiene deficiencies.
Infants with extremely low birth weight frequently develop retinopathy of prematurity — a vasoproliferative retinopathy threatening retinal detachment. The process is multifactorial, provoked by:
- fluctuations in oxygenation (both hypoxia and hyperoxia during mechanical ventilation);
- antioxidant deficiency (vitamins A and E);
- toxic effects of unconjugated bilirubin;
- adult donor blood transfusions (due to differences in hemoglobin oxygen affinity).
Severe forms of the disease are treated surgically using laser retinal photocoagulation.
Neurology and metabolic disorders
Perinatal nervous system damage is caused by profound immaturity of brain structures and its vascular network. In about 30% of cases, the morphological substrate is hemorrhage and ischemia: intraventricular hemorrhage (IVH) and parenchymal hemorrhage, decompensated hydrocephalus, and periventricular leukomalacia (PVL). Management requires a strict protective regimen, normothermia, and nootropic administration. For occlusive or communicating hydrocephalus, ventriculoperitoneal shunting is performed.
A group of metabolic disorders is associated with depletion of reserves and enzyme immaturity:
- Neonatal hyperbilirubinemia. Due to the high permeability of the blood-brain barrier, bilirubin encephalopathy develops at much lower free bilirubin concentrations than in full-term infants. Treated with phototherapy, dextrose and protein infusions, and exchange blood transfusion (EBT) for critical values.
- Hypoglycemia. Liver glycogen and brown fat stores are critically small. At glucose $\le$ 2.2 mmol/L (or $\le$ 2.6 mmol/L in the absence of enteral nutrition), intravenous administration of dextrose is indicated.
- Osteopenia. The fetus did not have time to accumulate calcium, phosphate, and magnesium reserves (this occurs in the third trimester). Breast milk fortifiers, special premature formulas, multi-component parenteral solutions, and specific rickets prevention are used for bone mineralization.
The "Three NOs" rule in the metabolism of premature infants: NO glycogen (hypoglycemia), NO blood-brain barrier maturity (kernicterus at low bilirubin), NO macronutrients obtained in the 3rd trimester (osteopenia).
Class and exam questions
At what temperature does surfactant production stop?
Endogenous surfactant synthesis completely stops if the child's body temperature drops below 35 °C.
What is the management strategy for patent ductus arteriosus (PDA)?
First, medical closure of the duct is used using cyclooxygenase inhibitors (ibuprofen, indomethacin). If the conservative approach is ineffective, surgical ligation is performed.
What most often provokes the development of necrotizing enterocolitis?
The trigger for the manifestation of the disease is often early or excessive enteral load, in particular, the use of cow's milk-based formulas.
Why are premature infants prone to osteopenia?
The main reserve of calcium, magnesium, and phosphates is received by the fetus in the third trimester of pregnancy. In premature birth, the child is deprived of this depot, which leads to insufficient bone mineralization.
What else to study on this topic
- Mechanisms of development of periventricular leukomalacia (PVL)
- Indications for exchange blood transfusion in premature infants
- Surgical treatment of retinopathy: laser photocoagulation
- Parenteral nutrition regimens and breast milk fortification
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