Prematurity (preterm Birth); Causes and Complications
A premature infant is a baby born before 37 completed weeks of gestation (more than 3 weeks before the due date). Prematurity is one of the common causes of infant mortality, especially in developing countries. In this article, we shall be covering the basics of prematurity, risk factors and the complications that are associated with preterm birth.
There are basic concepts that you may need to remind yourself of the classification of infants include:
- Term baby: ≥37 completed weeks' gestation
- Preterm baby: <37 completed weeks' gestation
- Post-term baby: >42 completed weeks' gestation
- Low birth weight (LBW): <2500 g
- Very low birth weight (VLBW): <1500 g
- Extremely low birth weight (ELBW): <1000 g
The premature infant
A premature infant is a baby born before 37 completed weeks of gestation (more than 3 weeks before the due date).
What are the causes of preterm birth?
In presence of a number of risk factors for preterm birth, about half of preterm births occur in the absence of recognized risk factors.
The incidence and severity of complications all decrease with increasing gestational age and birth weight as the survival rates increase.
Risk factors associated with preterm birth include;
Maternal Factors such as;
- Previous preterm birth
- Extremes of maternal age (too young or too old)
- Hypertensive disorders ie Pre-eclampsia/eclampsia
- Previous miscarriage or termination of pregnancy
- History of infertility
- In vitro fertilization (IVF)
- Uterine anomalies
- Cervical incompetence
- Low pre-pregnant weight
- Multiple gestations
- Fetal demise
- Fetal anomalies
- The first trimester threatened abortion
Placenta and membranes
- Abruptio placentae
- Placenta praevia
- Premature rupture of membranes
- Low socioeconomic status
- Smoking, alcohol abuse
- Psychological stress
- Heavy physical work
- Illicit drug abuse
complications of prematurity
Complications arising from prematurity can be categorized into short term complications that may occur immediately after birth or longterm complications that may develop some time after birth.
Short-term complications of prematurity
Respiratory distress syndrome/surfactant deficiency syndrome.
Immaturity of the respiratory system with surfactant deficiency results in respiratory distress.
RDS is managed with oxygen, nasal continuous positive airway pressure (NCPAP) and in more severe cases, surfactant administration and mechanical ventilation.
Corticosteroids such as dexamethasone injections given to the mother before preterm birth promote lung maturation reducing the incidence and severity of respiratory distress syndrome.
Periodic breathing/apnoea of prematurity
Apnoea is a cessation of breathing persisting for more than 20 seconds, or less than 20 seconds if there is associated bradycardia or desaturation. Premature babies commonly experience periodic breathing due to the immaturity of the respiratory centers of the brain.
They require cardiorespiratory and pulse oximetry monitoring to detect apnoea and associated bradycardia or desaturation.
Apnoea of prematurity occurs in almost all extremely premature babies and usually improves around 34–36 weeks' postmenstrual age.
Treatment includes methylxanthines such as caffeine or theophylline, which improve diaphragmatic contraction and stimulate the respiratory centers. NCPAP is also helpful, partly by reducing any obstructive component to the apnoea and reducing the work of breathing.
If apnoea is severe, the baby may have to be ventilated mechanically.
Apnoea can also be caused by many other complications of prematurity, such as infection, neurological problems, anemia, hypoxia, patent ductus arteriosus, and upper airway obstruction.
Patent ductus arteriosus
Before birth, the ductus arteriosus diverts blood from the right ventricle away from the lungs to the aorta. After birth it normally closes functionally within a few days. In premature babies, the closure may be delayed, leading to left-to-right shunting of blood from the aorta through the ductus to the lungs.
This results in pulmonary congestion, worsening lung disease and decreased blood flow to the gastrointestinal tract and brain. These changes have been implicated in the pathogenesis of necrotizing enterocolitis and intraventricular hemorrhage.
A significant patent ductus arteriosus (PDA) is often clinically silent, or there may be a continuous heart murmur, hyperdynamic precordium, bounding pulses, and widened pulse pressure.
The diagnosis is made by echocardiography.
A significant PDA may be treated by giving prostaglandin inhibitors (indomethacin or ibuprofen). If these are unsuccessful, surgical ligation may be necessary neurological
This is due to bleeding from the immature capillary bed of the germinal matrix lining the ventricles, often within the first 48 hours after birth.
Risk factors include asphyxia and changes in cerebral blood flow due to hypotension or rapid intravenous fluid infusion.
Intraventricular hemorrhage is diagnosed by cranial ultrasonography and varies in severity from grade I intraventricular hemorrhage (germinal matrix hemorrhage) to grade IV (intraparenchymal hemorrhage).
Although lower grades have a good prognosis, grades III and IV intraventricular hemorrhage is often associated with later hydrocephalus and neurological abnormalities such as cerebral palsy.
This is an uncommon problem, characterized by ischaemic necrosis of the white matter surrounding the lateral ventricles. Periventricular leukomalacia is diagnosed on head ultrasonography, usually at 4–6weeks of age.
It often results in cerebral palsy
Hypoglycemia is common because of decreased glycogen stores and increased glucose requirements in premature babies.
Hyperglycaemia can also occur in VLBW babies because of high glucose infusion rates, reduced insulin secretion, and impaired insulin sensitivity.
Hyperbilirubinaemia is common and due to hepatic immaturity coupled with a shorter half-life of red blood cells.
Premature babies require treatment at lower bilirubin levels than term babies because of their low albumin levels and immaturity of the blood-brain barrier place them at greater risk of bilirubin encephalopathy.
Immaturity of the kidneys results in a poor ability to concentrate or dilute the urine. This may be aggravated by immature skin leading to high insensible water losses, contributing to dehydration
hypernatraemia and hyponatremia
hyperkalemia metabolic acidosis due to inability to conserve Bicarbonate
This is an uncommon inflammatory process in the bowel wall that can lead to necrosis. Fluctuating gut blood flow, hypotension, hypoxia, infection, and feeding practices have all been implicated, but their exact contribution remains unclear.
Exclusive breast milk feeding is partially protective against necrotizing enterocolitis. Presentation of necrotizing enterocolitis can be non-specific, including apnoea, bradycardia and temperature instability, then with more focal abdominal signs such as distension, tenderness, feed intolerance, bloody stools, and bilious gastric aspirates.
Occasionally there may be rapid progression to sepsis, shock, and death. Classical X-ray findings are air in the bowel wall (pneumatosis intestinalis) and perforation of the gut.
Treatment is by the withholding of feeds, antibiotics and, if necessary, surgery.
There is emerging evidence that probiotics in the milk feeds may decrease the risk of developing necrotizing enterocolitis.
Premature babies have weak and uncoordinated suck and swallow reflexes, delayed gastric emptying and immature gut motility.
Feed intolerance and gastro-oesophageal reflux are common. Parenteral nutrition is usually required initially in extremely premature babies, with gradually increasing volumes of milk, preferably expressed breast milk, given by tube.
Supplemental vitamins, minerals, protein, and calories may also be required to allow adequate growth.
Sucking feeds are usually established at 34–36 weeks' postmenstrual age.
Anemia of prematurity
Anemia of prematurity is almost universal, as a result of low iron stores and red cell mass at birth, rapid growth, reduced erythropoiesis and decreased survival of red blood cells, aggravated by repeated blood sampling.
Treatment is supportive of transfusion in the early period and iron supplementation.
Premature babies have increased susceptibility to infection due to impaired cell-mediated immunity and reduced concentrations of complement and immunoglobulins, together with exposure to invasive procedures and monitoring.
Signs of sepsis are extremely nonspecific, including lethargy, temperature instability, apnoea, tachypnoea, feed intolerance, and jaundice.
Investigation usually requires a full blood count, blood culture, chest X-ray, bladder tap urine and lumbar puncture.
Because deterioration can be rapid, early treatment with antibiotics is an essential pending culture
This is a significant problem in the premature baby due to a relatively large body surface area, thin skin and subcutaneous tissues, and a lack of a keratinized epidermal barrier.
Nursing preterm infants in an incubator, with humidification, if necessary, maintains a stable temperature
Late-onset complications of prematurity
Retinopathy of prematurity
ROP results from disruption of the normal process of vascularization of the retina, with new vessel formation and fibrous scarring. Although ROP can result from excessive oxygen exposure, most cases occur in extremely premature babies with multiple other problems even when oxygen monitoring has been meticulous.
Severity is classified on the basis of the location and extent of ROP, from grade 1 (mild changes) to grade 4 (retinal detachment).
Most mild ROP regresses spontaneously; however, regular eye examinations are required to detect progressive ROP requiring laser therapy to reduce the chances of myopia and blindness.
Chronic lung Disease
This is usually defined as the need for supplemental oxygen at 36 weeks' postmenstrual age. It results from a combination of lung immaturity, oxygen toxicity, ventilator-induced lung injury, inflammatory, and free radical-mediated lung injury.
Babies with chronic lung disease may require supplemental oxygen for months or even years and are at increased risk of respiratory infections in the first year and adverse developmental outcomes.
Because premature babies often do not grow for 2–3 weeks after birth, most are still below birth centiles at discharge; however, steady catch-up growth is usual during the first 2 years of life. Permanent growth failure is more likely in premature babies who were also small for gestational age.
Severe impairments (cerebral palsy, mental retardation, blindness, deafness) occur in 10–15% of VLBW babies. More subtle delays in language, attention deficits, and social/behavioral difficulties are common.